Acute liver injury following a single dose of celecoxib: A rare case of rapid-onset hepatotoxicity

Maria Emilia Adenike V. Adedoja , Lovell B. Gatchalian
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Abstract

Celecoxib is a widely prescribed drug for symptomatic pain control. Data regarding its potential to cause deleterious hepatotoxicity is limited. This case report presents a 42-year old man who developed jaundice within 24 h after intake of one tablet of celecoxib (200 mg) for a tooth extraction. He did not have signs of hepatic encephalopathy, fever or rash. There was no previous drug allergy, herbal medicine or alcohol intake. Laboratory workup showed ALT 699, AST 631 U/L, Total bilirubin 5.17 mg/dL, alkaline phosphatase was elevated at 195 U/L and INR 1.2 with an R factor of 9 indicating a hepatocellular pattern of injury. Serologic tests for Hepatitis A, B & C were non-reactive. Antinuclear Antibody (ANA), anti-smooth muscle antibody (anti-SMA), serum immunoglobulin G, anti-mitochondrial antibody (AMA), and perinuclear anti-neutrophil cytoplasmic antibody (p-ANCA) were all negative. Imaging tests of the liver such as triphasic CT scan and Magnetic Resonance Cholangiopancreatography (MRCP) showed no evidence of biliary obstruction and dilatation. His cholestasis and course of liver disease were prolonged, and ultimately he underwent liver biopsy which showed portal and lobular inflammation and hepatocanalicular cholestasis favoring drug-induced liver injury. Celecoxib was withdrawn, ursodeoxycholic acid 300 mg/tab twice times daily and cetirizine 10 mg/tab OD were started to address his persistent pruritus. His liver biochemical and function tests gradually normalized with symptom resolution after 4 months. Conventional non-steroidal anti-inflammatory drugs like celecoxib may still be associated with significant hepatotoxicity. Swift recognition and cessation of the drug's use are crucial. This case highlights the potential for severe hepatotoxicity even with minimal exposure to celecoxib, underscoring the importance of recognizing this rare but serious adverse reaction.
单剂量塞来昔布引起的急性肝损伤:一例罕见的快速肝毒性病例
塞来昔布是一种广泛用于控制症状性疼痛的处方药。有关其可能引起有害肝毒性的数据有限。本病例报告介绍了一名42岁男性,在服用塞来昔布一片(200 mg)拔牙后24 小时内出现黄疸。他没有肝性脑病、发热或皮疹的症状。之前没有药物过敏,草药或酒精摄入。实验室检查显示ALT 699, AST 631 U/L,总胆红素5.17 mg/dL,碱性磷酸酶升高至195 U/L, INR为1.2,R因子为9,表明肝细胞损伤模式。A、B、C型肝炎血清学检测无反应。抗核抗体(ANA)、抗平滑肌抗体(anti-SMA)、血清免疫球蛋白G、抗线粒体抗体(AMA)、核周抗中性粒细胞胞浆抗体(p-ANCA)均为阴性。肝脏影像学检查如三相CT扫描和磁共振胆管胰胆管造影(MRCP)未显示胆道阻塞和扩张的证据。胆汁淤积和肝病病程延长,最终行肝活检,显示门静脉和小叶炎症及肝管胆汁淤积倾向于药物性肝损伤。停用塞来昔布,开始使用熊去氧胆酸300 mg/片,每日2次,西替利嗪10 mg/片OD治疗顽固性瘙痒。4个月后肝脏生化及功能指标逐渐恢复正常,症状逐渐缓解。传统的非甾体抗炎药,如塞来昔布,可能仍然与显著的肝毒性有关。迅速识别和停止使用药物是至关重要的。该病例强调了即使少量接触塞来昔布也可能发生严重肝毒性,强调了认识到这种罕见但严重的不良反应的重要性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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