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Abstract：
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.
OBJECTIVE: 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.
OBJECTIVE: 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.
摘要：
背景：胺碘酮在预防和缓解各种心律失常的心律失常学实践中处于领先地位。2型胺碘酮诱导的甲状腺毒症是该药物的常见副作用。就临床表现的严重程度而言，它是最复杂的甲状腺功能障碍类型，在理解发病机制方面，鉴别诊断和提供有效治疗的可能性。由于人口预期寿命的增加，心律失常的频率相应增加，这个问题并没有失去意义。预测因子的识别，评估和预测发生这种甲状腺病理的个体风险是日常临床实践中的必要条件，以便在处方药物时做出合理的决定，确定用于进一步动态监测患者的算法。
目的：评估胺碘酮诱导的甲状腺功能异常的结构，患病率,一项前瞻性队列研究发现2型胺碘酮诱发甲状腺毒症的发生时间和预测因素.材料和方法：本研究纳入124例首次接受胺碘酮治疗的无甲状腺功能不全患者。最初进行甲状腺功能状态的评估，在开药前3个月后，每月1次，在未来-每3个月。随访时间平均为12-24个月。观察结束时发生胺碘酮诱导的甲状腺功能障碍或患者拒绝进一步参与研究。对于胺碘酮诱导的甲状腺毒症的类型的鉴别诊断，测定了抗TSH受体抗体水平和高tech酸tech的甲状腺闪烁显像.甲状腺功能障碍的类型和频率，评估了2型胺碘酮诱导的甲状腺毒症的发生时间和预测因子.
结果：胺碘酮诱导的甲状腺功能障碍的结构表现为19,3％（n=24）的甲状腺功能减退，1型甲状腺毒症占1.6%(n=2)，2型甲状腺毒症占23,4％（n=29）。其发展的中位时间为92,0[69,0;116,0]周；平均生存期-150,2±12,6周（95％CI：125,5-175,0），中位数-144±21,7周（95%CI：101,4-186,6）。2型胺碘酮诱发甲状腺毒症的主要预测因素是：年龄（OR=0.931;95％CI：0.895-0.968;p＆lt;0.001），BMI（OR=0.859；95%CI：0.762-0.967；p=0.012），从胺碘酮治疗开始的时间(OR=1,023;95%CI:1,008-1,038;p=0,003)。年龄≤60岁与功能障碍风险增加2.4倍相关（OR=2,352；95％CI：1,053-5,253；p=0,037），BMI≤26,6kg/m2-2,3倍（OR=2,301；95％CI：1,025-5,165；p=0,043）。结论：该结果允许个性化评估2型胺碘酮诱发甲状腺毒症的风险，并确定患者的治疗策略。
目的：评估胺碘酮诱导的甲状腺功能异常的结构，患病率,一项前瞻性队列研究发现2型胺碘酮诱发甲状腺毒症的发生时间和预测因素.材料和方法：本研究纳入124例首次接受胺碘酮治疗的无甲状腺功能不全患者。最初进行甲状腺功能状态的评估，在开药前3个月后，每月1次，在未来-每3个月。随访时间平均为12-24个月。观察结束时发生胺碘酮诱导的甲状腺功能障碍或患者拒绝进一步参与研究。对于胺碘酮诱导的甲状腺毒症的类型的鉴别诊断，测定了抗TSH受体抗体水平和高tech酸tech的甲状腺闪烁显像.甲状腺功能障碍的类型和频率，评估了2型胺碘酮诱导的甲状腺毒症的发生时间和预测因子.
结果：胺碘酮诱导的甲状腺功能障碍的结构表现为19,3％（n=24）的甲状腺功能减退，1型甲状腺毒症占1.6%(n=2)，2型甲状腺毒症占23,4％（n=29）。其发展的中位时间为92,0[69,0;116,0]周；平均生存期-150,2±12,6周（95％CI：125,5-175,0），中位数-144±21,7周（95%CI：101,4-186,6）。2型胺碘酮诱发甲状腺毒症的主要预测因素是：年龄（OR=0.931;95％CI：0.895-0.968;p＆lt;0.001），BMI（OR=0.859；95%CI：0.762-0.967；p=0.012），从胺碘酮治疗开始的时间(OR=1,023;95%CI:1,008-1,038;p=0,003)。年龄≤60岁与功能障碍风险增加2.4倍相关（OR=2,352；95％CI：1,053-5,253；p=0,037），BMI≤26,6kg/m2-2,3倍（OR=2,301；95％CI：1,025-5,165；p=0,043）。结论：该结果允许个性化评估2型胺碘酮诱发甲状腺毒症的风险，并确定患者的治疗策略。
