• 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • 2019-06
  • The exact incidences of amiodarone induced hyperthyroidism a


    The exact incidences of amiodarone-induced hyperthyroidism and amiodarone-induced hypothyroidism currently remain unknown; however, the reported frequencies of amiodarone-induced hyperthyroidism and amiodarone-induced hypothyroidism vary widely from 0.8% to 37.8% [7–16] and from 1% to 32% [13,17–20], respectively. Although amiodarone-induced hypothyroidism is easily controlled by supplementation with L-thyroxine without requiring the discontinuation of amiodarone, the treatment of amiodarone-induced hyperthyroidism is more complex [21]. Amiodarone-induced hyperthyroidism is difficult to treat because of the large accumulation of iodine in the thyroid gland, and withdrawal of the drug is not effective because of its extremely prolonged hcv protease inhibitors of 50–100 days [6,22]. Furthermore, the discontinuation of life-sustaining antiarrhythmic medication is not recommended for patients with life-threatening arrhythmias. A younger age, male gender, thyroid autoantibody production, goiter, and low body mass index are associated with amiodarone-induced hyperthyroidism [12,13,16,23–25], while an older age, higher baseline thyroid-stimulating hormone (TSH) level, lower left ventricular ejection fraction, diabetes mellitus, and thyroid autoantibody production in women are possible risk factors for amiodarone-induced hypothyroidism [9,12,13,26–28]. Amiodarone-induced hyperthyroidism appears to occur more frequently in geographical areas with low dietary iodine intake, whereas amiodarone-induced hypothyroidism is more common in iodine-sufficient areas [26,29,30]. A daily iodine intake of 1–3mg in Japan results in a six- to fifteen-fold excess over the recommended daily intake [31]. Therefore, a higher incidence of amiodarone-induced hypothyroidism may be more common than amiodarone-induced hyperthyroidism. Meanwhile, subclinical thyroid dysfunction, defined as altered TSH and normal thyroxine (T4) levels, has been reported in more than 10% of patients with heart failure or dilated cardiomyopathy (DCM) [32–34]. This suggests that subclinical thyroid dysfunction is not so rare in patients with cardiovascular diseases treated with amiodarone, whereas previous reports regarding the prevalence of risk factors for amiodarone-induced thyroid dysfunction have focused only on patients with euthyroidism before amiodarone therapy [11,35]. Consequently, the impact of subclinical thyroid dysfunction on the development of amiodarone-induced hyperthyroidism and amiodarone-induced hypothyroidism is unclear.
    Materials and methods
    Results Fig. 1 shows the flowchart for study inclusion. Between January 2012 and December 2013, a total of 621 patients for whom amiodarone was prescribed for arrhythmia, were identified from the computer database of the hospital. Forty patients who were treated with antithyroid drugs or thyroid hormone preparations and eight patients diagnosed with thyroid dysfunction at the time of initiation of amiodarone therapy were excluded from the study. Eighty-six patients without tests for thyroid function within three months prior to the initiation of amiodarone therapy and 170 patients without tests for thyroid function more than three months after the initiation of amiodarone therapy were excluded from the study. A total of 317 patients fulfilled the inclusion criteria and were enrolled in the study. The baseline characteristics of the study patients are summarized in Table 1. DCM was the most common underlying cardiac abnormality (27.8%) for patients receiving amiodarone therapy. The mean age for the start of amiodarone therapy was 58.5±16.6 years, and 73.5% of the patients were males. There were 256 patients with euthyroidism, 9 patients with subclinical hyperthyroidism, and 52 patients with subclinical hypothyroidism. The characteristics of patients with normal and abnormal thyroid function after amiodarone therapy are presented in Table 2. After being treated with amiodarone, 30 (9.5%) and 60 (18.9%) patients developed amiodarone-induced hyperthyroidism and amiodarone-induced hypothyroidism, respectively. At the end of the follow-up period, there were 9 patients (2.8%) with subclinical hyperthyroidism, 81 (25.6%) with subclinical hypothyroidism, and 22 (6.9%) were “undetermined”. The remaining patients (36.3%) maintained a euthyroidism state throughout the study period.