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Treatment of Type II Amiodarone-Induced Thyrotoxicosis by Either Iopanoic Acid or Glucocorticoids: A Prospective, Randomized Study

Departments of Endocrinology and Metabolism, University of Pisa (F.B., C.C., S.B., E.D., L.G., F.A.-L., A.P., E.M.) and University of Insubria (L.B.), 21100 Varese, Italy; Department of Epidemiology and Biostatistics, Institute of Clinical Physiology (G.R.), National Research Council, 56124 Pisa, Italy; and Section of Endocrinology, Diabetes and Nutrition (L.E.B.), Boston Medical Center, Boston, Massachusetts 02118

Address all correspondence and requests for reprints to: Fausto Bogazzi, M.D., Dipartimento di Endocrinologia e Metabolismo, Università di Pisa, Ospedale Cisanello, Via Paradisa 2, 56124, Pisa, Italy. E-mail: fbogazzi{at}hotmail.com or f.bogazzi{at}endoc.med.unipi.it.

Amiodarone-induced thyrotoxicosis (AIT) may occur either in the presence of underlying thyroid disease (type I AIT) or in apparently normal thyroid glands (type II AIT). Type II AIT, a destructive thyroiditis, often favorably responds to glucocorticoids. Iopanoic acid (IopAc) is an iodinated cholecystographic agent that inhibits deiodinase activity and reduces the conversion of T₄ toT₃. It has recently been reported that cholecystographic agents restore euthyroidism in patients with type II AIT. We describe the results of a prospective randomized study conducted in 12 patients with type II AIT treated with either iopanoic acid (group A, n = 6) or glucocorticoids (group B, n = 6). Serum free T₃ levels normalized rapidly in both groups after 7 d, from 0.75 ± 0.20 ng/dl (11.5 ± 3.1 pmol/liter) to 0.46 ± 0.10 ng/d (7.1 ± 1.7 pmol/liter), P < 0.01, and from 0.58 ± 0.10 ng/dl (9.0 ± 1.2 pmol/liter) to 0.34 ± 0.03 ng/dl (5.2 ± 0.5 pmol/liter), P < 0.003, in groups A and B, respectively (P = NS). Serum free T₄ levels reduced at 6 months in group B [from 2.70 ± 0.32 ng/dl (35.1 ± 4.1 pmol/liter) to 1.0 ± 0.04 ng/dl (13.4 ± 0.6 pmol/liter), P < 0.0001] but not in group A (from 2.90 ± 0.6 ng/dl (38.0 ± 7.5 pmol/liter) to 2.30 ± 0.4 ng/dl (35.6 ± 6.1 pmol/liter, P = 0.39; P = 0.005 group B vs. group A). All patients in both groups became euthyroid and had their amiodarone-induced destructive thyroiditis cured as defined by normalization of both serum free T₄ and free T₃ levels, during both drugs therapy. However, patients in group B were cured more rapidly than patients in group A (43 ± 34 d vs. 221 ± 111 d, respectively, P < 0.002). This study shows that, albeit both drugs are effective, glucocorticoids are probably the drug of choice for more rapidly curing type II AIT.

This work was partially supported by grants from the University of Pisa (Fondi d’Ateneo) and Ministero dell’ Istruzione, dell’ Università, della Ricerca, Rome (to E.M.) and from the University of Insubria at Varese (to L.B.).

Abbreviations: AIT, Amiodarone-induced thyrotoxicosis; CFDS, color flow Doppler sonography; FT₃, free T₃; FT₄, free T₄; IopAc, iopanoic acid; KClO₄, potassium perchlorate; OCA, cholecystographic agent; RAIU, radioiodine uptake; TgAb, antithyroglobulin; TPOAb, antithyroperoxidase; TRAb, anti-TSH receptor.

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