BACKGROUND: Amiodarone takes a leading position in arrhythmological practice in the prevention and relief of various cardiac arrhythmias. Type 2 amiodarone-induced thyrotoxicosis is a frequent side effect of the drug. It is the most complex type of thyroid dysfunction both in terms of the severity of clinical manifestations, and in terms of understanding the mechanisms of pathogenesis, possibility of differential diagnosis and providing effective treatment. Due to the increasing life expectancy of the population, corresponding increase in the frequency of cardiac arrhythmias, the problem does not lose its relevance. Identification of predictors, assessment and prediction of the individual risk of developing this thyroid pathology is a necessity in daily clinical practice for making a reasonable decision when prescribing the drug, determining the algorithm for further dynamic monitoring of the patient.AIM: To evaluate the structure of amiodarone-induced thyroid dysfunction, prevalence, time and predictors of development type 2 amiodarone-induced thyrotoxicosis in a prospective cohort study. MATERIALS AND METHODS: The study involved 124 patients without thyroid dysfunction who received amiodarone therapy for the first time. Evaluation of the functional state of the thyroid gland was performed initially, after prescribing the drug for the first 3 months 1 time per month, in the future – every 3 months. The follow-up period averaged 12-24 months. The end of the observation occurred with the development of amiodaron-induced thyroid dysfunction or patient's refusal to further participate in the study. For the differential diagnosis of the type of amiodarone-induced thyrotoxicosis, the level of anti-TSH receptor antibodies and thyroid scintigraphy with technetium pertechnetate were determined. The type and frequency of thyroid dysfunction, time and predictors of development type 2 amiodarone-induced thyrotoxicosis were evaluated.RESULTS: The structure of amiodarone-induced thyroid dysfunction was represented by hypothyroidism in 19,3% (n=24), type 1 thyrotoxicosis in 1,6% (n=2), type 2 thyrotoxicosis in 23,4% (n=29). The median time of its development was 92,0 [69,0;116,0] weeks; the average period of common survival – 150,2±12,6 weeks (95% CI: 125,5–175,0), median – 144±21,7 weeks (95% CI: 101,4–186,6). The main predictors of type 2 amiodarone-induced thyrotoxicosis were: age (OR=0,931; 95% CI: 0,895–0,968; p<0.001), BMI (OR=0,859; 95% CI: 0,762–0,967; p=0,012), time from the start of amiodarone therapy (OR=1,023; 95% CI: 1,008–1,038; p=0,003). Age ≤60 years was associated with increased risk of the dysfunction by 2.4 times (OR=2,352; 95% CI: 1,053–5,253; p=0,037), BMI≤26,6 kg/m2 – 2,3 times (OR=2,301; 95% CI: 1,025–5,165; p=0,043). CONCLUSION: The results allow to personalized estimate the risk of type 2 amiodarone-induced thyrotoxicosis and determine the patient's management tactic.
