Trowbridge A A, Green J B, Bonnett J D, Shohet S B, Ponnappa B D, McCombs W B
Am J Clin Pathol. 1981 Oct;76(4):493-8. doi: 10.1093/ajcp/76.4.493.
A case of fulminant hemolytic anemia associated with a leptospiral infection is presented with morphologic and erythrocyte lipid studies. Both the frequency and pathogenesis of anemia in human leptospirosis is poorly understood. The anemia frequently observed in Weil's syndrome has been ascribed on clinical impression to blood loss, renal failure, and/or an ill-defined hemolytic process. However, hemolytic anemia associated with leptospirosis in animals is well documented and is due to hemolysins with phospholipase activity. Our patient's erythrocyte morphologic abnormalities on bright light and electron microscopy included particles of cells and cells with a thorny or spiculated surface suggesting that the hemolytic process was due to membrane injury. Measurement of the erythrocyte membrane lipids showed reductions in sphingomyelin and phosphatidylethanolamine suggesting that the observed hemolysis and morphologic changes resulted from phospholipases produced by the infecting leptospirae.
本文报告了一例与钩端螺旋体感染相关的暴发性溶血性贫血病例,并进行了形态学和红细胞脂质研究。人类钩端螺旋体病贫血的发生率和发病机制尚不清楚。韦尔综合征中常见的贫血,根据临床印象归因于失血、肾衰竭和/或不明原因的溶血过程。然而,动物中与钩端螺旋体病相关的溶血性贫血已有充分记录,是由具有磷脂酶活性的溶血素引起的。我们患者在明视野显微镜和电子显微镜下的红细胞形态异常包括细胞颗粒以及表面有棘状或锯齿状的细胞,提示溶血过程是由于膜损伤所致。红细胞膜脂质测量显示鞘磷脂和磷脂酰乙醇胺减少,提示观察到的溶血和形态学变化是由感染的钩端螺旋体产生的磷脂酶所致。