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  • order Clozapine N-oxide As shown in Fig out of the patients

    2019-05-15

    As shown in Fig. 2, 40 out of the 60 patients (66.6%) who developed amiodarone-induced hypothyroidism, and 10 out of the 30 patients (33.3%) who developed amiodarone-induced hyperthyroidism, were diagnosed within two years of order Clozapine N-oxide of amiodarone therapy. Amiodarone-induced hypothyroidism developed significantly earlier than amiodarone-induced hyperthyroidism following initiation of amiodarone therapy (P<0.003). The relationship between thyroid function status before and after amiodarone therapy is presented in Table 3, which shows the distribution of patients with thyroid dysfunction before and after amiodarone therapy. Among 256 patients with euthyroidism at baseline, 27 (10.5%) and 41 patients (16.0%) developed amiodarone-induced hyperthyroidism and amiodarone-induced hypothyroidism, respectively. However, 17 out of the 52 patients (32.7%) with subclinical hypothyroidism at baseline developed amiodarone-induced hypothyroidism after the therapy. Two out of the 52 patients (3.8%) with subclinical hypothyroidism at baseline developed amiodarone-induced hyperthyroidism. A stepwise multivariate logistic regression analysis identified patient age at baseline [Adjusted OR 0.95 (95% CI: 0.92–0.97)], DCM [Adjusted OR 3.30 (95% CI: 1.26–8.90)], and cardiac sarcoidosis [Adjusted OR 6.47 (95% CI: 1.60–25.77)] as predictors of amiodarone-induced hyperthyroidism (Table 4). In the analysis of amiodarone-induced hypothyroidism, baseline free T4 level [Adjusted OR 0.13 (95% CI: 0.03–0.63)], TSH level [Adjusted OR1.47 (95% CI: 1.26–1.74)], and average dose of amiodarone per day [Adjusted OR 1.01 (95% CI: 1.00–1.01)] were identified as predictors (Table 5).
    Discussion The prevalence of amiodarone-induced hyperthyroidism was higher in our study than in previous studies conducted in Asian countries [13,19,35] that included only patients with euthyroidism. The prevalence of amiodarone-induced hyperthyroidism was previously reported to be 4.0% in Taiwan [19] and 6% in the Chinese population living in Hong Kong [13]. Additionally, a recent study found that the prevalence of amiodarone-induced hyperthyroidism was 5.8% in Japan [35]. In our study, patients with subclinical hyperthyroidism and hypothyroidism were included in the analysis in order to determine the predictors of amiodarone-induced hypothyroidism and amiodarone-induced hyperthyroidism in clinical practice. Patients with subclinical thyroid dysfunction are also treated with amiodarone. Therefore, predictors associated with the clinical use of amiodarone therapy need to be investigated. In our analysis of 256 patients with euthyroidism at baseline, 10.5% and 16.0% of patients developed amiodarone-induced hyperthyroidism and amiodarone-induced hypothyroidism, respectively. Therefore, the high prevalence of amiodarone-induced hyperthyroidism in our study may not be attributable to the inclusion of patients with subclinical thyroid dysfunction. Meanwhile, the prevalence of amiodarone-induced hypothyroidism was similar to previously reported prevalences in Asian countries (13.1% in Taiwanese and 22% in the Hong Kong Chinese population). We identified several candidates as potential predictors of amiodarone-induced hyperthyroidism and amiodarone-induced hypothyroidism in the patient characteristic analysis. Baseline free T4 and baseline TSH levels, and the duration of amiodarone therapy, were considered as candidate predictors of amiodarone-induced hypothyroidism. Patients with subclinical hypothyroidism at the initiation of amiodarone therapy were more likely to develop amiodarone-induced hypothyroidism. In the present study, 41 out of the 256 patients (16.0%) with euthyroidism at the initiation of amiodarone therapy developed amiodarone-induced hypothyroidism. Meanwhile, 17 out of the 52 patients (32.7%) with subclinical hypothyroidism at the initiation of amiodarone therapy developed amiodarone-induced hypothyroidism. Subclinical hypothyroidism may be a potential risk factor for amiodarone-induced hypothyroidism. In order to test this hypothesis, a stepwise multivariate logistic regression analysis was performed. Consequently, lower baseline free T4 level, higher baseline TSH level, and higher average dose of amiodarone per day were identified as independent risk factors for the development of amiodarone-induced hypothyroidism. Higher baseline TSH level supports the hypothesis that subclinical hypothyroidism is a predictor of the development of amiodarone-induced hypothyroidism. Although average dose of amiodarone per day was also statistically significant as a predictor of amiodarone-induced hypothyroidism, the relationship between amiodarone dosage and amiodarone-induced hypothyroidism currently remains unclear. Additionally, both sample size and effect size of the odds ratios were small in the present study. Therefore, we cannot conclude that average dose of amiodarone per day is a clinically significant risk factor, and further studies are needed to elucidate this issue. In the present study, 40 out of the 60 patients (66.6%) who developed amiodarone-induced hypothyroidism were diagnosed within two years of initiation of amiodarone therapy. This result is consistent with previous studies, suggesting that a shorter duration of amiodarone use is associated with the development of amiodarone-induced hypothyroidism [19,37]. Lower baseline free T4 and higher baseline TSH levels, including those for subclinical hypothyroidism, appear to be potential risk factors for amiodarone-induced hypothyroidism in patients receiving amiodarone therapy. These findings suggest that careful medical surveillance for amiodarone-induced hypothyroidism is needed in patients with subclinical hypothyroidism at baseline.