Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.7 (plasmin)
9,023 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hormonal contraception for men requires administration of testosterone and gestagens. The effects of a long-acting testosterone ester and 2 different progestins on hemostatic activation parameters were studied in relation to cardiovascular risk. In phase 1, 7 healthy men aged 28-38 years received a single intramuscular injection of 200 mg norethisterone-enanthate (NET-EN) on Day 0. Plasma samples were obtained on Days 0, 14, 41, and 84. In phase 2, 3 groups of 14 healthy men aged 18-45 years received four injections (every 6 weeks) of 1000 mg testosterone undecanoate (TU), plus daily oral placebo or daily oral levonorgestrel (LNG, 250 microg); or four injections (every 6 weeks) of NET-EN. Treatment lasted 24 weeks. Plasma samples were obtained at weeks 0, 16, 24, and 52. All samples were assayed for levels of coagulation factors VIIc, VIIa, XIIc, and XIIa; prothrombin fragment F1+2 (F1+2); antithrombin; plasmin-alpha(2)-antiplasmin-complex (PAP); and fibrinogen. NET-EN alone led to a depletion of sexual hormones and a marked shift in hemostatic parameters with increasing levels of FXIIc, fibrinogen, antithrombin, and F1+2, whereas FVIIc and FVIIa levels decreased. PAP levels increased significantly. Opposite effects were seen in the TU/placebo group, with a significant down-regulation of fibrinolysis and the hemostatic turnover rate. Testosterone effects were attenuated by additional administration of gestagens. The effect of hormonal male contraception using long-acting testosterone esters with or without gestagens was significantly measurable within the hemostatic system. Down-regulation of the hemostatic system with testosterone alone may indicate an antithrombotic effect, whereas clinical consequences of an additional gestagen compound cannot be derived.
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PMID:Contraceptive steroids influence the hemostatic activation state in healthy men. 1206 57

Thrombophlebitis and pulmonary embolism are major causes of disability and death in both medical and surgical patients. Etiological factors are still poorly understood. Preventive measures as currently practised are non-specific and based on questionable premises. Diagnostic measures to predict the silent fatal embolus are inadequate. Currently accepted treatment measures are designed to prevent extension of the thrombus but have no effect on the existing clot. Theoretically, thrombolytic preparations now being marketed offer some hope for dissolution of preformed thrombi. An experimental study was carried out on artificially induced thrombi in jugular and femoral veins of mongrel dogs. Human fibrinolysin (Actase, Ortho) was infused locally and systemically in varying doses. No thrombi were successfully lyzed by either method. Thirty-six cases of acute deep thrombophlebitis in the leg, one of axillary thrombosis, three of chronic postphlebitis of a lower limb with massive edema and eight of pulmonary emboli were observed and carefully documented clinically. All these patients received anticoagulants unless there was a contraindication. Fibrinolysin infusions in varying dosages were administered to 27 patients; 10 served as controls. The observers were unaware of the identity of those receiving the actual drug or of those given the placebo until completion of the study. Progress of the disease was judged by the rate of dis-appearance of symptoms and signs. No significant benefit could be noted in the treated as compared to the control group, in terms of rate of recovery or incidence of embolus.
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PMID:Fibrinolysin therapy of thrombophlebitis and pulmonary embolism--a double-blind study. 1397 84