POTENTIAL PATHOGENIC ROLE OF COMPLEMENT IN DENGUE HEMORRHAGIC-SHOCK SYNDROME
POTENTIAL PATHOGENIC ROLE OF COMPLEMENT IN DENGUE HEMORRHAGIC-SHOCK SYNDROME
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DOI：
10.1056/nejm197311082891902
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发表时间：
1973-01-01
影响因子：
158.5
通讯作者：
MULLEREB.HJ
中科院分区：
文献类型：
--
作者：
BOKISCH, VA;TOP, FH;MULLEREB.HJ
在泰国曼谷，127名登革出血热患者中有49人出现休克。在系列血清样品中测量的9种补体蛋白的浓度在休克期间下降，但C9除外。在严重病例中，C3和C5降至正常值的20%至40%。血浆纤维蛋白原减少、纤维蛋白原分裂产物出现、血小板减少提示血管内凝血的发生。对24例患者进行的C3和C1 q代谢研究表明，特别是在休克期间，分解率明显增强。这些结果支持了补体激活可能是登革出血性休克发病机制中的主要因素的概念。（《新英格兰医学杂志》289：996-1000，1973）
In Bangkok, Thailand, 49 of 127 patients with dengue hemorrhagic fever experienced shock. The concentration of nine complement proteins measured in serial serum samples decreased during shock with the exception of C9. C3 and C5 were reduced to 20 to 40 per cent of normal in severe cases. Decrease of plasma fibrinogen, appearance of fibrinogen split products and thrombocytopenia indicated occurence of intravascular coagulation. Metabolic studies of C3 and C1q, performed on 24 patients, indicated a markedly enhanced fractional catabolic rate especially during shock. These results support the concept that activation of complement can constitute a major factor in the pathogenesis of dengue hemorrhagic shock. (N Engl J Med 289:996–1000, 1973)