Amiodarone is an iodine-based, potent antiarrhythmic drug bearing a structural resemblance to thyroxine (T4). It is understood to produce thyroid abnormalities ranging from abnormal thyroid function testing to overt hypothyroidism or thyrotoxicosis. Amiodarone, a benzofuranic iodine-rich antiarrhythmic drug, causes thyroid dysfunction in 15-20% of cases. These unfavorable effects may occur in patients with or without preexisting thyroid disease.

Although amiodarone-induced hypothyroidism poses no particular problem, amiodarone-induced thyrotoxicosis (AIT) is a diagnostic and therapeutic challenge.

Amiodarone-induced thyrotoxicosis is a diagnostic and therapeutic challenge. It may develop in patients with underlying occult functional autonomy (type 1) or in patients with regular thyroid (type 2), although the two forms may, sometimes, superimpose.

There are two stamps of amiodarone-induced thyrotoxicosis (AIT). Type 1 AIT is defined as tincture of iodine-induced hyperthyroidism, underdeveloped in individuals with underlying thyroid disease or positive circulating thyroid peroxidase antibodies (TPOAb) and is due to increased composition and release of thyroid hormone (Jod-Basedow effect). Type 2 AIT is a drug-induced destructive thyroiditis that occurs in individuals with no underlying thyroid disease and is more frequent in tincture of iodine-sufficient areas. However, distinguishing one type from the other may be wearisome, and some cases may in reality represent mixed forms, where individuals may have characteristics of both AIT subtypes. Because of this heterogeneity, AIT poses a difficult diagnostic and therapeutic challenge.

Diagnosis of thyrotoxicosis is easy, supported on the finding of increased free thyroid hormone concentrations and suppressed TSH levels. Thyroid radioactive iodine (RAI) uptake values are usually very low/suppressed in type 2 AIT, most commonly low or burn-normal, but sometimes average or increased in type 1 AIT despite the iodine load.

Color inundate Doppler sonography shows absent-minded hypervascularity in type 2 and increased vascularity in type 1 AIT. Mixed/indefinite forms may have features of both AIT types.

Interleukin-6 (IL-6), a cytokine associated with inflammation, was proposed as a biomarker to distinguish between amiodarone-induced thyroiditis and iodine-induced hyperthyroidism. Marked elevations of IL-6 levels correlated closely with subacute thyroiditis in patients without preexisting thyroid disease. Normal to mild elevations of IL-6 were also found in patients with AIT1 .

Identification of amiodarone-induced thyrotoxicosis types is crucial for why medical therapies are distinct for the two types: thionamides (accompanying with potassium perchlorate, when feasible) are the utmost choice for type 1 amiodarone-induced thyrotoxicosis, whereas glucocorticoids are used for typify 2; in the latter group, serum thyroid hormone levels and shield-shaped volume may predict response to glucocorticoids. Total thyroidectomy is the preferred treat when thyrotoxicosis is refractory to medical therapeutics or when euthyroidism should be rapidly replace. A narrow course with iopanoic acid, when feasible, rapidly normalizes serum T3 concentrations before surgery.