A 51-year-old Chinese man came to our hospital complaining of weight loss of 4 kg, finger tremors, sweating, and palpitations for 1 month in May 2013. Physical examination showed that his thyroid gland was slightly enlarged and tender. No other clinically relevant physical findings were recorded. His thyroid function was presented as increased free thyroxine (FT4), free triiodothyronine (FT3) along with low thyroid-stimulating hormone (TSH). At that time, his blood count, liver function test, erythrocyte sedimentation rate, and C-reactive protein were within the normal range. A thyroid scan using 99mTcO4 - revealed diffuse increased uptake in the thyroid area and ultrasound showing increased color Doppler flow was in the symmetrically enlarged thyroid. He was diagnosed as having hyperthyroidism due to Graves' disease and started treatment with MMI (10 mg twice daily) and propranolol (10 mg thrice daily). Four weeks after taking these drugs, he had a sore throat with high fever (40.0 C), skin rash, cholestatic symptoms including dark urine, pruritus, and jaundice. He went to the hospital and got laboratory analyses. The results showed total WBCs 1.1 x 109/L with no neutrophils, total serum bilirubin (TB) 385 mumol/L, conjugated bilirubin (DB) 299 mumol/L, alanine aminotransferase (ALT) 89 U/L, aspartate aminotransferase (AST) 30 U/L, prothrombin time (PT) 17 s, FT4 37.1 ng/dL, FT3 5.61 pg/mL, and TSH 0.001 mulU/mL. He was recommended to stop MMI immediately. Further examination results were as follows: his electrocardiogram and ultrasonic cardiogram were normal; abdominal ultrasonograph showed no evidence of biliary dilatation or gallbladder disease; chest X-ray showed no abnormalities. He was negative for antinuclear antibody, anti-smooth-muscle antibody, antineutrophil cytoplasm antibodies, and hepatitis A, B, C, and E. He has no history of alcohol addiction, smoking, additional drug, blood transfusion, or recent overseas travel. So we considered this to be a diagnosis of MMI-induced severe cholestatic hepatotoxicity with agranulocytosis. Initial management included cessation of MMI, empiric antibiotic treatment (IV Sulperazone, oral levofloxacin) and hepatoprotective treatment (IV atomolam and glycyrrhizinate). By day 5, the patient was afebrile. At the 2nd week, his granulocytes count had risen to 3.1 x 109/L, his liver function tests were all improving, and TB had fallen to 158 mumol/L. Three weeks after MMI stopped, 296 MBq dose of 131I was given. Five weeks later, the values of liver function decreased to normal. His symptoms of hyperthyroidism were improved in the 3rd month after 131I treatment and his thyroid function remained at normal levels in the 6th month. During the course of the patient, changes in his thyroid function, liver function, and blood counts are shown in Table 1.