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EN100024
|
Exam: Ki-67
|
not available
| 7 |
The patient referred to our unit for consideration for coronary artery bypass grafting was a 56 year old teacher who had been managed for Ischaemic Heart Disease (IHD) at a private cardiology facility in Lagos. She had presented in July 2009 with a history suggestive of IHD and angina class III (Canadian Cardiovascular society classification) which was worsening despite medical therapy. Coronary angiography done demonstrated significant lesions in the mid portion of the Left Descending Coronary Artery (LAD) and the proximal Circumflex Coronary Artery (Cx). The Right Coronary Artery was a dominant artery with some minor irregularities. Percutaneous transluminal coronary angioplasty of both the LAD and Cx was done. A 3.0 mm Drug Eluting Stent was deployed to stent the LAD and the Cx was stented with a 3.0mm Bare Metal Stent. The patient was angina-free for one year but represented in July 2010 again with angina class III. Repeat coronary angiogram was done which showed that both stents were patent and there was no new coronary lesion. She was controlled on medical therapy. However she presented again in November 2011, this time with unstable angina. An urgent coronary angiogram carried out showed that the previous stents were still patent but with a 50% left main stem stenosis and a 95% proximal LAD stenosis. She was subsequently referred for surgical revascularization. Physical examination on admission revealed a middle aged woman who was clinically obese with a body mass index of 32kg/m 2. There were no significant physical findings. Associated risk factors were intermittent claudication (Ankle-Brachial Index bilaterally was 0.57), bilateral carotid bruits, poorly controlled diabetes mellitus and hyperlipidemia. Her calculated euroscore was 6. Medications on admission were Aspirin, Glyceryl trinitrate sublingual spray, Metformin, Glibenclamide, Fluvastatin, Metoprolol and Isosorbide Dinitrate. Investigations done included transthoracic echocardiogram which showed good left ventricular ejection fraction with no evidence of ventricular dysfunction. Chest radiogram, 12 lead electrocardiogram and pulmonary function tests were normal. All blood parameters were within acceptable limits. Following review of her coronary angiogram she was scheduled for single vessel grafting of the LAD as an off pump procedure. Surgery was performed in November 2011. The cardiopulmonary bypass circuit was not primed. Following median sternotomy and harvesting of the Left Internal Mammary Artery (LIMA) the Octopus 3 Off-pump stabilizer and foot plate were used to immobilize the anterior myocardial surface with good visualization of the LAD. The LAD which was a 2.5mm vessel was snugged proximally and an arteriotomy performed in its mid-portion. The arteriotomy site was kept bloodless with CO2 insufflation via an improvised blow-mister. The LIMA to LAD anastomosis was performed with 6-0 prolene suture. The procedure was uneventful and the patient was transferred to the Intensive Care Unit on minimal inotropic support. She was weaned off the ventilator after 4 hours and inotropic support was discontinued after 24 hours. Postoperative recovery was delayed by the need to achieve glycaecmic control. She was discharged home 2 weeks postoperatively. She has been reviewed in clinic and remains free of angina.
|
EN100024
|
Exam: pressure
|
not available
| 7 |
The patient referred to our unit for consideration for coronary artery bypass grafting was a 56 year old teacher who had been managed for Ischaemic Heart Disease (IHD) at a private cardiology facility in Lagos. She had presented in July 2009 with a history suggestive of IHD and angina class III (Canadian Cardiovascular society classification) which was worsening despite medical therapy. Coronary angiography done demonstrated significant lesions in the mid portion of the Left Descending Coronary Artery (LAD) and the proximal Circumflex Coronary Artery (Cx). The Right Coronary Artery was a dominant artery with some minor irregularities. Percutaneous transluminal coronary angioplasty of both the LAD and Cx was done. A 3.0 mm Drug Eluting Stent was deployed to stent the LAD and the Cx was stented with a 3.0mm Bare Metal Stent. The patient was angina-free for one year but represented in July 2010 again with angina class III. Repeat coronary angiogram was done which showed that both stents were patent and there was no new coronary lesion. She was controlled on medical therapy. However she presented again in November 2011, this time with unstable angina. An urgent coronary angiogram carried out showed that the previous stents were still patent but with a 50% left main stem stenosis and a 95% proximal LAD stenosis. She was subsequently referred for surgical revascularization. Physical examination on admission revealed a middle aged woman who was clinically obese with a body mass index of 32kg/m 2. There were no significant physical findings. Associated risk factors were intermittent claudication (Ankle-Brachial Index bilaterally was 0.57), bilateral carotid bruits, poorly controlled diabetes mellitus and hyperlipidemia. Her calculated euroscore was 6. Medications on admission were Aspirin, Glyceryl trinitrate sublingual spray, Metformin, Glibenclamide, Fluvastatin, Metoprolol and Isosorbide Dinitrate. Investigations done included transthoracic echocardiogram which showed good left ventricular ejection fraction with no evidence of ventricular dysfunction. Chest radiogram, 12 lead electrocardiogram and pulmonary function tests were normal. All blood parameters were within acceptable limits. Following review of her coronary angiogram she was scheduled for single vessel grafting of the LAD as an off pump procedure. Surgery was performed in November 2011. The cardiopulmonary bypass circuit was not primed. Following median sternotomy and harvesting of the Left Internal Mammary Artery (LIMA) the Octopus 3 Off-pump stabilizer and foot plate were used to immobilize the anterior myocardial surface with good visualization of the LAD. The LAD which was a 2.5mm vessel was snugged proximally and an arteriotomy performed in its mid-portion. The arteriotomy site was kept bloodless with CO2 insufflation via an improvised blow-mister. The LIMA to LAD anastomosis was performed with 6-0 prolene suture. The procedure was uneventful and the patient was transferred to the Intensive Care Unit on minimal inotropic support. She was weaned off the ventilator after 4 hours and inotropic support was discontinued after 24 hours. Postoperative recovery was delayed by the need to achieve glycaecmic control. She was discharged home 2 weeks postoperatively. She has been reviewed in clinic and remains free of angina.
|
EN100024
|
Exam: HIV
|
not available
| 7 |
The patient referred to our unit for consideration for coronary artery bypass grafting was a 56 year old teacher who had been managed for Ischaemic Heart Disease (IHD) at a private cardiology facility in Lagos. She had presented in July 2009 with a history suggestive of IHD and angina class III (Canadian Cardiovascular society classification) which was worsening despite medical therapy. Coronary angiography done demonstrated significant lesions in the mid portion of the Left Descending Coronary Artery (LAD) and the proximal Circumflex Coronary Artery (Cx). The Right Coronary Artery was a dominant artery with some minor irregularities. Percutaneous transluminal coronary angioplasty of both the LAD and Cx was done. A 3.0 mm Drug Eluting Stent was deployed to stent the LAD and the Cx was stented with a 3.0mm Bare Metal Stent. The patient was angina-free for one year but represented in July 2010 again with angina class III. Repeat coronary angiogram was done which showed that both stents were patent and there was no new coronary lesion. She was controlled on medical therapy. However she presented again in November 2011, this time with unstable angina. An urgent coronary angiogram carried out showed that the previous stents were still patent but with a 50% left main stem stenosis and a 95% proximal LAD stenosis. She was subsequently referred for surgical revascularization. Physical examination on admission revealed a middle aged woman who was clinically obese with a body mass index of 32kg/m 2. There were no significant physical findings. Associated risk factors were intermittent claudication (Ankle-Brachial Index bilaterally was 0.57), bilateral carotid bruits, poorly controlled diabetes mellitus and hyperlipidemia. Her calculated euroscore was 6. Medications on admission were Aspirin, Glyceryl trinitrate sublingual spray, Metformin, Glibenclamide, Fluvastatin, Metoprolol and Isosorbide Dinitrate. Investigations done included transthoracic echocardiogram which showed good left ventricular ejection fraction with no evidence of ventricular dysfunction. Chest radiogram, 12 lead electrocardiogram and pulmonary function tests were normal. All blood parameters were within acceptable limits. Following review of her coronary angiogram she was scheduled for single vessel grafting of the LAD as an off pump procedure. Surgery was performed in November 2011. The cardiopulmonary bypass circuit was not primed. Following median sternotomy and harvesting of the Left Internal Mammary Artery (LIMA) the Octopus 3 Off-pump stabilizer and foot plate were used to immobilize the anterior myocardial surface with good visualization of the LAD. The LAD which was a 2.5mm vessel was snugged proximally and an arteriotomy performed in its mid-portion. The arteriotomy site was kept bloodless with CO2 insufflation via an improvised blow-mister. The LIMA to LAD anastomosis was performed with 6-0 prolene suture. The procedure was uneventful and the patient was transferred to the Intensive Care Unit on minimal inotropic support. She was weaned off the ventilator after 4 hours and inotropic support was discontinued after 24 hours. Postoperative recovery was delayed by the need to achieve glycaecmic control. She was discharged home 2 weeks postoperatively. She has been reviewed in clinic and remains free of angina.
|
EN100024
|
Exam: HCV
|
not available
| 7 |
The patient referred to our unit for consideration for coronary artery bypass grafting was a 56 year old teacher who had been managed for Ischaemic Heart Disease (IHD) at a private cardiology facility in Lagos. She had presented in July 2009 with a history suggestive of IHD and angina class III (Canadian Cardiovascular society classification) which was worsening despite medical therapy. Coronary angiography done demonstrated significant lesions in the mid portion of the Left Descending Coronary Artery (LAD) and the proximal Circumflex Coronary Artery (Cx). The Right Coronary Artery was a dominant artery with some minor irregularities. Percutaneous transluminal coronary angioplasty of both the LAD and Cx was done. A 3.0 mm Drug Eluting Stent was deployed to stent the LAD and the Cx was stented with a 3.0mm Bare Metal Stent. The patient was angina-free for one year but represented in July 2010 again with angina class III. Repeat coronary angiogram was done which showed that both stents were patent and there was no new coronary lesion. She was controlled on medical therapy. However she presented again in November 2011, this time with unstable angina. An urgent coronary angiogram carried out showed that the previous stents were still patent but with a 50% left main stem stenosis and a 95% proximal LAD stenosis. She was subsequently referred for surgical revascularization. Physical examination on admission revealed a middle aged woman who was clinically obese with a body mass index of 32kg/m 2. There were no significant physical findings. Associated risk factors were intermittent claudication (Ankle-Brachial Index bilaterally was 0.57), bilateral carotid bruits, poorly controlled diabetes mellitus and hyperlipidemia. Her calculated euroscore was 6. Medications on admission were Aspirin, Glyceryl trinitrate sublingual spray, Metformin, Glibenclamide, Fluvastatin, Metoprolol and Isosorbide Dinitrate. Investigations done included transthoracic echocardiogram which showed good left ventricular ejection fraction with no evidence of ventricular dysfunction. Chest radiogram, 12 lead electrocardiogram and pulmonary function tests were normal. All blood parameters were within acceptable limits. Following review of her coronary angiogram she was scheduled for single vessel grafting of the LAD as an off pump procedure. Surgery was performed in November 2011. The cardiopulmonary bypass circuit was not primed. Following median sternotomy and harvesting of the Left Internal Mammary Artery (LIMA) the Octopus 3 Off-pump stabilizer and foot plate were used to immobilize the anterior myocardial surface with good visualization of the LAD. The LAD which was a 2.5mm vessel was snugged proximally and an arteriotomy performed in its mid-portion. The arteriotomy site was kept bloodless with CO2 insufflation via an improvised blow-mister. The LIMA to LAD anastomosis was performed with 6-0 prolene suture. The procedure was uneventful and the patient was transferred to the Intensive Care Unit on minimal inotropic support. She was weaned off the ventilator after 4 hours and inotropic support was discontinued after 24 hours. Postoperative recovery was delayed by the need to achieve glycaecmic control. She was discharged home 2 weeks postoperatively. She has been reviewed in clinic and remains free of angina.
|
EN100024
|
Exam: HB
|
not available
| 7 |
The patient referred to our unit for consideration for coronary artery bypass grafting was a 56 year old teacher who had been managed for Ischaemic Heart Disease (IHD) at a private cardiology facility in Lagos. She had presented in July 2009 with a history suggestive of IHD and angina class III (Canadian Cardiovascular society classification) which was worsening despite medical therapy. Coronary angiography done demonstrated significant lesions in the mid portion of the Left Descending Coronary Artery (LAD) and the proximal Circumflex Coronary Artery (Cx). The Right Coronary Artery was a dominant artery with some minor irregularities. Percutaneous transluminal coronary angioplasty of both the LAD and Cx was done. A 3.0 mm Drug Eluting Stent was deployed to stent the LAD and the Cx was stented with a 3.0mm Bare Metal Stent. The patient was angina-free for one year but represented in July 2010 again with angina class III. Repeat coronary angiogram was done which showed that both stents were patent and there was no new coronary lesion. She was controlled on medical therapy. However she presented again in November 2011, this time with unstable angina. An urgent coronary angiogram carried out showed that the previous stents were still patent but with a 50% left main stem stenosis and a 95% proximal LAD stenosis. She was subsequently referred for surgical revascularization. Physical examination on admission revealed a middle aged woman who was clinically obese with a body mass index of 32kg/m 2. There were no significant physical findings. Associated risk factors were intermittent claudication (Ankle-Brachial Index bilaterally was 0.57), bilateral carotid bruits, poorly controlled diabetes mellitus and hyperlipidemia. Her calculated euroscore was 6. Medications on admission were Aspirin, Glyceryl trinitrate sublingual spray, Metformin, Glibenclamide, Fluvastatin, Metoprolol and Isosorbide Dinitrate. Investigations done included transthoracic echocardiogram which showed good left ventricular ejection fraction with no evidence of ventricular dysfunction. Chest radiogram, 12 lead electrocardiogram and pulmonary function tests were normal. All blood parameters were within acceptable limits. Following review of her coronary angiogram she was scheduled for single vessel grafting of the LAD as an off pump procedure. Surgery was performed in November 2011. The cardiopulmonary bypass circuit was not primed. Following median sternotomy and harvesting of the Left Internal Mammary Artery (LIMA) the Octopus 3 Off-pump stabilizer and foot plate were used to immobilize the anterior myocardial surface with good visualization of the LAD. The LAD which was a 2.5mm vessel was snugged proximally and an arteriotomy performed in its mid-portion. The arteriotomy site was kept bloodless with CO2 insufflation via an improvised blow-mister. The LIMA to LAD anastomosis was performed with 6-0 prolene suture. The procedure was uneventful and the patient was transferred to the Intensive Care Unit on minimal inotropic support. She was weaned off the ventilator after 4 hours and inotropic support was discontinued after 24 hours. Postoperative recovery was delayed by the need to achieve glycaecmic control. She was discharged home 2 weeks postoperatively. She has been reviewed in clinic and remains free of angina.
|
EN100024
|
Exam: Platelets
|
not available
| 7 |
The patient referred to our unit for consideration for coronary artery bypass grafting was a 56 year old teacher who had been managed for Ischaemic Heart Disease (IHD) at a private cardiology facility in Lagos. She had presented in July 2009 with a history suggestive of IHD and angina class III (Canadian Cardiovascular society classification) which was worsening despite medical therapy. Coronary angiography done demonstrated significant lesions in the mid portion of the Left Descending Coronary Artery (LAD) and the proximal Circumflex Coronary Artery (Cx). The Right Coronary Artery was a dominant artery with some minor irregularities. Percutaneous transluminal coronary angioplasty of both the LAD and Cx was done. A 3.0 mm Drug Eluting Stent was deployed to stent the LAD and the Cx was stented with a 3.0mm Bare Metal Stent. The patient was angina-free for one year but represented in July 2010 again with angina class III. Repeat coronary angiogram was done which showed that both stents were patent and there was no new coronary lesion. She was controlled on medical therapy. However she presented again in November 2011, this time with unstable angina. An urgent coronary angiogram carried out showed that the previous stents were still patent but with a 50% left main stem stenosis and a 95% proximal LAD stenosis. She was subsequently referred for surgical revascularization. Physical examination on admission revealed a middle aged woman who was clinically obese with a body mass index of 32kg/m 2. There were no significant physical findings. Associated risk factors were intermittent claudication (Ankle-Brachial Index bilaterally was 0.57), bilateral carotid bruits, poorly controlled diabetes mellitus and hyperlipidemia. Her calculated euroscore was 6. Medications on admission were Aspirin, Glyceryl trinitrate sublingual spray, Metformin, Glibenclamide, Fluvastatin, Metoprolol and Isosorbide Dinitrate. Investigations done included transthoracic echocardiogram which showed good left ventricular ejection fraction with no evidence of ventricular dysfunction. Chest radiogram, 12 lead electrocardiogram and pulmonary function tests were normal. All blood parameters were within acceptable limits. Following review of her coronary angiogram she was scheduled for single vessel grafting of the LAD as an off pump procedure. Surgery was performed in November 2011. The cardiopulmonary bypass circuit was not primed. Following median sternotomy and harvesting of the Left Internal Mammary Artery (LIMA) the Octopus 3 Off-pump stabilizer and foot plate were used to immobilize the anterior myocardial surface with good visualization of the LAD. The LAD which was a 2.5mm vessel was snugged proximally and an arteriotomy performed in its mid-portion. The arteriotomy site was kept bloodless with CO2 insufflation via an improvised blow-mister. The LIMA to LAD anastomosis was performed with 6-0 prolene suture. The procedure was uneventful and the patient was transferred to the Intensive Care Unit on minimal inotropic support. She was weaned off the ventilator after 4 hours and inotropic support was discontinued after 24 hours. Postoperative recovery was delayed by the need to achieve glycaecmic control. She was discharged home 2 weeks postoperatively. She has been reviewed in clinic and remains free of angina.
|
EN100024
|
Exam: INR
|
not available
| 7 |
The patient referred to our unit for consideration for coronary artery bypass grafting was a 56 year old teacher who had been managed for Ischaemic Heart Disease (IHD) at a private cardiology facility in Lagos. She had presented in July 2009 with a history suggestive of IHD and angina class III (Canadian Cardiovascular society classification) which was worsening despite medical therapy. Coronary angiography done demonstrated significant lesions in the mid portion of the Left Descending Coronary Artery (LAD) and the proximal Circumflex Coronary Artery (Cx). The Right Coronary Artery was a dominant artery with some minor irregularities. Percutaneous transluminal coronary angioplasty of both the LAD and Cx was done. A 3.0 mm Drug Eluting Stent was deployed to stent the LAD and the Cx was stented with a 3.0mm Bare Metal Stent. The patient was angina-free for one year but represented in July 2010 again with angina class III. Repeat coronary angiogram was done which showed that both stents were patent and there was no new coronary lesion. She was controlled on medical therapy. However she presented again in November 2011, this time with unstable angina. An urgent coronary angiogram carried out showed that the previous stents were still patent but with a 50% left main stem stenosis and a 95% proximal LAD stenosis. She was subsequently referred for surgical revascularization. Physical examination on admission revealed a middle aged woman who was clinically obese with a body mass index of 32kg/m 2. There were no significant physical findings. Associated risk factors were intermittent claudication (Ankle-Brachial Index bilaterally was 0.57), bilateral carotid bruits, poorly controlled diabetes mellitus and hyperlipidemia. Her calculated euroscore was 6. Medications on admission were Aspirin, Glyceryl trinitrate sublingual spray, Metformin, Glibenclamide, Fluvastatin, Metoprolol and Isosorbide Dinitrate. Investigations done included transthoracic echocardiogram which showed good left ventricular ejection fraction with no evidence of ventricular dysfunction. Chest radiogram, 12 lead electrocardiogram and pulmonary function tests were normal. All blood parameters were within acceptable limits. Following review of her coronary angiogram she was scheduled for single vessel grafting of the LAD as an off pump procedure. Surgery was performed in November 2011. The cardiopulmonary bypass circuit was not primed. Following median sternotomy and harvesting of the Left Internal Mammary Artery (LIMA) the Octopus 3 Off-pump stabilizer and foot plate were used to immobilize the anterior myocardial surface with good visualization of the LAD. The LAD which was a 2.5mm vessel was snugged proximally and an arteriotomy performed in its mid-portion. The arteriotomy site was kept bloodless with CO2 insufflation via an improvised blow-mister. The LIMA to LAD anastomosis was performed with 6-0 prolene suture. The procedure was uneventful and the patient was transferred to the Intensive Care Unit on minimal inotropic support. She was weaned off the ventilator after 4 hours and inotropic support was discontinued after 24 hours. Postoperative recovery was delayed by the need to achieve glycaecmic control. She was discharged home 2 weeks postoperatively. She has been reviewed in clinic and remains free of angina.
|
EN100024
|
Exam: AFP
|
not available
| 7 |
The patient referred to our unit for consideration for coronary artery bypass grafting was a 56 year old teacher who had been managed for Ischaemic Heart Disease (IHD) at a private cardiology facility in Lagos. She had presented in July 2009 with a history suggestive of IHD and angina class III (Canadian Cardiovascular society classification) which was worsening despite medical therapy. Coronary angiography done demonstrated significant lesions in the mid portion of the Left Descending Coronary Artery (LAD) and the proximal Circumflex Coronary Artery (Cx). The Right Coronary Artery was a dominant artery with some minor irregularities. Percutaneous transluminal coronary angioplasty of both the LAD and Cx was done. A 3.0 mm Drug Eluting Stent was deployed to stent the LAD and the Cx was stented with a 3.0mm Bare Metal Stent. The patient was angina-free for one year but represented in July 2010 again with angina class III. Repeat coronary angiogram was done which showed that both stents were patent and there was no new coronary lesion. She was controlled on medical therapy. However she presented again in November 2011, this time with unstable angina. An urgent coronary angiogram carried out showed that the previous stents were still patent but with a 50% left main stem stenosis and a 95% proximal LAD stenosis. She was subsequently referred for surgical revascularization. Physical examination on admission revealed a middle aged woman who was clinically obese with a body mass index of 32kg/m 2. There were no significant physical findings. Associated risk factors were intermittent claudication (Ankle-Brachial Index bilaterally was 0.57), bilateral carotid bruits, poorly controlled diabetes mellitus and hyperlipidemia. Her calculated euroscore was 6. Medications on admission were Aspirin, Glyceryl trinitrate sublingual spray, Metformin, Glibenclamide, Fluvastatin, Metoprolol and Isosorbide Dinitrate. Investigations done included transthoracic echocardiogram which showed good left ventricular ejection fraction with no evidence of ventricular dysfunction. Chest radiogram, 12 lead electrocardiogram and pulmonary function tests were normal. All blood parameters were within acceptable limits. Following review of her coronary angiogram she was scheduled for single vessel grafting of the LAD as an off pump procedure. Surgery was performed in November 2011. The cardiopulmonary bypass circuit was not primed. Following median sternotomy and harvesting of the Left Internal Mammary Artery (LIMA) the Octopus 3 Off-pump stabilizer and foot plate were used to immobilize the anterior myocardial surface with good visualization of the LAD. The LAD which was a 2.5mm vessel was snugged proximally and an arteriotomy performed in its mid-portion. The arteriotomy site was kept bloodless with CO2 insufflation via an improvised blow-mister. The LIMA to LAD anastomosis was performed with 6-0 prolene suture. The procedure was uneventful and the patient was transferred to the Intensive Care Unit on minimal inotropic support. She was weaned off the ventilator after 4 hours and inotropic support was discontinued after 24 hours. Postoperative recovery was delayed by the need to achieve glycaecmic control. She was discharged home 2 weeks postoperatively. She has been reviewed in clinic and remains free of angina.
|
EN100024
|
Exam: Her2neu
|
not available
| 7 |
The patient referred to our unit for consideration for coronary artery bypass grafting was a 56 year old teacher who had been managed for Ischaemic Heart Disease (IHD) at a private cardiology facility in Lagos. She had presented in July 2009 with a history suggestive of IHD and angina class III (Canadian Cardiovascular society classification) which was worsening despite medical therapy. Coronary angiography done demonstrated significant lesions in the mid portion of the Left Descending Coronary Artery (LAD) and the proximal Circumflex Coronary Artery (Cx). The Right Coronary Artery was a dominant artery with some minor irregularities. Percutaneous transluminal coronary angioplasty of both the LAD and Cx was done. A 3.0 mm Drug Eluting Stent was deployed to stent the LAD and the Cx was stented with a 3.0mm Bare Metal Stent. The patient was angina-free for one year but represented in July 2010 again with angina class III. Repeat coronary angiogram was done which showed that both stents were patent and there was no new coronary lesion. She was controlled on medical therapy. However she presented again in November 2011, this time with unstable angina. An urgent coronary angiogram carried out showed that the previous stents were still patent but with a 50% left main stem stenosis and a 95% proximal LAD stenosis. She was subsequently referred for surgical revascularization. Physical examination on admission revealed a middle aged woman who was clinically obese with a body mass index of 32kg/m 2. There were no significant physical findings. Associated risk factors were intermittent claudication (Ankle-Brachial Index bilaterally was 0.57), bilateral carotid bruits, poorly controlled diabetes mellitus and hyperlipidemia. Her calculated euroscore was 6. Medications on admission were Aspirin, Glyceryl trinitrate sublingual spray, Metformin, Glibenclamide, Fluvastatin, Metoprolol and Isosorbide Dinitrate. Investigations done included transthoracic echocardiogram which showed good left ventricular ejection fraction with no evidence of ventricular dysfunction. Chest radiogram, 12 lead electrocardiogram and pulmonary function tests were normal. All blood parameters were within acceptable limits. Following review of her coronary angiogram she was scheduled for single vessel grafting of the LAD as an off pump procedure. Surgery was performed in November 2011. The cardiopulmonary bypass circuit was not primed. Following median sternotomy and harvesting of the Left Internal Mammary Artery (LIMA) the Octopus 3 Off-pump stabilizer and foot plate were used to immobilize the anterior myocardial surface with good visualization of the LAD. The LAD which was a 2.5mm vessel was snugged proximally and an arteriotomy performed in its mid-portion. The arteriotomy site was kept bloodless with CO2 insufflation via an improvised blow-mister. The LIMA to LAD anastomosis was performed with 6-0 prolene suture. The procedure was uneventful and the patient was transferred to the Intensive Care Unit on minimal inotropic support. She was weaned off the ventilator after 4 hours and inotropic support was discontinued after 24 hours. Postoperative recovery was delayed by the need to achieve glycaecmic control. She was discharged home 2 weeks postoperatively. She has been reviewed in clinic and remains free of angina.
|
EN100024
|
Exam: ER
|
not available
| 7 |
The patient referred to our unit for consideration for coronary artery bypass grafting was a 56 year old teacher who had been managed for Ischaemic Heart Disease (IHD) at a private cardiology facility in Lagos. She had presented in July 2009 with a history suggestive of IHD and angina class III (Canadian Cardiovascular society classification) which was worsening despite medical therapy. Coronary angiography done demonstrated significant lesions in the mid portion of the Left Descending Coronary Artery (LAD) and the proximal Circumflex Coronary Artery (Cx). The Right Coronary Artery was a dominant artery with some minor irregularities. Percutaneous transluminal coronary angioplasty of both the LAD and Cx was done. A 3.0 mm Drug Eluting Stent was deployed to stent the LAD and the Cx was stented with a 3.0mm Bare Metal Stent. The patient was angina-free for one year but represented in July 2010 again with angina class III. Repeat coronary angiogram was done which showed that both stents were patent and there was no new coronary lesion. She was controlled on medical therapy. However she presented again in November 2011, this time with unstable angina. An urgent coronary angiogram carried out showed that the previous stents were still patent but with a 50% left main stem stenosis and a 95% proximal LAD stenosis. She was subsequently referred for surgical revascularization. Physical examination on admission revealed a middle aged woman who was clinically obese with a body mass index of 32kg/m 2. There were no significant physical findings. Associated risk factors were intermittent claudication (Ankle-Brachial Index bilaterally was 0.57), bilateral carotid bruits, poorly controlled diabetes mellitus and hyperlipidemia. Her calculated euroscore was 6. Medications on admission were Aspirin, Glyceryl trinitrate sublingual spray, Metformin, Glibenclamide, Fluvastatin, Metoprolol and Isosorbide Dinitrate. Investigations done included transthoracic echocardiogram which showed good left ventricular ejection fraction with no evidence of ventricular dysfunction. Chest radiogram, 12 lead electrocardiogram and pulmonary function tests were normal. All blood parameters were within acceptable limits. Following review of her coronary angiogram she was scheduled for single vessel grafting of the LAD as an off pump procedure. Surgery was performed in November 2011. The cardiopulmonary bypass circuit was not primed. Following median sternotomy and harvesting of the Left Internal Mammary Artery (LIMA) the Octopus 3 Off-pump stabilizer and foot plate were used to immobilize the anterior myocardial surface with good visualization of the LAD. The LAD which was a 2.5mm vessel was snugged proximally and an arteriotomy performed in its mid-portion. The arteriotomy site was kept bloodless with CO2 insufflation via an improvised blow-mister. The LIMA to LAD anastomosis was performed with 6-0 prolene suture. The procedure was uneventful and the patient was transferred to the Intensive Care Unit on minimal inotropic support. She was weaned off the ventilator after 4 hours and inotropic support was discontinued after 24 hours. Postoperative recovery was delayed by the need to achieve glycaecmic control. She was discharged home 2 weeks postoperatively. She has been reviewed in clinic and remains free of angina.
|
EN100024
|
Exam: PR
|
not available
| 7 |
The patient referred to our unit for consideration for coronary artery bypass grafting was a 56 year old teacher who had been managed for Ischaemic Heart Disease (IHD) at a private cardiology facility in Lagos. She had presented in July 2009 with a history suggestive of IHD and angina class III (Canadian Cardiovascular society classification) which was worsening despite medical therapy. Coronary angiography done demonstrated significant lesions in the mid portion of the Left Descending Coronary Artery (LAD) and the proximal Circumflex Coronary Artery (Cx). The Right Coronary Artery was a dominant artery with some minor irregularities. Percutaneous transluminal coronary angioplasty of both the LAD and Cx was done. A 3.0 mm Drug Eluting Stent was deployed to stent the LAD and the Cx was stented with a 3.0mm Bare Metal Stent. The patient was angina-free for one year but represented in July 2010 again with angina class III. Repeat coronary angiogram was done which showed that both stents were patent and there was no new coronary lesion. She was controlled on medical therapy. However she presented again in November 2011, this time with unstable angina. An urgent coronary angiogram carried out showed that the previous stents were still patent but with a 50% left main stem stenosis and a 95% proximal LAD stenosis. She was subsequently referred for surgical revascularization. Physical examination on admission revealed a middle aged woman who was clinically obese with a body mass index of 32kg/m 2. There were no significant physical findings. Associated risk factors were intermittent claudication (Ankle-Brachial Index bilaterally was 0.57), bilateral carotid bruits, poorly controlled diabetes mellitus and hyperlipidemia. Her calculated euroscore was 6. Medications on admission were Aspirin, Glyceryl trinitrate sublingual spray, Metformin, Glibenclamide, Fluvastatin, Metoprolol and Isosorbide Dinitrate. Investigations done included transthoracic echocardiogram which showed good left ventricular ejection fraction with no evidence of ventricular dysfunction. Chest radiogram, 12 lead electrocardiogram and pulmonary function tests were normal. All blood parameters were within acceptable limits. Following review of her coronary angiogram she was scheduled for single vessel grafting of the LAD as an off pump procedure. Surgery was performed in November 2011. The cardiopulmonary bypass circuit was not primed. Following median sternotomy and harvesting of the Left Internal Mammary Artery (LIMA) the Octopus 3 Off-pump stabilizer and foot plate were used to immobilize the anterior myocardial surface with good visualization of the LAD. The LAD which was a 2.5mm vessel was snugged proximally and an arteriotomy performed in its mid-portion. The arteriotomy site was kept bloodless with CO2 insufflation via an improvised blow-mister. The LIMA to LAD anastomosis was performed with 6-0 prolene suture. The procedure was uneventful and the patient was transferred to the Intensive Care Unit on minimal inotropic support. She was weaned off the ventilator after 4 hours and inotropic support was discontinued after 24 hours. Postoperative recovery was delayed by the need to achieve glycaecmic control. She was discharged home 2 weeks postoperatively. She has been reviewed in clinic and remains free of angina.
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EN100029
|
Exam: radiogram
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
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EN100029
|
Exam: electrocardiogram
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
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EN100029
|
Exam: phosphokinase
|
59000U/L.
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
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EN100029
|
Exam: troponin
|
21ng/ml.
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
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EN100029
|
Exam: lymphopenia
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
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EN100029
|
Exam: globulin
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
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EN100029
|
Exam: nitrogen
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
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EN100029
|
Exam: cholesterol
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
|
EN100029
|
Exam: Echocardiogram
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
|
EN100029
|
Exam: hemoglobin
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
|
EN100029
|
Exam: amylase
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
|
EN100029
|
Exam: lipase
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
|
EN100029
|
Exam: cytokeratin
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
|
EN100029
|
Exam: CK7
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
|
EN100029
|
Exam: synaptophysin
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
|
EN100029
|
Exam: CD56
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
|
EN100029
|
Exam: SCAN
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
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EN100029
|
Exam: fever
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not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
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EN100029
|
Exam: WBC
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
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EN100029
|
Exam: aminotransferase
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
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EN100029
|
Exam: ALT
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
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EN100029
|
Exam: LDH
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
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EN100029
|
Exam: phosphatase
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
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EN100029
|
Exam: Entamoeba
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
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EN100029
|
Exam: echinococcus
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
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EN100029
|
Exam: leismania
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
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EN100029
|
Exam: brucella
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
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EN100029
|
Exam: amikacin
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
|
EN100029
|
Exam: cefepime
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
|
EN100029
|
Exam: ciprofloxacin
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
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EN100029
|
Exam: gentamycin
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
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EN100029
|
Exam: meropenem
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
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EN100029
|
Exam: chromogranin
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
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EN100029
|
Exam: Synaptophysin
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
|
EN100029
|
Exam: CD10
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
|
EN100029
|
Exam: Ki-67
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
|
EN100029
|
Exam: pressure
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
|
EN100029
|
Exam: HIV
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
|
EN100029
|
Exam: HCV
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
|
EN100029
|
Exam: HB
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
|
EN100029
|
Exam: Platelets
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
|
EN100029
|
Exam: INR
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
|
EN100029
|
Exam: AFP
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
|
EN100029
|
Exam: Her2neu
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
|
EN100029
|
Exam: ER
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
|
EN100029
|
Exam: PR
|
not available
| 7 |
A 17 year-old woman with a history of moderate persistent allergic asthma has benefited from a first desensitization protocol at age 3. The protocol has been interrupted 4 years later because of a mild skin reaction. Her doctor decided to stop the specific immunotherapy. But another doctor restarted a new protocol of desensitization at age 16 against pollens because of a lack of control of his condition. She was never hospitalized, she was receiving no medication and she was doing well one year after she received a new regimen of pneumallergens (Alustal® Stallergenes SA, France). Indeed, 12 hours after initiation of treatment, she complained of abdominal pain, vomiting and diarrhea without fever. Several hours after, she consulted to the emergency department where a surgical emergency was ruled out. She was then admitted to the internal medicine ward. Two days later, she developed an acute respiratory failure and was referred to the intensive care unit where laboratory tests revealed multiorgan failure: liver enzymes, 5000U/L (normal level, 0-37U/L); creatine phosphokinase, 59000U/L (normal level, 10-200U/L); cardiac troponin T, 21ng/ml (normal level, under 0,01ng/ml); leucopenia, 2600/mm 3 (normal level, 4000-9000/ mm 3); thrombocytopenia, 13000/ mm 3 (normal level, 150000-400000/ mm 3); prothrombin time, 38% (normal level, 70-100%). Chest X-ray demonstrated bilateral interstitial markings with a normal cardiac silhouette. Viral serology was normal for hepatitis A, B, C, D, and E, Epstein-Barr virus and Cytomegalovirus. A skin morbilliform rash and facial edema appeared later. The patient received a fluid resuscitation, platelet and erythrocyte transfusion, steroids and antibiotics. A hypoxic coma occurred on day 4 leading to intubation and mechanical ventilation. Rapidly, she experienced intractable shock and acute renal impairment despite inotropic agents leading to death on day 5.
|
EN100310
|
Exam: radiogram
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: electrocardiogram
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: phosphokinase
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: troponin
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: lymphopenia
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: globulin
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: nitrogen
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: cholesterol
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: Echocardiogram
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: hemoglobin
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: amylase
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: lipase
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: cytokeratin
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: CK7
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: synaptophysin
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: CD56
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: SCAN
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: fever
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: WBC
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: aminotransferase
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: ALT
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: LDH
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: phosphatase
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: Entamoeba
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: echinococcus
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: leismania
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: brucella
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: amikacin
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: cefepime
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: ciprofloxacin
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: gentamycin
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: meropenem
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: chromogranin
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: Synaptophysin
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: CD10
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: Ki-67
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: pressure
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: HIV
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: HCV
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: HB
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: Platelets
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: INR
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
EN100310
|
Exam: AFP
|
not available
| 7 |
We present a case of a 32-year-old woman with a history of gradual enlargement of the anterior neck. The medical history was unremarkable and no comorbidities existed. There was no history of radiation exposure. Clinical examination revealed a multinodular goiter.
Computed tomography showed a thyroid nodule of the left lobe extended to the isthmus and the right lobe with anterior and posterior capsular rupture contracting close contact with the vascular axis left carotid-jugular plunging into the cervicothoracic away from the hole aortic arch.
There was no evidence of lung lesions. The patient underwent a surgical exploration. There was a hard left lobe nodule of 5 cm infiltrating the adjacent muscles and partially infiltrates the trachea. The intraoperative consultation pathology diagnosis was: undifferentiated carcinoma. A total thyroidectomy was realized. Histological examination showed a proliferation of elongated spindle-shaped cells, arranged in interweaving fascicles of varying sizes, intersected at right angles. Tumor cells are atypical with strange nuclei. Chromatin is distributed inhomogeneously. The cytoplasmic membrane is irregular and thick. The nucleolus is very large. The tumor realize a pushing against thyroid parenchyma which is separated with a fibrous capsule. The mitotic rate was extremely high (19 mitosis/10 high power field), and atypical mitotic figures were also present. The neoplasia showed invasion of the peri-glandular fat tissue.
Immuno-histochemical staining of the slides with caldesmon, desmin, PanCK, CK5-6, CK7, myogenin, epithelial membrane antigen (EMA), CEA, thyroid transcription factor (TTF-1), pancytokeratin, smooth muscle actin (SMA), MelanA, S 100 protein, CD 45, CD3, CD30, CD 20, CD 15, CD34, ALK, calcitonin and KI 67 protein was performed. The tumour was strongly positive for caldesmon, SMA, desmin, and negative for pancytokeratin and other epithelial, lymphoid and melanocytic markers. On the basis of the clinical, radiographic, histopathological and immunohistochemical features, the final diagnosis was primary thyroid leiomyosarcoma, FNCLCC grade 3.
In multidisciplinary tumour board, it was decided that adjuvant loco regional RT and chemotherapy by ifosfamide and doxorubicin.
|
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