BACKGROUND: Type 2 amiodarone-induced thyrotoxicosis remains a significant problem of endocrinology and cardiology. Due to the increase a life expectancy of the population, the prevalence of cardiac arrhythmias and prescribing of amiodarone are increasing. Thyrotoxicosis aggravates the existing cardiovascular disease in patients, leads to the progression of left ventricular dysfunction, relapses of arrhythmias, increasing the risk of adverse outcomes. The tactic of further management of patients is complicated: it is necessary to resolve the issue of canceling or continuing the use of antiarrhythmic drugs necessary for a patient with a history of cardiac arrhythmia, as well as competent therapy of the thyroid pathology that has arisen. Oral glucocorticoids are the first-line drugs for the treatment of patients with moderate and severe type 2 amiodarone-induced thyrotoxicosis. Despite the appearance of clinical recommendations, opinions on the management of patients are differ, both among cardiologists and among endocrinologists. Often thyrostatics are prescribed to patients simultaneously with glucocorticoids, although it doesn’t have pathogenetic basis.AIM: To evaluate the efficacy of various therapy options in patients with type 2 amiodarone-induced thyrotoxicosis.MATERIALS AND METHODS: The retrospective study included 38 patients (20 men and 18 women aged 35 to 85 years) with type 2 amiodarone-induced thyrotoxicosis. All patients underwent an analysis of anamnestic, anthropometric data, complex laboratory and instrumental diagnostics. According to the treatment options, 3 groups were retrospectively formed: without therapy (n=19), taking glucocorticoids (n=11) and combination of glucocorticoids and thyrostatics (n=8). The follow-up period was 6–18 months, including the treatment. The efficacy of treatment in the groups was evaluated by the time of reaching euthyroidism on the background of glucocorticoid therapy and duration of thyrotoxicosis; the search was conducted for potential predictors of delayed response to glucocorticoid therapy and long-term course of thyrotoxicosis.RESULTS: The average age was 62.0 [52.9; 66.3] years. The level of free thyroxine was significantly decreased after 1 month from the start of therapy in both groups: from 38.1 [32.1; 58.4] to 23.4 [19.6; 29.3] pmol/l (p<0.001) in the group taking glucocorticoids; from 73.9 [42.2; 75.6] to 39.3 [22.4; 47.2] pmol/l (p<0.001) in the combination therapy group. The time of reaching euthyroidism was longer in the combination therapy group (p=0.047), didn’t depend on the dose (p=0.338) and duration of taking thiamazole (p=0.911), the delayed response to therapy correlated with age (p=-0.857; p=0.007) and time interval from the appearance of clinical symptoms of thyrotoxicosis to the start of glucocorticoid therapy (p=0.881; p<0.001).CONCLUSION: The results demonstrate the dependence of glucocorticoid response on the age of the patient and start time of therapy relative to the duration of thyrotoxicosis, inexpediency of additional prescribing thyrostatics in type 2 amiodarone-induced thyrotoxicosis.

На данный момент во всем мире существует большое количество разнообразных методик хирургического лечения хронического тонзиллита, в частности классическая тонзиллэктомия, криохирургическое воздействие на небные миндалины, шейверная тонзиллэктомия, монополярная и биполярная тонзиллэктомия, тонзиллэктомия при помощи ультразвукового скальпеля, биполярная диссекция с использованием режущего инструментария, лазерная тонзиллэктомия, коблация. В данной статье проанализированы существующие методы, описана принципиальная техника их выполнения, а также рассмотрены их преимущества и недостатки. С учетом обилия различных хирургических подходов к лечению хронического тонзиллита возрастает необходимость в проведении исследований, направленных на сравнительное изучение их клинической и микробиологической эффективности, включая послеоперационный период.

Possible triggers and genetic markers involved in pathogenesis of amiodarone-induced thyrotoxicosis (AIT) or amiodarone-induced hypothyroidism (AIH) are currently unknown. This study aimed to analyze the association between polymorphisms in the genes involved in thyroid hormones biosynthesis and metabolism. Thirty-nine consecutive patients with confirmed type 2 amiodarone-induced thyrotoxicosis were enrolled; 39 patients on the same therapy for at least 6 months without thyroid pathology were included as a control group. A comparative study was carried out to determine the distribution and genotypes of polymorphic markers of the (Na)-iodide symporter (NIS) genes (rs7250346, C/G substitution), thyroid stimulating hormone receptor (TSHR) (rs1991517, C/G substitution), thyroid peroxidase (TPO) (rs 732609, A/C substitution), DUOX 1-1 (C/T substitution), DUOX 1-2 (G/T substitution), DUOX 1-3 (C/T substitution), glutathione peroxidase 3 (GPX3) (C/T substitution), glutathione peroxidase 4 (GPX4) (C/T substitution). Statistical analysis was performed using Prism (Version 9.0.0 (86)). This study showed that the risk of AIT2 is 3.18 times higher in the G/T of the DUOX1 gene carriers. This study is the first report of genetic markers associated with amiodarone-related adverse events conducted in humans. The obtained results indicate the necessity for a personalized approach to amiodarone administration.

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.

Introduction.There is an abundance of various methods of surgical treatment in the world, which include: classical tonsillectomy (TE), shaver TE, unipolar and bipolar bilateral TE, laser TE, palatine tonsil coblation, etc. However, there is still a risk of recurrence of chronic tonsillitis after TE there is a need for a study in the late postoperative period.Purpose of the study.Improving the efficiency of surgical treatment of patients with chronic tonsillitis based on the analysis of five main methods of surgical treatment of chronic tonsillitis according to clinical and laboratory criteria.Materials and methods.Patients were divided into 5 study groups depending on the method of tonsillectomy: The first group consisted of 60 patients after classical tonsillectomy. In the second group there were 55 patients after palatine tonsil coblation. The third group included 48 patients after laser tonsillectomy. The fourth group consisted of 64 patients after tonsillectomy using the surgitron apparatus. The fifth group consisted of 58 patients after microdebrider tonsillectomy.Results.By analysis, it was found that the best results were obtained in patients of the 1^stgroup, who underwent classical tonsillectomy. In this group, there are fewer cases of subjective and objective clinical symptoms (sore throat, signs of subatrophic pharyngitis, hypertrophy of the lateral folds of the pharynx, remnants of the lymphoid tissue of the palatine tonsils, as well as postoperative cicatricial changes). In a laboratory study, patients of the 1^stgroup had the lowest values of the indicators (ASL-O titer, CRP and DNase B levels, negative results of the Streptatest).

Background: Glucocorticoids are the first-line pharmacotherapy for amiodarone-induced destructive thyroiditis. Despite the availability of clinical guidelines, there is no unified approach to patient management (indications for prescription, starting dose, duration of therapy and withdrawal algorithm). The issues of dose-dependent effect of glucocorticoids, verification of factor of delayed treatment response, prediction of severity and duration of thyrotoxicosis remain unresolved. Aim: To evaluate the efficacy of various regimens of tablet glucocorticoids in patients with type 2 amiodarone-induced thyrotoxicosis. Methods: This was a prospective randomized open-label comparative controlled trial of the efficacy of two starting doses of prednisolone 30 mg (n = 22) and 60 (n = 22) mg daily. The study groups were comparable for gender (men to women ratio 2:1), age, anthropometric and main clinical and laboratory characteristics. After euthyroidism has been achieved, thyroid function was assessed twice at 1 and 2 months during the dose reduction and at 1, 3, 6, 9, and 12 months after prednisolone withdrawal. The follow up was 15 to 24 months. The efficacy of therapy was evaluated by the time to euthyroidism, thyrotoxicosis duration, rate of recurrent waves of destruction and relapses. We looked for predictors of delayed treatment response and severe and prolonged thyrotoxicosis. Results: There were no significant differences in the time to euthyroidism (Mantel-Cox log rank test 0.859), duration of thyrotoxicosis (Mantel-Cox log rank test 0.813), rate of recurrent waves of destruction (0.721) and relapses (0.464). Within 30 days of therapy, remission was obtained in 11/22 (50.0%) patients in active control group (prednisolone 30 mg) and in 12/22 (54.5%) patients in the 60 mg group. Delayed response ( 60 days) was defined by recurrent waves of destruction (RR = 34.7, 95% CI: 3.7–321.8; R² = 0.430; p = 0.002). High risk of severe thyrotoxicosis was predicted by the age ≤ 54 years (AUC 0.749 ± 0.095, 95% CI: 0.562–0.936; p = 0.038; sensitivity 71.4%, specificity 62.2%). The duration of thyrotoxicosis was associated with body mass index (B = -7.4, R = 0.481, R² = 0.0231; p = 0.024) and cumulative amiodarone dose (B = 0.4, R = 0.472, R² = 0.223; p = 0.026). A combination of adverse events (hyperglycemia, infection, proximal myopathy, change in appearance, hematomas) and their severity were more frequent in the patients who had received the 60 mg prednisolone starting dose (p = 0.014). Conclusion: Compared to lower doses, the use of high doses of glucocorticoids is associated with a greater severity of side effects and does not ensure any significant acceleration of thyrotoxicosis remission. The potential factors of unfavorable clinical course of type 2 amiodarone-induced thyrotoxicosis are age, body mass index, and cumulative dose of amiodarone.