Hong Kong medical journal = Xianggang yi xue za zhi · 2010
Amiodarone-induced thyroid dysfunction in the Hong Kong Chinese population.
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Lee K F, Lee K M, Fung T T
Аннотация
OBJECTIVE: To determine the frequency, risk factors, clinical features, and management of amiodarone-induced thyroid dysfunctions.
DESIGN: Retrospective study.
SETTING: A regional hospital in Hong Kong.
PATIENTS: Patients who had been prescribed amiodarone for at least 6 months from 1 October 2005 to 30 September 2007.
RESULTS: A total of 390 patients (mean age, 70 years; standard deviation, 9 years; 54% male) with a median follow-up of 43 (interquartile range, 25-69) months were studied. Hypothyroidism developed in 87 (22%) of the patients (mean age, 72 years; standard deviation, 7 years; 56% male) and thyrotoxicosis in 24 (6%) of the patients (65 years; 11 years; 54% male). Increased baseline thyrotropin (thyroid-stimulating hormone) level appeared to be predictive of amiodarone-induced hypothyroidism, in which a thyroid-stimulating hormone level of 4 mIU/L or above was associated with a 4.7-fold increase in the risk (95% confidence interval, 1.9-11.7; P<0.001). Compared with those who remained euthyroid on amiodarone, thyrotoxicosis developed in younger patients. In these patients, the classical symptoms of thyroid dysfunction were frequently absent, although worsening of underlying arrhythmias, their cardiac condition, weight loss, and over-warfarinisation were suggestive of amiodarone-induced thyrotoxicosis. In both amiodarone-induced thyrotoxicosis and hypothyroidism, the disease course was benign. Patients with the former showed a good response to anti-thyroid drugs and steroid therapy.
CONCLUSIONS: Amiodarone-induced thyroid dysfunction is common among our population. As the clinical presentations are usually vague and atypical, regular biochemical monitoring of thyroid function is warranted, particularly in patients with elevated baseline thyroid-stimulating hormone level. The disease course of amiodarone-induced thyrotoxicosis is usually benign and remits with timely administration of anti-thyroid medications, with or without corticosteroids.
DESIGN: Retrospective study.
SETTING: A regional hospital in Hong Kong.
PATIENTS: Patients who had been prescribed amiodarone for at least 6 months from 1 October 2005 to 30 September 2007.
RESULTS: A total of 390 patients (mean age, 70 years; standard deviation, 9 years; 54% male) with a median follow-up of 43 (interquartile range, 25-69) months were studied. Hypothyroidism developed in 87 (22%) of the patients (mean age, 72 years; standard deviation, 7 years; 56% male) and thyrotoxicosis in 24 (6%) of the patients (65 years; 11 years; 54% male). Increased baseline thyrotropin (thyroid-stimulating hormone) level appeared to be predictive of amiodarone-induced hypothyroidism, in which a thyroid-stimulating hormone level of 4 mIU/L or above was associated with a 4.7-fold increase in the risk (95% confidence interval, 1.9-11.7; P<0.001). Compared with those who remained euthyroid on amiodarone, thyrotoxicosis developed in younger patients. In these patients, the classical symptoms of thyroid dysfunction were frequently absent, although worsening of underlying arrhythmias, their cardiac condition, weight loss, and over-warfarinisation were suggestive of amiodarone-induced thyrotoxicosis. In both amiodarone-induced thyrotoxicosis and hypothyroidism, the disease course was benign. Patients with the former showed a good response to anti-thyroid drugs and steroid therapy.
CONCLUSIONS: Amiodarone-induced thyroid dysfunction is common among our population. As the clinical presentations are usually vague and atypical, regular biochemical monitoring of thyroid function is warranted, particularly in patients with elevated baseline thyroid-stimulating hormone level. The disease course of amiodarone-induced thyrotoxicosis is usually benign and remits with timely administration of anti-thyroid medications, with or without corticosteroids.