Van Steenbergen W, Peeters P, De Bondt J, Staessen D, Büscher H, Laporta T, Roskams T, Desmet V
Department of Internal Medicine, University Hospital Gasthuisberg-St Rafaël, Catholic University of Leuven, Belgium.
J Hepatol. 1998 Jul;29(1):135-41. doi: 10.1016/s0168-8278(98)80188-8.
BACKGROUND/AIMS: A number of nonsteroidal anti-inflammatory drugs have been reported to provoke hepatic injury. Nimesulide is a new agent of the sulfonanilide class, and is a more selective inhibitor of cyclooxygenase type 2 than of type 1. Well-documented cases of acute hepatitis have not yet been reported with this drug. We report on six patients who developed acute liver damage after initiation of nimesulide.
Between April 1996 and January 1997, six patients with apparent nimesulide-induced liver injury were admitted. Clinical, laboratory, serologic, radiological, and histologic data of all six cases were extensively analyzed. The causal relationship between nimesulide and liver injury was assessed, using a scoring system elaborated by the French and International consensus meeting group.
Four women developed a centrilobular (three) or panlobular (one) bridging necrosis, whereas two men showed a bland intrahepatic cholestasis. Jaundice was the presenting symptom in five of the six cases. One patient with hepatocellular necrosis and one with cholestasis had hallmarks of hypersensitivity with an increased blood and tissue eosinophilia. The causal relationship could be designated as "highly probable" in one, "probable" in four, and "possible" in one patient. One patient died from a pancreatic tumor 5 months after the diagnosis of toxic liver injury. In all other patients, liver tests returned to completely normal values within a late follow-up period of 6 to 17 months.
Nimesulide-induced liver injury can present with hepatocellular necrosis or with pure cholestasis. From clinical and histologic data, it appears that both immunologic and metabolic idiosyncratic reactions can be invoked as the pathogenic mechanisms of nimesulide-induced liver disease.
背景/目的：据报道，多种非甾体类抗炎药可引发肝损伤。尼美舒利是一种新型磺酰苯胺类药物，对环氧化酶-2的抑制作用比对环氧化酶-1更具选择性。目前尚未见关于该药物引发急性肝炎的确切病例报道。我们报告了6例在开始使用尼美舒利后发生急性肝损伤的患者。
1996年4月至1997年1月，收治了6例明显由尼美舒利引起肝损伤的患者。对所有6例患者的临床、实验室、血清学、放射学和组织学数据进行了广泛分析。采用法国和国际共识会议小组制定的评分系统评估尼美舒利与肝损伤之间的因果关系。
4名女性发生了中央小叶性（3例）或全小叶性（1例）桥接坏死，而2名男性表现为单纯性肝内胆汁淤积。黄疸是6例中的5例的首发症状。1例肝细胞坏死患者和1例胆汁淤积患者具有超敏反应的特征，血液和组织嗜酸性粒细胞增多。因果关系在1例患者中被判定为“极有可能”，4例为“很可能”，1例为“可能”。1例患者在被诊断为中毒性肝损伤5个月后死于胰腺肿瘤。在所有其他患者中，肝功能检查在6至17个月的后期随访期内恢复到完全正常水平。
尼美舒利引起的肝损伤可表现为肝细胞坏死或单纯胆汁淤积。从临床和组织学数据来看，免疫和代谢特异反应似乎都可被认为是尼美舒利所致肝病的致病机制。
