Omeprazole

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Immune-mediated drug-induced liver injury: case report A 72-year-old woman developed immune-mediated drug-induced liver injury (DILI) during treatment with omeprazole for dyspepsia. The woman, who had hypertension, subclinical hyperthyroidism and type 2 diabetes, presented with jaundice associated with dark urine, fatigue, pale stool and poor appetite for a period of 2 weeks. Her diabetes medication included metformin and sitagliptin. Two weeks prior to the presentation, she was seen in primary healthcare with mild dyspepsia for a period of 1 month. She was prescribed omeprazole [route not stated] 20mg daily scheduled for 4 weeks, to which she was compliant. She had no recent travel history outside Qatar. She exhibited yellow discoloration (jaundice) of the eyes. She was hospitalised. Laboratory tests showed increased values of the following: total and direct bilirubin, ALP, ALT and AST. Other tests were normal. Abdominal ultrasound demonstrated a 13cm liver with normal echotexture. No lesions or intra hepatic biliary radicle dilatation were detected. The common bile duct was 2.6mm. Hepatitis antigens and antibodies were negative. Her biochemistry was suggesting apossibility of AIH vs DILI. Omeprazole was suspected to be the culprit drug as it was the only medicine that was initiated recently. Therefore, omeprazole was discontinued on day 3. The woman’s liver enzymes revealed a mixed picture of cholestasis and hepatitis with no obvious obstruction of the biliary tract. Magnetic resonance cholangiopancreatography showed unremarkable pancreas and biliary tree without any evidence of underlying neoplastic process. Periportal oedema and trace of perihepatic free fluid were observed, which were indicative of diffuse liver disease. On day 4, the AIH work up results were obtained. Anti-nuclear antibodies (ANA) and anti-smooth muscle antibodies (ASMA) were positive with titers of 1:160 (nucleolar pattern) and 1:80, respectively. IgG and IgG subclass increased. Rest of the work up was unremarkable. Although her liver enzymes were decreasing slowly but were still considerably high; therefore, on day 10, an ultrasound-guided liver biopsy was performed, which showed confluent zone three necrosis with moderate portal tract inflammation as well as focal lobular inflammation. These features were highly indicative of DILI and were not entirely consistent with AIH. During her hospital stay, her liver enzymes kept decreasing. Her condition did not require steroid treatment. Her jaundice improved gradually, and she was discharged. After 1 month, she was followed-up. She had no residual jaundice, and her liver enzymes were normalised. A repeated ANA, anti-liver kidney microsomal antibody and ASMA titers were negative, indicating the diagnosis of immune-mediated DILI (DILI with positive autoantibodies) secondary to omeprazole. Her liver injury resolved. Rechallenge with omeprazole was not performed. Seife Hassen S, et al. Immune-mediated drug-induced liver injury secondary to Omeprazole: A case report. Clinical Case Reports : 2020