氯贝丁酯对高脂蛋白血症血管内凝血的影响。

Effect of clofibrate on intravascular coagulation in hyperlipoproteinemia.

作者信息

Carvalho A C, Lees R S, Vaillancourt R A, Colman R W

出版信息

Circulation. 1977 Jul;56(1):114-8. doi: 10.1161/01.cir.56.1.114.

DOI:10.1161/01.cir.56.1.114

Abstract

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.

摘要

通过检测血浆中可溶性纤维蛋白复合物（SFC），对19例II型和11例IV型高脂血症患者在氯贝丁酯治疗前后的血管内凝血（IVC）情况进行了评估；通过定量血清中纤维蛋白（原）降解产物来估计纤维蛋白溶解情况。未经治疗的II型和IV型患者的SFC升高（P<0.01）。前者还存在内源性凝血途径的激活，表现为血浆前激肽释放酶降低（P<0.001）、激肽释放酶抑制剂降低（P<0.001）以及因子XII降低（P<0.02）。尽管对II型患者进行氯贝丁酯治疗并未改变血脂水平，但它降低了血管内凝血，显然是通过降低因子XII的激活以及刺激纤维蛋白溶解来实现的。相比之下，接受治疗的IV型患者尽管血浆甘油三酯降低（P<0.01），但其SFC和纤维蛋白降解产物（FDP）水平并未改变。氯贝丁酯引起的血液凝固变化与降脂作用无关。氯贝丁酯治疗可降低II型患者的血管内凝血，并可能有助于预防血栓栓塞后遗症。