Abstract
The review presents recent data on the pathogenesis, diagnosis and treatment of amiodarone-induced thyrotoxicosis (AIT), which is a frequent complication of amiodarone (Am) therapy. Changes in secretion and metabolism of thyroid hormones are described under the influence of short-term and long-term therapy. The development of AIT leads to worsening of arrhythmias, aggravation of circulatory insufficiency, deterioration of the patient’s condition. Two types of AIT are distinguished, as well as mixed form. Diagnostic criteria of AIT type 1 and AIT type 2 are described. The most informative test for differential diagnosis between first and second types of AIT and mixed forms is ultrasound examination of the thyroid gland with Doppler blood flow evaluation and radionuclide scanning with 99 mTc-sestaMIBI. Medical management is determined by the type of AIT, the state of cardiovascular system and the risk of recurrent arrhythmias. Pharmacological management of AIT depends on it’s type and comprises the use of anti-thyroid medications or glucocorticoids. The possibility of continuing antiarrhythmic amiodarone therapy in patients who underwent AIT is discussed. In patients with AIT type 1 and mixed form drug cancellation is required, if this is not possible – radical treatment of thyrotoxicosis (radioiodine therapy, thyroidectomy) is applied. AIT type 2 is a self-limiting process with life-threatening arrhythmias, and amiodarone therapy can be continued. The effectiveness of radioiodine therapy for radical treatment of AIT type 1 and type 2 is shown in spite of low radioiodine capture. However, this issue requires further investigation and discussion. Plasmapheresis and thyroidectomy are used for rapid restoration of euthyroidfunction in severe patients.
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