某些治疗性药物引起溶血,国内外文献已有较多的报导。一般认为关于药物溶血作用,归之于药物过量中毒,可以直接破坏红细胞:也可能机体对药物的过敏,则与药量无关。近年来发现某些治疗性药物所致溶血与红细胞代谢缺陷及其与遗传有关,已证实系由于酶的缺乏或异常。某些学者建议“药物遗传学”(Pharmacogenetics)一名,作为对药物反应异常的遗传学研究的统称。本文就是最近有关药物性溶血与红细胞代谢缺陷的关系,作一简述。敏感红细胞代谢缺陷过去认为某些治疗量药物所引起的溶血是属过敏性,但大多数溶血反应却不能用免疫机制来解释。近年来,国外文献报告中已证实对某些药物敏感者的红细胞中缺乏6-磷酸葡萄糖脱氢酶(G-6-PD),此酶 Some therapeutic drugs cause hemolysis, the literature has been more reported at home and abroad. Generally believed that the role of drug hemolysis, due to excessive drug poisoning, can directly damage the red blood cells: the body may also be allergic to drugs, it has nothing to do with the dose. In recent years, hemolysis caused by some therapeutic drugs has been found to be associated with genetic defects in erythrocyte metabolism and has been confirmed due to lack of or abnormal enzyme. Some scholars recommend “Pharmacogenetics” as a generic term for genetic studies that indicate abnormalities in drug response. This article is the recent drug-related hemolysis and erythrocyte metabolism defects, for a brief review. Sensitive defects in the metabolism of red blood cells in the past that some therapeutic drugs caused by hemolysis is anaphylactoid, but most hemolysis can not be used to explain the immune mechanism. In recent years, foreign literature reports have confirmed the lack of 6-phosphoglucose dehydrogenase (G-6-PD) in erythrocytes susceptible to certain drugs, this enzyme