Ersöz Galip, Vardar Rukiye, Akarca Ulus Salih, Tekın Fatih, Yilmaz Funda, Günşar Fulya, Karasu Zeki
Department of Gastroenterology, Ege University, School of Medicine, İzmir, Turkey.
Turk J Gastroenterol. 2011 Oct;22(5):494-9. doi: 10.4318/tjg.2011.0245.
BACKGROUND/AIMS: Certain drugs including oxyphenisatin, methyldopa, nitrofurantoin, diclofenac, interferon, infliximab, pemoline, minocycline, atorvastatin, and rosuvastatin can induce hepatocellular injury that mimics autoimmune hepatitis. Whether drugs and herbs unmask or induce autoimmune hepatitis or simply cause a drug-induced hepatitis with accompanying autoimmune features is unclear. We describe the clinicopathologic details of eight cases with ornidazole-induced hepatitis with autoimmune features.
Patients who presented with acute hepatitis between February 2001 and March 2009 were reevaluated for the etiology of liver disease. Patients with acute viral hepatitis, metabolic liver disease, vascular liver disease such as Budd-Chiari syndrome, biliary obstruction, or alcohol consumption were excluded. The autoimmune hepatitis scores, which were calculated at the time of diagnosis according to the criteria of the International Autoimmune Hepatitis Group, were recorded. In addition, the simplified criteria of the same group were applied retrospectively to each patient. Patients with ornidazole-induced toxic hepatitis with autoimmune hepatitis were included to constitute the study group of this report. All patients underwent initial liver biopsy, and one patient underwent liver biopsy three years later. All biopsies were scored according to the hepatitis scoring system by Ishak et al. (10).
Overall, eight patients (all female) were diagnosed as drug-induced autoimmune hepatitis. With the exception of one patient, all were treated with prednisolone 30 mg/day + azathioprine 50 mg/day. The prednisolone dose was tapered according to the decrease in the level of transaminases. A two-year treatment program was planned for all patients.
Ornidazole may cause drug-induced autoimmune hepatitis. Withdrawal of the drug may not provide the recovery despite a rather long wait. Thus, immunosuppressive therapy may be suggested in these cases.
背景/目的：某些药物，包括奥昔芬净、甲基多巴、呋喃妥因、双氯芬酸、干扰素、英夫利昔单抗、匹莫林、米诺环素、阿托伐他汀和瑞舒伐他汀，可诱发类似自身免疫性肝炎的肝细胞损伤。药物和草药是揭示或诱发自身免疫性肝炎，还是仅仅导致伴有自身免疫特征的药物性肝炎，目前尚不清楚。我们描述了8例具有自身免疫特征的奥硝唑诱发肝炎的临床病理细节。
对2001年2月至2009年3月期间出现急性肝炎的患者重新评估肝病病因。排除急性病毒性肝炎、代谢性肝病、布加综合征等血管性肝病、胆道梗阻或饮酒患者。记录根据国际自身免疫性肝炎小组标准在诊断时计算的自身免疫性肝炎评分。此外，同一小组的简化标准被回顾性应用于每位患者。纳入具有自身免疫性肝炎的奥硝唑诱发中毒性肝炎患者，构成本报告的研究组。所有患者均接受了初次肝活检，1例患者在3年后接受了肝活检。所有活检均根据Ishak等人的肝炎评分系统进行评分（10）。
总体而言，8例患者（均为女性）被诊断为药物性自身免疫性肝炎。除1例患者外，所有患者均接受30mg/天泼尼松龙+50mg/天硫唑嘌呤治疗。泼尼松龙剂量根据转氨酶水平的下降逐渐减少。为所有患者制定了为期两年的治疗方案。
奥硝唑可能导致药物性自身免疫性肝炎。尽管等待时间较长，但停药可能无法实现康复。因此，在这些病例中可能建议进行免疫抑制治疗。
