Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An 86-year-old woman with a 13-year history of hypertension was admitted because of consciousness disturbance, hypotension, tachycardia, and cyanosis at her extremities. Enhanced computed tomography showed a thrombus in the truncus pulmonalis and right pulmonary artery, and also showed a left renal mass and a right renal cyst. Under a diagnosis of pulmonary embolism we started anticoagulant therapy, but the patient died five days after admission. At autopsy, a saddle-like thrombus was found in the truncus pulmonalis and bilateral trunks of pulmonary arteries. Microscopic examination showed smooth muscle cells in the thrombus. We could not find any other thrombus in the inferior vena cava, intrapelvic veins, nor in veins of lower extremities by milking. We also found tumors in both kidneys. Microscopically all tumors were diagnosed as angiomyolipoma. There were many fibrin thrombi in the sinuses of the tumors but there was no evidence of malignancy. We finally diagnosed pulmonary embolism due to renal angiomyolipoma because there was no other thrombus origin and microscopically the same smooth muscle cells were found both in the renal tumor and the pulmonary thrombus. There is only one case report concerning pulmonary embolism due to renal angiomyolipoma which happened during operative treatment. The treatment method of renal angiomyolipoma is determined by tumor size and symptoms, and usually intensive treatment is not performed in cases without symptoms. Our patient had no symptoms until the onset of severe complication of pulmonary embolism, suggesting that radical treatment is necessary for renal angiomyolipoma with a thrombus even when there are no symptoms.
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PMID:[An autopsy case of pulmonary embolism due to renal angiomyolipoma in an elderly woman]. 1051 15

Pulmonary embolism (PE) is a major health problem. Mortality in untreated PE is high, but with adequate (anticoagulant) treatment, can be reduced. Multiple primary and secondary risk factors are responsible for PE. But there is rare association of mixed adrenal tumor with PE. Here, we report a case of adrenocortical adenoma with Cushing's syndrome coexistent with pheochromocytoma with recurrent PE in an elderly patient with prostate adenocarcinoma. A 78-year-old Taiwanese retired veteran was admitted in July, 2002 with the presentation of syncope. Three years before, he was diagnosed with prostate adenocarcinoma and had received Androcur therapy since then. Five months later, he was admitted with Cushingoid appearance and hypertension. Abdominal imaging studies revealed a left adrenal tumor. Laparoscopic adrenalectomy revealed an adrenocortical adenoma. Two years later, a recurrent left adrenal tumor was found. Repeated laparoscopic adrenalectomy revealed pheochromocytoma. One month after the repeat laparoscopic surgery, the patient was admitted due to syncope. Chest X-ray revealed cardiomegaly with pulmonary venous congestion. Echocardiogram showed impaired right ventricle global systolic function. Perfusion lung scan showed a high probability of PE. Heparin and coumadin were given but stopped 5 weeks later due to the development of severe skin ecchymosis. In December 2002, the patient was admitted again with consciousness disturbance. Chest computed tomography (CT) revealed bilateral PE, and he died 5 hours later due to cardiogenic shock. In conclusion, in elderly patients with Cushing's syndrome with pheochromocytoma and prostate carcinoma, there is probability of pulmonary embolism.
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PMID:Recurrent pulmonary embolism in an elderly patient with Cushing's syndrome, adrenocortical adenoma, pheochromocytoma and prostate adenocarcinoma. 1551 Sep 34

A 67-year-old woman was admitted to the hospital for lethargy, fever, hemolytic anemia, thrombocytopenia, and consciousness disturbance. Direct Coombs test was positive, and anti-cardiolipin beta2-glycoprotein I antibody was detected. She was diagnosed with antiphospholipid syndrome complicated with autoimmune hemolytic anemia (AIHA). She demonstrated variable consciousness disturbance, inability to distinguish right from left, dysgraphia and dyscalculia. Multiple cerebral infarctions, especially dominant cerebral hemisphere infarctions, were observed on magnetic resonance imaging. A ventilation-perfusion scan demonstrated the presence of a ventilation-perfusion mismatch in both lung fields, and multiple veinous embolisms in the right femoral, bilateral the great saphenous and popliteal veins. Therefore, pulmonary embolism and thrombophlebitis were diagnosed. Based on these findings, it was necessary to distinguish this diagnosis from thrombotic thrombocytopenic purpura (TTP). As ADAMTS-13 activity was within the normal range, TTP was denied. Thereafter, the patient was treated with 1 mg/kg of prednisolone for AIHA, 3 mg of warfarin, and 3500 units of low-molecular-weight heparin for thrombosis, and her condition improved.
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PMID:[Antiphospholipid syndrome with autoimmune hemolytic anemia which mimics thrombotic thrombocytopenic purpura]. 2046 25

Akinetic crisis (AC) is a life-threatening complication of parkinsonism characterized by an acute severe akinetic-hypertonic state, consciousness disturbance, hyperthermia, and muscle enzymes elevation. Injectable dopaminomimetic drugs, high-dose methylprednisolone, and dantrolene are advocated as putative specific treatments. The course of the illness is frequently complicated by infections, pulmonary embolism, renal failure, disseminated intravascular coagulation, and cardiac arrhythmias. Critical illness neuromyopathy (CINM) is an acquired neuromuscular disorder characterized by flaccid quadriparesis and muscle enzyme elevation, often occurring in intensive care units and primarily associated with inactivity, sepsis, multiorgan failure, neuromuscular blocking agents, and steroid treatment. In 3 parkinsonian patients, during the course of AC we observed disappearance of rigidity but persistent hypoactivity. In all, neurological examination showed quadriparesis with loss of tendon reflexes and laboratory investigation disclosed a second peak of muscle enzymes elevation, following the first increment due to AC. Electrophysiological studies showed absent or reduced sensory nerve action potentials and compound muscular action potentials, myopathic changes, and fibrillation potentials at electromyography recordings, and reduced excitability or inexcitability of tibialis anterior at direct muscle stimulation, leading to a diagnosis of CINM in all 3 patients. In 1 patient, the diagnosis was also confirmed by muscle biopsy. Outcome was fatal in 2 of the 3 patients. Although AC is associated with most of the known risk factors for CINM, the cooccurrence of the 2 disorders may be difficult to recognize and has never been reported. We found that CINM can occur as a severe complication of AC, and should be suspected when hypertonia-rigidity subsides despite persistent akinesia. Strict monitoring of muscle enzyme levels may help diagnosis. This finding addresses possible caveats in the use of putative treatments for AC.
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PMID:Critical Illness Neuromyopathy Complicating Akinetic Crisis in Parkinsonism: Report of 3 Cases. 2618 47

We present a case of isolated adrenocorticotropic hormone (ACTH) deficiency complicated by acute adrenal crisis and severe myocardial dysfunction. A 54-year-old woman developed consciousness disturbance, hypoglycemia, hyponatremia, and rhabdomyolysis. Initial echocardiographic examinations on the sixth hospital day revealed marked right-sided atrial and ventricular dilatation and severe tricuspid regurgitation. A computed tomography scan for pulmonary embolism was negative. On the 14th hospital day, she became dyspneic and hypotensive. Repeated echocardiographic examinations demonstrated diffuse and severe hypokinesis of the left ventricle. The previous right-sided chamber dilatation became less apparent. Congestive heart failure and severe hypotension were refractory to catecholamines, while she was eventually diagnosed as having acute adrenal crisis due to isolated ACTH deficiency. Hydrocortisone replacement therapy was started, and echocardiographic examinations revealed that the left ventricular dysfunction completely returned to normal in the following eight days. Severe myocardial dysfunction is an uncommon but serious complication of acute adrenal insufficiency. The present case was unique in that diffuse left ventricular dysfunction was preceded by right ventricular dysfunction.
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PMID:Isolated ACTH deficiency presenting with severe myocardial dysfunction. 3054 10