Amiodarone-induced thyrotoxicosis with paroxysmal supraventricular (ectopic atrial) tachycardia: case report and review of the literature

The most common side effects of amiodarone therapy include disruptions of thyroid function with the incidence range from 14-18% [1, 2]. In fact this antiarrhythmic drug is rich in iodine and during common therapy the oversupply of iodine is 50-100 times higher than its optimal intake. Moreover, due to its intrinsic qualities (not related to iodine load), such as structural resemblance to thyroid hormones, the ability of inhibiting deiodinase enzymes or tissue toxicity, amiodarone can alter thyroid balance via different mechanisms [1, 2]. Impaired functioning of the thyroid has various forms: from subclinical changes in hormone concentrations, to overt clinical problems: amiodarone-induced thyrotoxicosis (AIT) and amiodarone-induced hypothyroidism (AIH). In areas rich in iodine, AIH is often observed, whereas in areas of low iodine supply, AIT is often observed. Amiodarone-induced thyrotoxicosis occurs in men more frequently, while AIH is more common in women. In contrast to the more easily treatable hypothyroidism, AIT poses a challenge for clinicians. Amiodarone-induced thyrotoxicosis can present as AIT I, AIT II or as a mixed type [1, 2]. They differ from each other in the pathogenesis, laboratory test results, ultrasound image and iodine uptake observed. The necessity to indicate the type of AIT is important in order to provide the appropriate prompt treatment of the patient. Amiodarone-induced thyrotoxicosis I usually develops in abnormal thyroid glands (mainly multinodular goiter or in preexisting Graves’ disease) where an oversupply of iodine due to the amiodarone therapy is responsible for the overproduction of thyroid hormones. Amiodarone-induced thyrotoxicosis I usually shows high radioactive iodine uptake and increased blood flow on ultrasonography. The presence of thyroid stimulating receptor antibodies (TRAb) in the patient’s serum might be indicative. In contrast, AIT II presents as a destructive drug-induced thyroiditis with low radioactive iodine uptake and normal blood flow [1, 2]. Some inflammation markers as C-reactive protein (CRP) or interleukin-6 (IL-6) might be helpful in the diagnostic process. Some authors underline the beneficial role of Tc-99m sestamibi scintigraphy in AIT type differentiation. Nevertheless, the most reliable tests are iodine-uptake and colorflow Doppler sonography (CFDS) [6, 7]. In the case of AIT I, first line treatCorresponding author: Assoc. Prof. Marek Niedziela MD, PhD Department of Pediatric Endocrinology and Rheumatology Poznan University of Medical Sciences 27/33 Szpitalna St 60-572 Poznan, Poland Phone: +48 61 849 1481 Fax: +48 61 848 0291 E-mail: [email protected] Letter to the Editor