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ABSTRACT
Amiodarone (AMD) is a potent antiarrhythmic drug, liposoluble bensophuran derivative, containig 75 mg of iodide per 200 mg of active substance with elimination half-life of several months. Metabolism of 300 mg of AMD yields approximately 9 mg/day of iodide. In susceptible patients chronical iodine overload can induce thyroid disfunction – hypothyreosis or thyrotoxicosis.
The aim of the the article is the evaluation of clinical characteristics of patients with AIH. Eight patients from 120 on chronical AMD treatment, followed clinically and biochemicaly, developed hypothyreosis – 5 males and 3 females.
The mean age was 59. The mean duration of AMD teratment before induced hypothyreosis was 20 months. Clinical manifestations were absent in 3 patiens along with the elevated TSH and decreased FT4. Others had typical clinical signs and symptoms of hypothyreosis. In all the patients hypothyreosis was transient. In all the patients AMD was withdrawn; 5 of them received substitution (Levothyroxine tbl. 100 mcg/day) for the mean duration of 4,2 months. None of the patiens had previous history of thyroid disorder, nor positive family history.
All patients receiving chronical AMD treatment should be screened periodically (eg. two times a year) clinically and bichemically for thyroid disfunction.
Keywords: hypothyreoidism, amiodarone
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