S5558 Oral N-Acetylcysteine in Hepatitis C-Induced Acute Liver Injury: A Case Report

Introduction: While N-acetylcysteine (NAC) is well-established for acetaminophen-induced liver failure, its role in non-acetaminophen acute liver injury (e.g., viral hepatitis, drug-induced) remains debated. Prior studies demonstrate improved survival with intravenous (IV) NAC in non-acetaminophen liver failure, but data on oral NAC in hepatitis C (HCV) are limited. This case highlights a patient with chronic liver diseases of HCV and non-alcoholic fatty liver disease (NAFLD) who was started on oral NAC in the setting of non-acetaminophen liver failure. Case Description/Methods: A 54-year-old man with a past medical history of HCV (previously treated/sustained virological response), NAFLD, and recent cocaine/methamphetamine use presented with cough and markedly elevated transaminases (aspartate aminotransferase [AST] 778, alanine aminotransferase [ALT] 1,069). Workup ruled out acetaminophen toxicity, malignancy, and acute viral hepatitis. On hospital day 5, oral NAC (600 mg BID) was initiated for suspected drug-induced liver injury superimposed on chronic liver diseases of HCV and NAFLD. Liver enzymes downtrended by discharge (AST 505, ALT 1351). Discussion: This case highlights oral NAC as a potential adjunct in HCV-related acute liver injury, despite its primary use for acetaminophen toxicity. The patient’s improvement aligns with proposed NAC mechanisms: glutathione replenishment and mitigation of oxidative stress. Notably, prior studies focused on intravenous (IV) NAC in heterogeneous liver failure etiologies; our report adds to limited evidence supporting oral NAC in HCV. Oral NAC may benefit select patients with HCV and acute liver injury, particularly when IV formulations are unavailable or contraindicated. Further studies are needed to define optimal dosing, timing, and patient selection.