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致命性胺碘酮肝毒性。

Fatal amiodarone hepatoxicity.

作者信息

Gilinsky N H, Briscoe G W, Kuo C S

机构信息

Department of Medicine, Albert B. Chandler Medical Center, University of Kentucky, Lexington.

出版信息

Am J Gastroenterol. 1988 Feb;83(2):161-3.

PMID:3341340
Abstract

The antiarrhythmic agent amiodarone is associated with numerous adverse effects, but clinically significant liver disease is rare. A patient is described who presented with muscle weakness, hepatomegaly, and ascites following 28 months of amiodarone usage. His condition deteriorated despite discontinuation of amiodarone therapy. A postmortem liver biopsy demonstrated necrosis, fibrosis, hyalin, and phospholipid-laden lysosomal lamellar bodies. Resolution of hepatic dysfunction may not necessarily occur on withdrawal of amiodarone if irreversible damage is already established. We speculate as to the reasons for the reportedly low incidence of overt liver disease, and suggest that hepatic enzyme levels, as well as other indicators of hepatic function, such as the serum albumin concentration, be monitored indefinitely in all patients while taking amiodarone.

摘要

抗心律失常药物胺碘酮会引发多种不良反应,但临床上显著的肝脏疾病较为罕见。本文描述了一名患者,在使用胺碘酮28个月后出现肌肉无力、肝肿大和腹水症状。尽管停用了胺碘酮治疗,其病情仍继续恶化。尸检肝脏活检显示有坏死、纤维化、透明蛋白及充满磷脂的溶酶体层状小体。如果已经造成不可逆损伤,停用胺碘酮后肝功能障碍不一定会得到缓解。我们推测了明显肝脏疾病报道发病率较低的原因,并建议在所有服用胺碘酮的患者中持续监测肝酶水平以及其他肝功能指标,如血清白蛋白浓度。

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