Capron-Chivrac D, Reix N, Quénum C, Capron J P
Gastroenterol Clin Biol. 1985 Jun-Jul;9(6-7):535-9.
The authors report the case of a non-alcoholic 73-year-old man, treated for arrhythmia with amiodarone for 2 months, and hospitalized because of jaundice and hepatomegaly. There was an important increase in serum alkaline phosphatase activity (4 times the normal value) and a moderate increase in the serum activity of transaminases (3-4 times the normal value). Endoscopic retrograde cholangiography was normal. Serum markers of virus B and tissue antibodies were absent. Histological examination of a liver specimen disclosed portal and periportal fibrosis, mixed inflammatory infiltrate of the portal spaces, and ductular proliferation. Lamellar lysosomal inclusions were demonstrated on electron microscopy. Outcome was favorable after withdrawal of amiodarone. This report, as well as the 7 previously published cases, cannot explain the pathogenesis of amiodarone-induced liver changes.
作者报告了一例73岁非酒精性男性病例，该患者用胺碘酮治疗心律失常2个月，因黄疸和肝肿大住院。血清碱性磷酸酶活性显著升高（为正常值的4倍），转氨酶血清活性中度升高（为正常值的3 - 4倍）。内镜逆行胆管造影正常。未检测到乙型肝炎病毒血清标志物和组织抗体。肝组织标本的组织学检查显示门静脉和门静脉周围纤维化、门静脉间隙混合性炎症浸润以及小胆管增生。电子显微镜检查发现板层状溶酶体包涵体。停用胺碘酮后预后良好。本报告以及之前发表的7例病例均无法解释胺碘酮所致肝脏改变的发病机制。
