title: Iopanoic acid rapidly controls type I amiodarone-induced thyrotoxicosis prior to thyroidectomy.
abstract: Amiodarone-induced thyrotoxicosis (AIT) may develop either in apparently normal thyroid glands (Type II AIT) or in the presence of sub-clinical thyroid abnormalities (either autonomous goiter or latent Graves' disease; Type I AIT). Mixed forms also occur. While Type I AIT is due to iodine-induced excess thyroid hormone synthesis, Type II AIT is a form of amiodarone (possibly iodine) -induced destructive thyroiditis. Type I AIT is usually treated by combined thionamide and potassium perchlorate therapy, but may be resistant to therapy. On the other hand, Type II AIT often responds favorably to glucocorticoids and may not require further therapy once euthyroidism has been restored. Not infrequently, however, AIT (especially Type I) is resistant to conventional treatment, and several weeks or months may elapse before euthyroidism is restored. Thyroidectomy has been carried out in Type I AIT patients, but thyroid surgery in thyrotoxic patients, especially those with underlying cardiac problems, carries a high surgical risk. In this study we describe 3 patients with Type I AIT, who were successfully treated with a short course of iopanoic acid (IOP), an oral cholecystographic agent, which is rich in iodine and is a potent inhibitor of 5'-deiodinase, resulting in a marked decrease in the peripheral tissue conversion of T4 to T3, in preparation for thyroid surgery. Euthyroidism was rapidly restored in 7-12 days, allowing a subsequent safe and uneventful thyroidectomy in all cases. These patients were then treated with L-T4 for their hypothyroidism and amiodarone was safely re-instituted. We suggest that IOP is the drug of choice in the rapid restoration of euthyroidism prior to definitive thyroidectomy in patients with drug resistant Type I AIT.
authors.affiliation: Department of Endocrinology and Metabolism, University of Pisa, Italy.
authors.forename: F
authors.initials: F
authors.lastname: Bogazzi
authors.forename: F
authors.initials: F
authors.lastname: Aghini-Lombardi
authors.forename: C
authors.initials: C
authors.lastname: Cosci
authors.forename: I
authors.initials: I
authors.lastname: Lupi
authors.forename: F
authors.initials: F
authors.lastname: Santini
authors.forename: M L
authors.initials: ML
authors.lastname: Tanda
authors.forename: P
authors.initials: P
authors.lastname: Miccoli
authors.forename: F
authors.initials: F
authors.lastname: Basolo
authors.forename: A
authors.initials: A
authors.lastname: Pinchera
authors.forename: L
authors.initials: L
authors.lastname: Bartalena
authors.forename: L E
authors.initials: LE
authors.lastname: Braverman
authors.forename: E
authors.initials: E
authors.lastname: Martino
mesh_terms: D000368:Aged; D000638:Amiodarone / Q000009:adverse effects* / Q000627:therapeutic use; D001145:Arrhythmias, Cardiac / Q000188:drug therapy; D004351:Drug Resistance; D004791:Enzyme Inhibitors / Q000627:therapeutic use; D005260:Female; D006801:Humans; D007453:Iodide Peroxidase / Q000037:antagonists & inhibitors; D007480:Iopanoic Acid / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D013965:Thyroidectomy; D013971:Thyrotoxicosis / Q000139:chemically induced* / Q000188:drug therapy* / Q000601:surgery; D013974:Thyroxine / Q000627:therapeutic use
chemical_list: D004791:Enzyme Inhibitors; D007453:Iodide Peroxidase; D007480:Iopanoic Acid; D000638:Amiodarone; D013974:Thyroxine