
IATROGENIC CHANGES IN THYROID GLAND OF PATIENTS WITH ATRIAL FIBRILLATION AFTER THERAPY WITH AMIODARON
Author(s) -
Oksana Danyliuk
Publication year - 2021
Publication title -
aktualʹnì problemi sučasnoï medicini: vìsnik ukraïnsʹkoï medičnoï stomatologìčnoï akademì
Language(s) - English
Resource type - Journals
eISSN - 2077-1126
pISSN - 2077-1096
DOI - 10.31718/2077-1096.21.1.11
Subject(s) - amiodarone , medicine , euthyroid , thyroid , atrial fibrillation , cardiology , bisoprolol , heart failure , triiodothyronine , endocrinology
Objective of the study: to analyze the frequency of structural and functional changes in the thyroid gland of the patients with atrial fibrillation who took amiodarone for 12 months on regular basis. The study was based on findings obtained by examining 80 patients (28 women and 52 men) with cardiosclerosis (diffuse and postinfarction), atrial fibrillation and heart failure IIA at the age of 63.5 ± 1.3 years and 15 healthy individuals of the relevant age (62,4 ± 2,4 years) and relevant sex proportions. The main inclusion criterion was the euthyroid state of the thyroid gland before the beginning of antiarrhythmic therapy. To assess the functional state of the thyroid gland, we studied the content of free thyroxine, triiodothyronine, and antibodies to thyroid peroxidase. The examination was carried out before the therapy, and in 3, 6, 9 and 12 months after the beginning of the study during the course of antiarrhythmic therapy. To detect structural changes in the thyroid gland, we used ultrasound scanning. Depending on the prescribed treatment, the participants were divided into the following groups: group I included the patients who received amiodarone in a dosage of 200 mg per day and basic therapy (n = 60); control group involved the patients who received the basic therapy with antiarrhythmic drugs, digoxin and bisoprolol (n = 20). Results. The therapy with amiodarone for a year resulted in thyroid dysfunction in 33.3% of the patients. Hypothyroidism (20.0%) is leading in the structure of amiodarone-associated thyroid dysfunctions; this condition is subclinically manifested in 11.7% of the patients. The development of amiodarone-induced thyrotoxicosis was observed in 13.3% of the patients, and the first cases of hyperthyroidism were detected not earlier than six months. Under the effect of amiodarone in the first months of the therapy, serum levels of free thyroxine may increase, while free triiodothyronine may decrease, therefore there may be a tendency to slightly increased levels of thyroid-stimulating hormone in the first weeks of the therapy. The above changes in laboratory parameters are transient and are not accompanied by the deterioration of the antiarrhythmic action of amiodarone.