The use of several groups of medications may result in thyroid dysfunction including thyrotoxicosis or hypothyroidism of various degree (from subclinical to full-clinical syndrome). The mentioned disturbances may develop either on the basis of normal euthyroid gland or may overlap the previously-existing oceult changes (first of all different forms of autoimmune thyroiditis). Amiodarone is a widely used anti-arrythmic drug with considerable potential to cause thyroid dysfunction because of its 35% iodine content. Besides amiodarone particles are known to inhibit T4 to T3 conversion, they work as inhibitors of nuclear receptors for thyroid hormones, exert cytotoxic effect and induce immune/inflammatory process in thyroid gland. Both thyrotoxicosis (AIT - amiodarone induced thyrotoxicosis) and hypothyroidism (AIH - amiodarone induce hypothyroidism) may develop during amiodarone therapy. AIT appears to occur more frequently in geographical areas with low iodine intake, whereas AIH is more frequent in iodine-sufficient areas. Two forms of AIT are known. Their differentiation is very important for further therapeutical procedures. Because thyrotoxicosis and hypothyroidism symptoms during amiodarone therapy are scanty, there is need for periodic determination of thyroid function. Normal ranges for amiodarone patients differ from those for the rest of population. They are presented in this review. Treatment of AIT is very complicated. Sometimes there is need to use few methods together, especially when amiodarone treatment can not be stopped.