Endocrine Abstracts

Introduction: Graves’ thyrotoxicosis has been known to affect other organ systems in the body including the liver. However, severe hepatitis in this clinical context is quite rare.

Case report: We report a 55-year-old man who presented with marked weight loss and jaundice. In addition, he had a diffuse goitre with fine tremors in the hands. Laboratory work-up revealed thyrotoxicosis with FT₄ of 87.9 pmol/l and TSH of <0.01 mIU/l. He had abnormal liver function with total bilirubin 258.3 μmol/l, Direct Bilirubin 217 μmol/l, indirect bilirubin 41.2 μmol/l, ALP 306 U/l and ALT at 54 U/l. Serological tests excluded viral hepatitis. Ultrasound of the thyroid and hepatobiliary system together with MRCP were normal. In view of the hepatitis, he was given a potassium iodide solution and dexamethasone (10 mg daily) to prevent the peripheral conversion of T₄ to T₃. The jaundice and liver function test improved within a few days. Carbimazole 20 mg daily was slowly commenced with the resulting drop of FT₄ to 25 pmol/l. However the ALP increased to 359 mmo/l requiring the reduction of carbimazole dose down to 10 mg daily. Subsequent FT₄ came down to 15 pmol/l and he successfully underwent an RAI therapy 2 months later, which was uneventful.

Discussion: Acute icteric hepatitis occurs in <1% of Graves’ thyrotoxicosis, posing a management dilemma. This has to do with the close association between liver enzyme abnormalities and oral antithyroid medications. Propylthiouracil and carbimazole, may cause elevation in aminotransferase levels (28%) usually 6 weeks to 2 months after administration. In our patient the elevated aminotransferase level preceded the administration of the drug which lead to rapid aggravation of the hepatocyte damage.

In conclusion, derangement of liver enzymes associated with Graves’ thyrotoxicosis even in fulminant cases tends to be transient and most patients recover with no long-term sequeale.