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Acute Cholestatic Liver Injury From Hydralazine Intake

机译:硫吡嗪摄入急性胆固性肝损伤

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Hydralazine is a commonly used oral antihypertensive agent. We report a rare case of hydralazine-induced hepatotoxicity in the form of subacute hepatic necrosis. A 75-year-old African American woman presented with jaundice of 7-day duration. She was started on hydralazine 100 mg 3 times a day 10 weeks before presentation. On physical examination, scleral icterus was noted. Workup revealed elevated liver transaminases, alkaline phosphatase, and conjugated bilirubin. She had no history of liver disease, and liver function tests had been normal before starting hydralazine. Other etiologies, including viruses, common toxins, drugs, autoimmune, and copper-induced hepatitis, were excluded. Abdominal imaging studies did not show any evidence of intrahepatic or extrahepatic biliary ductal dilatation, and no pathologies were seen in the liver and pancreas. The patient's liver biopsy revealed extensive lobular hepatitis, significant necrosis, mixed inflammatory infiltrate, and no significant fibrosis, supporting a diagnosis of drug-induced liver injury. Hydralazine was immediately discontinued. She showed improvement of clinical and laboratory abnormalities within 5 days after discontinuation of hydralazine. To establish the diagnosis of hydralazine-induced liver injury, we used assessment tool outlined by the Council for International Organization of Medical Sciences (CIOMS) scale that led to high probable relationship. Although rare, clinically significant, and potentially life-threatening liver injury can result from use of hydralazine. Both clinical and histological presentations in our patient suggest acute liver injury. The hydralazine-induced hepatitis seems to be reversible as discontinuation of the drug improves clinical outcomes. We highly recommend monitoring of the liver function during hydralazine treatment.
机译:氢氮嗪是一种常用的口服抗高血压剂。我们以亚急性肝脏坏死的形式报告稀有含氢吡嗪诱导的肝毒性的含量。一名75岁的非洲裔美国女性举办了7天持续时间的黄疸。在介绍前10周,她在碘嗪100毫克100毫克3次开始。关于体检,注意到巩膜捷。上次揭示肝脏转氨酶,碱性磷酸酶和共轭胆红素的升高。她没有肝病的历史,肝功能试验在开始碘嗪之前已经正常。其他病因,包括病毒,常见的毒素,药物,自身免疫和铜诱导的肝炎,被排除在外。腹部成像研究没有显示出肝内或脱毛胆道导管扩张的任何证据,并且在肝脏和胰腺中没有观察到病理学。患者的肝脏活组织检查显示出广泛的小叶肝炎,显着的坏死,混合炎症性浸润,无明显纤维化,支持诊断药物诱导的肝损伤。立即停止氢吡啶。她在碘嗪停止后5天内显示出改善临床和实验室异常。为建立碘嗪诱导的肝损伤的诊断,我们使用了国际医学组织理事会(CIOM)规模概述的评估工具,导致了高可能的关系。虽然罕见,临床显着和潜在的危及生命的肝脏损伤可能是由氢氮嗪产生的。我们患者的临床和组织学介绍均表明急性肝损伤。由于药物的停药改善了临床结果,氢嗪诱导的肝炎似乎是可逆的。我们强烈建议在碘嗪治疗期间监测肝功能。

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