Energy Drink-Associated Mixed Liver Injury With Cholestatic Histology After Long-Term High-Volume Consumption: A Case...

Energy drinks are multi-ingredient beverages whose clinically apparent hepatotoxicity is described mainly in case reports. A 25-year-old man with obesity and approximately three years of daily high-volume energy drink consumption (1-2.5 L/day) presented with epigastric pain, dark urine, jaundice, and systemic inflammation. His admission total bilirubin was 8.0 mg/dL, alanine aminotransferase 380 U/L, aspartate aminotransferase 187 U/L, gamma-glutamyl transferase 471 U/L, and alkaline phosphatase 232 U/L. The resulting R ratio was 4.5, indicating a mixed biochemical pattern. Computed tomography and magnetic resonance cholangiopancreatography excluded biliary obstruction and demonstrated hepatosplenomegaly, diffuse hepatic edema, and enlarged porta hepatis lymph nodes. Viral and autoimmune investigations were unrevealing. Core liver biopsy showed centrilobular and midzonal cholestasis with bilirubinostasis, minimal lobular inflammation, portal lymphogranulocytic infiltrates, preserved bile ducts, and no fibrosis. The energy drink exposure was stopped. Empiric antibiotics, ursodeoxycholic acid, and intravenous methylprednisolone were administered. By discharge on hospital day 18, bilirubin and C-reactive protein had substantially decreased; aminotransferases remained elevated but were declining from their peak. At four months, aspartate aminotransferase, alkaline phosphatase, and C-reactive protein were within the supplied institutional reference ranges, while alanine aminotransferase and gamma-glutamyl transferase had markedly improved. A retrospective updated Roussel Uclaf Causality Assessment Method score of 3 supported only a possible product-level association. This case illustrates that biochemical classification and histology may diverge and that causality should not be assigned to a single energy drink ingredient when the exact formulation, dose, and untreated dechallenge are unavailable.