Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.73 (urokinase-type plasminogen activator)
 10,685 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In various connective tissue disorders, a depressed fibrinolytic activity of the blood, attributed a contributory role in the development of disease, has been reported. We have determined selected fibrinolysis variables of the blood in 16 patients (7 patients with mixed connective tissue disease, 4 with systemic lupus erythematosus, 3 with rheumatoid arthritis and 2 with systemic sclerosis) and in 16 apparently healthy, age- and sex-matched controls. A significantly reduced mean activity of the intrinsic derived, urokinase-like plasminogen activator was found in the patient group. None of the other variables, including the extrinsic plasminogen activator (t-PA), differed from the control group. Possible implications of our findings in relation to the patho-physiology of these connective tissue diseases are discussed.
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PMID:Depressed plasma fibrinolytic activity in a group of patients with connective tissue diseases. 251 38

A woman with mixed connective tissue disease (MCTD) developed pulmonary hypertension after delivery of a child, but had little evidence of parenchymal lung disease. This 29-year-old woman had been given a diagnosis of MCTD when she was 19 years old. She was admitted to our department two days after delivery of a child, because of dyspnea on exertion. Acute thromboembolism was suspected because of: (1) chest roentgenogram showing cardiomegaly and enlargement of the left main pulmonary artery, (2) a lung perfusion scan showing a segmental defect in the left S6 and S8 areas, (3) laboratory studies showing abnormally high WBC, LDH, FDP, and D-D dimer, and (4) arterial blood gas analyses showing mild hypoxemia and hypocapnia. Thrombolytic therapy with heparin and urokinase was begun, and was followed by a loop diurtic and anticoagulation with warfarin. One month after admission, cardiac enlargement and the A-aDO2 were found to have decreased. At that time, cardiac catheterization was done and revealed pulmonary hypertension (mean PA pressure: 45 mmHg) and low cardiac output with no detectable thrombosis in the left pulmonary artery. The patient was subsequently treated with a calcium antagonist and a prostacyclin derivative, and her condition was stable for 5 months. Then her exercise tolerance gradually decreased due to shortness of breath, and cardiomegaly gradually increased over the next 3 months. Eight months after delivery of the child, the patient died of right heart failure. In clinically stable patients with MCTD, delivery of a child may lead to pulmonary thromboembolism and pulmonary hypertension.
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PMID:[Puerperal secondary pulmonary hypertension in a patient with mixed connective tissue disease]. 747 71