A Diagnostic Challenge: Uncovering Autoimmune Hepatitis Masked by Choledocholithiasis and Unsupervised Ivermectin Use.

Autoimmune hepatitis (AIH) is a chronic immune-mediated liver disease diagnosed by the clustering of compatible biochemical, serological, and histological features after exclusion of competing causes. Concurrent biliary obstruction or drug-induced injury can obscure the underlying autoimmune process and misdirect the initial diagnosis toward a purely obstructive or toxic cause. A 65-year-old woman with a remote cholecystectomy presented with one week of painless jaundice, dark urine, fatigue, and pruritus on a background of a year of slowly progressive aminotransferase elevation. She had also completed an unprescribed two-week course of oral ivermectin shortly before presentation. Admission studies showed marked hepatocellular injury (aspartate aminotransferase (AST): 2,109 U/L, alanine aminotransferase (ALT): 1,652 U/L), conjugated hyperbilirubinemia (total bilirubin: 8.4 mg/dL), mildly elevated alkaline phosphatase (ALP) (253 U/L), hypergammaglobulinemia (globulin: 5 g/dL; subsequent immunoglobulin G (IgG): 2,925 mg/dL), and an international normalized ratio (INR) of 1.6. With a negative viral hepatitis panel, a normal acetaminophen level, and bland cross-sectional imaging, empiric intravenous corticosteroids were begun on hospital day 2. Aminotransferases and bilirubin fell briskly over the next 72 hours, before any mechanical relief of obstruction. Magnetic resonance cholangiopancreatography (MRCP) on hospital day 4 revealed a 7-mm common bile duct stone, extracted at endoscopic retrograde cholangiopancreatography on hospital day 5. Smooth muscle antibody (SMA) returned at a titer of ≥1:640, with negative antinuclear antibodies (ANA) and antimitochondrial antibodies (AMA), a profile consistent with type 1 AIH. By a simplified International Autoimmune Hepatitis Group (IAIHG) score of 6, the combination of high-titer SMA, markedly elevated IgG, and a corticosteroid response that preceded biliary decompression identified AIH as the most likely dominant driver of injury, with choledocholithiasis as a concurrent second insult and ivermectin as a possible contributor of indeterminate magnitude. Obstructive imaging findings can anchor clinicians away from a concurrent, treatable autoimmune process, and a corticosteroid response that precedes mechanical decompression carries genuine diagnostic weight. Because histology was not obtained during the index admission, the relative contributions of the biliary stone and ivermectin cannot be fully excluded; long-term follow-up, including confirmatory biopsy and a structured trial of corticosteroid withdrawal, will clarify whether the disease is best classified as idiopathic AIH unmasked by concurrent insults or as a drug-related variant.