A diagnostic conundrum: Cholestatic liver injury during graves’ disease management revealing psc–aih overlap

Introduction

Liver dysfunction in Graves’ disease is usually attributed to thyrotoxicosis or antithyroid drug-induced liver injury. Methimazole-induced liver injury is a known cause of cholestatic liver injury pattern in patients treated for Graves’ disease. Persistent or progressive cholestatic liver dysfunction despite drug withdrawal indicates an underlying autoimmune hepatobiliary disorder. Differentiating Drug-induced liver injury from autoimmune liver disease is challenging, when autoimmune serology and radiological investigations are unremarkable. Case Report and Results: A 49-year-old gentleman presented with 2-months history suggestive of thyrotoxicosis. Diagnosis of Graves’ disease was confirmed with biochemical investigations(tsh-0.05miu/ml, total t4-21.5mcg/dl, totalt3349ng/dl and echnetium-99m thyroid scintigraphy. Baseline liver enzymes were normal. Methimazole and propranolol were initiated, with subsequent dose reduction according to thyroid function test. Nine weeks after treatment initiation, patient presented with jaundice and pruritis and liver function was suggestive of cholestatic pattern. Despite drug withdrawal, liver function worsened, (AST/ALT 61/76 U/L, ALP 235 U/L, total bilirubin 5.27 mg/dL). Viral hepatitis screening, autoimmune serology (ANA, AMA, ASMA, LKM-1), serum IgG, and Magnetic Resonance Cholangiopancreatography (MRCP) were within normal range. Liver biopsy was suggestive of interface hepatitis, intrahepatic cholestasis, onion-skin periductal fibrosis with bile duct obliteration, granulomas, and portal fibrosis (Ishak 1/6), consistent with primary sclerosing cholangitis with autoimmune hepatitis overlap. Prednisolone (40 mg/day) was initiated, methimazole was replaced with lithium, and definitive treatment with radioiodine I131 (10 mCi) was done. Liver function progressively normalized with corticosteroid therapy, which was successfully tapered over 20 weeks. Patient after 20 weeks of radioiodine ablation became hypothyroid and is currently euthyroid on levothyroxine replacement.