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Elevation of Liver Enzymes in a Patient with Obesity and Dyslipidemia on Statin Therapy: Importance of the Differential Diagnosis Between PBC and Drug-Induced HepatitisJHJ

Laura JOVELL and Daniel ALCANTARILLA

Liver enzyme abnormalities are frequently detected in routine primary care testing. In patients with obesity and dyslipidemia, these abnormalities are often attributed to metabolic causes. However, when autoantibodies are present, the differential diagnosis must be broadened to include autoimmune liver disease and drug-induced liver injury. Statins, although safe, can rarely trigger immune-mediated hepatitis.A 52-year-old woman with obesity, mixed dyslipidemia, elevated Lp(a), and hepatic steatosis was receiving atorvastatin. Routine blood tests revealed persistent elevation of AST, ALT, GGT, and IgG. Autoimmune screening showed ANA 1/1280, AMA positive, and anti–smooth muscle antibodies 1/640. An abdominal ultrasound was normal. Elastography measured 9.6 kPa. Given the mixed analytical pattern, a liver biopsy was performed. Atorvastatin was discontinued and serial blood tests were monitored.This case illustrates how statin-induced hepatotoxicity may present with positive autoantibodies, closely resembling Primary Biliary Cholangitis (PBC) or autoimmune hepatitis. Such autoimmune-like drug reactions are rare and poorly recognized in primary carePrimary care clinicians should consider statins as a potential cause of immune-mediated liver injury—even when autoantibodies suggest autoimmune disease. Liver biopsy and temporal correlation with medication exposure are key to establishing the correct diagnosis. Future protocols could incorporate earlier evaluation of drug-related causes in atypical autoimmune serologies.The coexistence of AMA positivity, elevated IgG, and steatosis initially suggested PBC. However, the biochemical pattern was not predominantly cholestatic, symptoms were absent, and imaging was normal. Liver biopsy revealed findings consistent with drug-induced hepatitis rather than autoimmune disease. Importantly, liver enzymes and IgG improved markedly after stopping atorvastatin, confirming causality. Recognizing this pattern prevents misdiagnosis and unnecessary immunosuppressive treatment.In patients with metabolic risk factors on statin therapy, elevated liver enzymes with autoantibodies require careful interpretation. This case highlights that statin-induced hepatitis can mimic PBC or autoimmune hepatitis. Biopsy and drug withdrawal were decisive for diagnosis and full recovery. Primary Care plays a crucial role in identifying, evaluating, and correctly attributing these abnormalities.