Baker N M, Mills A E, Rachman I, Thomas J E
Br Med J. 1974 Apr 13;2(5910):84-7. doi: 10.1136/bmj.2.5910.84.
Among 48 patients with a typhoid infection 6 (12.5%) developed the haemolytic-uraemic syndrome. Neither glucose-6-phosphate dehydrogenase deficiency nor therapy with chloramphenicol could be incriminated as the causal factor. Evidence presented here suggests that the mechanism is localized intravascular coagulation.The presence of leucocytosis in typhoid fever suggests a complication and should alert one to the possibility of the haemolytic-uraemic syndrome. Furthermore, in our area typhoid should be suspected as a cause in any patient presenting with acute renal failure.
在48例伤寒感染患者中，有6例（12.5%）发生了溶血尿毒综合征。葡萄糖-6-磷酸脱氢酶缺乏症和氯霉素治疗均不能被认定为病因。此处提供的证据表明，其机制为局部血管内凝血。伤寒热时白细胞增多提示有并发症，应提醒人们注意溶血尿毒综合征的可能性。此外，在我们地区，任何出现急性肾衰竭的患者都应怀疑伤寒是病因。
