Recommended Citation
Stevenson JR, Ezeano C, Capelli G, Villavicencio Kim J. Postpartum Flare Unmasking Autoimmune Hepatitis After Apparent Resolution of Drug-Induced Liver Injury in Pregnancy. Poster presented at: American College of Gastroenterology (ACG) 2026 Annual Scientific Meeting; October 11, 2026; Nashville, TN. Poster P1897.
Presentation Notes
Poster presented at: American College of Gastroenterology (ACG) 2026 Annual Scientific Meeting; October 11, 2026; Nashville, TN. Poster P1897.
Abstract
Introduction: Drug-induced liver injury (DILI) can present as a drug-induced autoimmune-like hepatitis (DI-ALH) phenotype, mimicking idiopathic autoimmune hepatitis (AIH) on clinical, serologic, and histologic grounds. Pregnancy introduces further diagnostic complexity, as gestational immunotolerance may suppress AIH activity, potentially obscuring the underlying diagnosis until postpartum immune rebound unmasks the disease. Case Description/Methods: A 33-year-old woman with prior mild aminotransferase elevations was hospitalized for pyelonephritis with Escherichia coli bacteremia and treated with amoxicillin–clavulanate. Aminotransferases peaked at aspartate aminotransferase (AST) 788 U/L (30× the upper limit of normal [ULN]) and alanine aminotransferase (ALT) 1,141 U/L (46× ULN), downtrending at discharge, raising concern for DILI. Six weeks later, following metronidazole for bacterial vaginosis, she re-presented with jaundice, AST/ALT >1,000 U/L, and total bilirubin >20 mg/dL. Viral hepatitis serologies were negative; immunoglobulin G was 2,370 mg/dL and antinuclear antibody was 1:160. Liver biopsy demonstrated plasma cell–rich portal inflammation with interface activity, hepatocyte rosetting/emperipolesis, zone 3 dropout, and mild cholestasis without fibrosis—favoring AIH with possible DILI overlap. She improved with intravenous methylprednisolone followed by prednisone 60 mg daily, completing her taper. She became pregnant thereafter. Early pregnancy aminotransferases worsened (AST 421 U/L, ALT 649 U/L) but improved by the second trimester and near-normalized after delivery. Four weeks postpartum, after a preeclamptic delivery, enzymes rose to AST 65 U/L (2.5× ULN) and ALT 108 U/L (4.3× ULN) without new medications, prompting reinitiation of corticosteroids. Discussion: This case illustrates how gestational immunotolerance may suppress underlying AIH, mimicking DILI resolution and delaying diagnosis. The postpartum aminotransferase rise—occurring without new medication exposures—provided critical evidence distinguishing idiopathic AIH from DI-ALH. Clinicians should not interpret aminotransferase normalization during pregnancy as definitive DILI resolution when biopsy findings are consistent with AIH. Close biochemical monitoring through the postpartum period is essential, as immune rebound may unmask underlying autoimmune liver disease. AI use disclosure: Generative AI tools assisted with literature review and language editing; no patient-identifiable information was entered; authors verified content. Figure 1. Aspartate aminotransferase (AST) and alanine aminotransferase (ALT), in U/L, and total bilirubin (mg/dL) plotted across the clinical course. Shaded regions denote pregnancy (last menstrual period [LMP] March 2025 → delivery December 2025) and postpartum; treatment bar indicates intravenous (IV) methylprednisolone → prednisone → taper (completed March 2025). Numbered markers: (1) amoxicillin–clavulanate exposure; (2) discharge with improving labs; (3) liver biopsy (autoimmune hepatitis ± druginduced liver injury), corticosteroids initiated; (4) off-steroid worsening in early pregnancy; (5) biochemical improvement at 22 weeks; (6) near-normalization post-delivery; (7) postpartum rise, steroids restarted (date approximate). Upper limit of normal (ULN), female-specific: AST 26 U/L, ALT 25 U/L.
Type
Poster
Affiliations
Aurora Health Care, Aurora St. Luke's Medical Center