Methimazole or carbimazole can cause liver
dysfunction in patients with hyperthyroidism
(July 2002)
The background
of the study. The antithyroid drugs in wide use
- methimazole, carbimazole, and propylthiouracil - can cause liver
dysfunction. This article describes a patient with hyperthyroidism
who had liver disease during treatment with methimazole and summarizes
previous reports of liver dysfunction in patients with hepatic disorders
acquired during treatment with methimazole or carbimazole.
Case report. A
36-year-old woman with hyperthyroidism caused by Graves' disease
was treated with propranolol, 20 mg three times daily, and methimazole,
20 mg twice daily. At base line, she had a diffuse goiter, no ophthalmopathy,
and no liver enlargement. On day 19 of treatment, jaundice, abdominal
discomfort, and dark urine developed; methimazole was discontinued.
On day 23, physical examination revealed jaundice but no abdominal
tenderness or liver enlargement. Tests of liver function were abnormal.
Studies for hepatitis virus infection were negative. Abdominal ultrasonography
revealed inflammation of small bile ducts within the liver (cholestatic
hepatitis). The dose of propranolol was doubled, and she was given
15 mCi (555 MBq) of radioiodine on day 27. Her liver function initially
worsened, but then improved.
Review of reported cases.
Thirty-one patients, including this patient, with liver dysfunction
disorders acquired while taking methimazole or carbimazole have
been reported. Twenty patients had cholestatic hepatitis, like this
patient. The mean time of onset after starting treatment was 36
days (range, 12 to 90), and the mean daily dose of the drugs was
44 mg (range, 15 to 80). In most patients recovery was slow, but
complete, as in this patient. The other 11 patients had toxic hepatitis,
fatty liver, or other conditions.
The conclusions of the study.
Methimazole and carbimazole can in rare cases cause cholestatic
hepatitis or possibly other hepatic disorders.
The original article.
Woeber KA. Methimazole-induced hepatotoxicity. Endocr Pract
2002;8:222-4.
|
