[Effect of amiodarone on the thyroid function and safety of the therapy--what's new]

This paper presents the current state of knowledge on the effects of amiodarone (AM) on the thyroid gland function, including the question of epidemiology, pathogenesis and prognostic factors. Of all the antiarrhythmic drugs hitherto used, AM has the most adverse effects on the thyroid gland. In patients receiving AM, it may lead to a development of a full- symptomatic hyperthyroidism (AIT-Amiodarone-induced thyrotoxicosis) and hypothyroidism (AIH - Amiodarone-induced hypothyroidism). The time from the start of the treatment of AM to the onset of symptoms of thyrotoxicosis is varied and amounts approximately to 3 years. The AIT may develop up to 2 years after the cessation of the AM treatment because of the accumulation of the drug and its metabolites in the body. The AIT treatment is complicated and often requires multiple treatment methods, such as: antithyroid drugs, glucocorticoids, iopanic acid, plasmapheresis, thyroidectomy and radioiodine. AIH is associated with the Wolff-Chaikoffa phenomenon. Thyroid hormone synthesis is impaired by blocking iodine organification. Hypothyroidism can also arise and be exacerbated by the output of thyroid disease - autoimmune diseases. The paper also devotes much attention to the relationship between smoking and the toxicity of AM. The components of tobacco smoke increase the activity of enzymes involved in the metabolism of AM. Increased concentrations of desetyloamiodarone in lung tissue may be responsible for the increased toxicity in the lungs in smokers. In addition, the paper presents a new antiarrhythmic drug - dronedarone (DN), an attractive alternative, but, because of the high risk of heart failure, stroke and death from cardiovascular disease, with a limited potential.