Treatment of amiodarone-induced thyrotoxicosis, a difficult challenge: results of a prospective study.

Abstract

Amiodarone-induced thyrotoxicosis (AIT) occurs in both abnormal (type I) and apparently normal (type II) thyroid glands due to iodine-induced excessive thyroid hormone synthesis in patients with nodular goiter or latent Graves' disease (type I) or to a thyroid-destructive process caused by amiodarone or iodine (type II). Twenty-four consecutive AIT patients, 12 type I and 12 type II, were evaluated prospectively. Sex, age, severity of thyrotoxicosis, and cumulative amiodarone dose were similar. Type II patients had higher serum interleukin-6 (IL-6; median, 440 vs. 173 fmol/L; P < 0.001), but lower serum thyroglobulin levels. Several weeks of thionamide therapy in eight type II or prolonged glucocorticoid administration in two type I patients had previously failed to control hyperthyroidism. Type II patients were given prednisone (initial dose, 40 mg/day) for 3 months and achieved normal free T3 and IL-6 after an average of 8 and 6 days, respectively. Exacerbation of thyrotoxicosis with increased serum IL-6 values, observed in 4 patients while tapering steroid, was promptly corrected by increasing it. Type I patients, given methimazole (30 mg/day) and potassium perchlorate (1 g/day), achieved normal free T3 and IL-6 concentrations after an average of 4 weeks. Exacerbation of thyrotoxicosis with markedly increased IL-6 was controlled by prednisone in 3 of 4 cases. Distinction of different forms of AIT is essential for its successful management. Type II AIT should be treated with glucocorticoids; type I AIT should be treated with methimazole and potassium perchlorate. Exacerbation of thyrotoxicosis, which may occur in both forms and is probably related to destructive processes, should be controlled by the addition/increase in glucocorticoids.

Thyroid Disease and the Heart

“…As initially described in a large Italian patient population, 2 forms of amiodarone-induced hyperthyroidism exist. 115 Type 1 hyperthyroidism occurs in patients with preexistent thyroid disease and goiter and occurs more often in regions where iodine intake is low. Type 2 hyperthyroidism is caused by an inflammatory process that causes increased release of thyroid hormones from a previously normal thyroid gland.…”

“…114 It is frequently not possible to distinguish between these 2 types. 115 Signs of inflammation with elevated erythrocyte sedimentation rate and interleukin-6 levels are common, as are modest increases in thyroid gland size. Radioiodine uptake studies are almost always low.…”

“…Radioiodine uptake studies are almost always low. 113,115 The management of patients with amiodarone-induced hyperthyroidism can be difficult, and no uniform consensus exists among thyroidologists on the proper form of treatment. 116 It is important to measure serum TSH, total and free T 4 , and total T 3 as well as antithyroid antibodies.…”

“…52 A trial of glucocorticoids that used 20 to 30 mg of prednisone per day for 14 to 21 days in all but patients with diabetes mellitus quickly lowered T 4 levels. 115 Although most treatment protocols suggest cessation of the amiodarone and use of thioureas in relatively high doses, neither of these interventions have been shown to lead to predictable benefits. 115,117 The course of the disease may last for anywhere between 1 to 3 months.…”

“…115 Although most treatment protocols suggest cessation of the amiodarone and use of thioureas in relatively high doses, neither of these interventions have been shown to lead to predictable benefits. 115,117 The course of the disease may last for anywhere between 1 to 3 months. In rare cases, surgical thyroidectomy under local anesthesia has proven to be effective.…”