Kanwarpreet Sadhu, Rakshand Shetty, Prachi Mehmi, Lipi Patel, Zunera Shaikh, Rithvika Badugu, Ogundele Tosin Arinola, Ballu R
Losartan, a commonly prescribed angiotensin II receptor blocker, is generally well-tolerated but can rarely cause severe drug-induced liver injury (DILI), leading to acute liver failure. We report a 43-year-old man with hypertension and type 2 diabetes who developed jaundice, fatigue, and right upper quadrant pain six weeks after starting losartan (50 mg daily). Despite prompt discontinuation of the drug, he progressed to acute liver failure with hepatic encephalopathy, coagulopathy (international normalized ratio (INR): 2.8), and a Model for End-Stage Liver Disease (MELD) score of 28, meeting King's College criteria for poor prognosis. Comprehensive workup, including viral hepatitis panel (A, B, C, and E), cytomegalovirus (CMV), Epstein-Barr virus (EBV), herpes simplex virus (HSV), autoimmune markers, Wilson disease screening, acetaminophen levels, and exclusion of ischemic and metabolic causes, was negative. Liver biopsy showed severe centrilobular necrosis, eosinophilic infiltrate, portal inflammation, interface hepatitis, and cholestasis. Causality assessment using the Roussel Uclaf Causality Assessment Method (RUCAM) yielded a score of 8 (Probable DILI). The patient ultimately required liver transplantation despite early drug withdrawal. This case highlights that losartan-induced hepatotoxicity, although rare, can be life-threatening and underscores the importance of early recognition and a high index of suspicion in patients with unexplained liver injury.