[Possibilities of drug therapy in the fight against deep venous thrombosis].
The aim of treatment of this illness should be recovery of the circulation, i.e. the suppression of thrombi in the deep venous network. This goal may currently be reached, in the same way as embolic lysis, by the early administration of streptokinase and urokinase, whose mechanisms, dosage-problems and chances of success are discussed here. This thrombolytic treatment is charged with major risks. If it is not to be used then anticoagulants are indicated. These have only a prophylactic effect, that is: they prevent the growth of thrombi. Heparin is the most active anticoagulant but it can only be administered parenterally. The author discusses the mechanism and efficiency of heparin and the antagonists of vitamin K1. Anti-aggregates rather show prophylactic action in the formation of arterial thromboses. Their spectacular effect in vitro on coagulation in vivo has not always been clearly proved in the venous system. It can be seen from the varied effects on thrombocytes and the vascular wall why anti-aggregates are not ideal anti-coagulants.
D000925:Anticoagulants / Q000627:therapeutic use; D005342:Fibrinolysis / Q000187:drug effects; D006493:Heparin / Q000627:therapeutic use; D006801:Humans; D010974:Platelet Aggregation / Q000187:drug effects; D013300:Streptokinase / Q000627:therapeutic use; D013924:Thrombophlebitis / Q000188:drug therapy* / Q000503:physiopathology; D014568:Urokinase-Type Plasminogen Activator / Q000627:therapeutic use
D000925:Anticoagulants; D006493:Heparin; D013300:Streptokinase; D014568:Urokinase-Type Plasminogen Activator
Les possibilités thérapeutiques médicamenteuses dans la lutte contre la thrombophlébite profonde.