O'Connor D T, Weisman M H, Fierer J
Clin Exp Immunol. 1978 Nov;34(2):179-87.
Twenty-four patients with infective endocarditis (IE) are described, fourteen with Staph. aureus and ten with other organisms. Despite the acute nature of the infection, ten of the fourteen with Staph. aureus IE were hypocomplementaemic; six of these ten had normal levels of C4 associated with low C3 levels, suggesting activation of the alternate complement pathway. Factor B (C3PA) was also low in three of these six cases. In the ten patients with non-Staph. IE, three had hypocomplementaemia with low levels of C4, C3, and Factor B, probably due to C1 (classical pathway) activation with feedback activation of the alternate pathway. In addition, thrombocytopenia was noted in nine of the twenty-four patients and was associated with hypocomplementaemia; the degree of renal insufficiency noted in these patients also correlated with hypocomplementaemia. In Staph. aureus IE thrombocytopenia and hypocomplementaemia, occurring early in the course of the disease, may be due to a non-immune interaction of Staph. cell wall products (Protein A) with immunoglobulin, complement components, and thrombocytes.
本文描述了24例感染性心内膜炎（IE）患者，其中14例由金黄色葡萄球菌引起，10例由其他微生物引起。尽管感染具有急性性质，但14例金黄色葡萄球菌性IE患者中有10例补体水平降低；这10例中的6例C4水平正常而C3水平降低，提示旁路补体途径激活。这6例中的3例B因子（C3PA）水平也较低。在10例非金黄色葡萄球菌性IE患者中，3例补体水平降低，C4、C3和B因子水平均低，可能是由于C1（经典途径）激活并伴有旁路途径的反馈激活。此外，24例患者中有9例出现血小板减少，且与补体水平降低相关；这些患者的肾功能不全程度也与补体水平降低相关。在金黄色葡萄球菌性IE中，血小板减少和补体水平降低在疾病早期出现，可能是由于金黄色葡萄球菌细胞壁产物（蛋白A）与免疫球蛋白、补体成分和血小板之间的非免疫相互作用所致。
