Effect of clofibrate on intravascular coagulation in hyperlipoproteinemia.
Intravascular coagulation (IVC) was evaluated in 19 patients with type II and 11 with type IV hyperlipoproteinemia before and after clofibrate therapy by measurements of soluble fibrin complexes (SFC) in plasma; fibrinolysis was estimated by quantitation of fibrin (ogen) degradation products in serum. Untreated type II and type IV patients had increased SFC (P less than 0.01). The former also had activation of the intrinsic coagulation pathway as evidenced by decreased plasma prekallikrein (P less than 0.001), kallikrein inhibitors (P less than 0.001), and factor XII (P less than 0.02). Although clofibrate treatment of the type II patients did not change plasma lipids, it decreased intravascular coagulation, apparently via decreased factor XII activation and stimulation of fibrinolysis. In contrast, treated type IV patients had unchanged SFC and FDP levels, despite decreased plasma triglycerides (P less than 0.01). Clofibrate-induced changes in blood coagulation are independent of lipid-lowering. Clofibrate therapy decreases intravascular coagulation in type II patients and may help to prevent thromboembolic sequelae.
D000991:Antithrombins / Q000032:analysis; D007611:Aprotinin; D001161:Arteriosclerosis / Q000188:drug therapy; D002994:Clofibrate / Q000627:therapeutic use*; D004211:Disseminated Intravascular Coagulation / Q000188:drug therapy* / Q000209:etiology; D005174:Factor XII / Q000032:analysis; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D006801:Humans; D006949:Hyperlipidemias / Q000150:complications*; D011288:Prekallikrein / Q000032:analysis
D000991:Antithrombins; D005338:Fibrin Fibrinogen Degradation Products; D005174:Factor XII; D011288:Prekallikrein; D007611:Aprotinin; D002994:Clofibrate