Severe Acute Cholera Infection Mimicking Decompensated Liver Cirrhosis and Triggering Autoimmune Hepatitis

Abstract

Acute systemic infection may cause hepatic, hematological and radiologic abnormalities that closely mimic decompensated liver cirrhosis. Vibrio cholerae causes cholera, which does not typically imply hepatic involvement; however, in severe or complicated cases, there may be dysfunction of various organs, cholestatic hepatitis, coagulopathy, and false radiographic findings. In addition, acute infections can serve as immunological triggers for autoimmune hepatitis (AIH), an infrequent yet increasingly acknowledged finding. We report the case of an 18-year-old previously healthy Sudanese female refugee who presented with severe acute cholera infection complicated by deep cholestatic jaundice, disseminated intravascular coagulation, hemolysis, hepatic encephalopathy, and ascites. Early imaging and transient elastography (FibroScan) results showed findings consistent with decompensated liver cirrhosis. She later acquired progressive transaminitis with ongoing hyperbilirubinemia; the subsequent serological screen revealed positive antinuclear antibodies and smooth muscle antibodies, suggesting infection-induced AIH. Her response to corticosteroid treatment using prednisolone was dramatic, which was later combined with azathioprine as a steroid-sparing agent. A chronic relapsing course was confirmed by two relapses when treatment was discontinued. A follow-up FibroScan performed after biochemical remission showed that liver stiffness had normalized. To our knowledge, this is the first reported case of severe cholera infection initially mimicking decompensated cirrhosis, followed by the subsequent development of autoimmune hepatitis. Clinicians need to be aware that infection can trigger AIH and that imaging and elastography have significant limitations in acute inflammatory disease. Early identification, multidisciplinary assessment, and adequate long-term follow-up are essential.