ACTIVATION OF THE COAGULATION CASCADE IN SEVERE FALCIPARUM-MALARIA THROUGH THE INTRINSIC PATHWAY
ACTIVATION OF THE COAGULATION CASCADE IN SEVERE FALCIPARUM-MALARIA THROUGH THE INTRINSIC PATHWAY
复制标题
DOI：
10.1111/j.1365-2141.1994.tb04877.x
复制
发表时间：
1994-05-01
影响因子：
6.5
通讯作者：
WHITE, NJ
中科院分区：
文献类型：
--
作者：
CLEMENS, R;PRAMOOLSINSAP, C;WHITE, NJ
对22例18-45岁（平均+/- sd 31 +/- 11）的重症恶性疟疾患者（男19例，女3例）的凝血级联激活机制进行了研究。其中9人有多个重要器官功能障碍，4人出血，其中2人死亡。在急性疾病期间，血浆抗凝血酶III （AT III）浓度的降低和凝血酶-AT III复合物的升高与因子XII和预钾likrein活性的显著降低以及C1抑制剂抗原/活性比的增加相关。所有患者的系列纤溶酶原活性均保持在正常范围内，而蛋白C活性明显降低。所有患者血浆多形核白细胞弹性酶（pmn -弹性酶）水平均显著升高，α -2巨球蛋白轻度耗损，α -1抗胰蛋白酶浓度正常。pmn -弹性酶浓度与任何凝血参数或蛋白酶抑制剂浓度之间没有相关性。这些结果表明，凝血级联的内在途径在重症疟疾中被激活。这可能导致补体系统的激活和缓激肽和pmn弹性酶的释放，并可能有助于严重疟疾的发病机制。
The mechanisms involved in the activation of the coagulation cascade in severe falciparum malaria were studied in 22 adult patients (19 male, three female) aged 18-45 (mean +/-SD 31 +/- 11) years. Of these, nine had multiple vital organ dysfunction, and bleeding occurred in four patients, two of whom died. During acute illness the reduction in plasma antithrombin III (AT III) concentrations and elevation in thrombin-AT III complexes were associated with significant reductions in factor XII and prekallikrein activities, and an increase in the C1 inhibitor antigen/activity ratio. Serial plasminogen activity remained within the normal range in all patients while protein C activity was significantly reduced. All patients had markedly elevated plasma polymorphonuclear leucocyte elastase (PMN-elastase) levels with mild depletion of alpha-2 macroglobulin but normal concentrations of alpha-1 antitrypsin. There was no correlation between PMN-elastase concentrations and any of the coagulation parameters or concentrations of proteinase inhibitors. These results suggest that the intrinsic pathway of the clotting cascade is activated in severe malaria. This may cause activation of the complement system and release of bradykinin and PMN-elastase and could contribute to the pathogenesis of severe malaria.