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西咪替丁与血液学抑制:事情并非总是表面看上去的那样。

Cimetidine and hematologic suppression: things are not always as they appear.

作者信息

Richter J E, Gerhardt D C, Pasquale D N, Castell D O

出版信息

Dig Dis Sci. 1980 Dec;25(12):960-3. doi: 10.1007/BF01308047.

Abstract

A 67-year-old man with a bleeding ulcer developed fever, thrombocytopenia, and neutropenia with eosinophilia coincidental to receiving 3600 mg of cimetidine. Failure to reduplicate the hematologic suppression after cimetidine rechallenge suggests the drug was not responsible for the change in circulating cells. Our patient is similar to the earlier reported cases of cimetidine-associated hematologic suppression. The role of cimetidine in these cases is impossible to determine because of the multifactorial possibilities for bone-marrow suppression. Recently, a fatal case of agranulocytosis associated with cimetidine has been reported. The possible mechanisms of granulocytopenia are reviewed, and it is suggested cimetidine may cause bone-marrow suppression by an idiosyncratic reaction. We believe the possibility of fatal aplastic anemia secondary to cimetidine is very rare and does not preclude a drug rechallenge when the benefit-risk ration warrants.

摘要

一名患有出血性溃疡的67岁男性在接受3600毫克西咪替丁治疗期间出现发热、血小板减少、中性粒细胞减少伴嗜酸性粒细胞增多。再次使用西咪替丁后未能重现血液学抑制现象,提示该药物与循环细胞的变化无关。我们的患者与早期报道的西咪替丁相关血液学抑制病例相似。由于骨髓抑制存在多种因素,西咪替丁在这些病例中的作用无法确定。最近,有一例与西咪替丁相关的致命性粒细胞缺乏症的报道。本文对粒细胞减少的可能机制进行了综述,并提示西咪替丁可能通过特异反应导致骨髓抑制。我们认为西咪替丁继发致命性再生障碍性贫血的可能性非常罕见,当获益风险比合理时并不排除再次使用该药物。

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