title: Acute effects of amiodarone administration on thyroid function in patients with cardiac arrhythmia.
abstract: Because little has been published on early effects of treatment with amiodarone on thyroid function, we studied serum total and free thyroid hormone, reverse T3, and TSH levels in patients with cardiac arrhythmias during the first 10 days of treatment with a loading dose of amiodarone by iv infusion. Twenty-four patients were enrolled in the study. A standardized loading regimen for the i.v. infusion of amiodarone was used. The protocol provided the i.v. infusion of 20 mg/kg per day on day 1, the i.v. infusion of 10 mg/kg per day on day 2, then 600 mg/day per os for 7-10 days, and finally, in patients chronically treated with the drug, the dose was gradually reduced to 400-200 mg/day per os. Total and free concentrations of T4 tended to progressively and significantly increase (P < 0.0001 repeated measures ANOVA) starting from the fourth day of therapy, whereas total T3 decreased from the second day progressively (P < 0.0001) throughout the study; free T3 did not significantly change. TSH levels early and significantly (P < 0.001, by ANOVA) increased throughout the study, starting from the first day of therapy and reaching at 10 days a value 2.7 times higher than the basal value. Reverse T3 levels progressively and significantly (after 2 days of treatment) increased and paralleled the TSH values, reaching at the 10th day a value about 2 times higher than basal value. In conclusion, our data suggest that after i.v. treatment with amiodarone: 1) TSH is the first hormone to change significantly followed by reverse T3, T4, and T3; 2) the progressive fall of T3 levels reflects an inhibition of the peripheral conversion of T4 to T3; 3) the observed later increase of total and free T4 levels may be explained by a contribution of direct thyroidal stimulation by TSH and/or by a reduction in T4 clearance.
authors.affiliation: Laboratory of Cardiovascular Endocrinology, National Research Council Institute of Clinical Physiology, Pisa, Italy.
authors.forename: G
authors.initials: G
authors.lastname: Iervasi
authors.forename: A
authors.initials: A
authors.lastname: Clerico
authors.forename: R
authors.initials: R
authors.lastname: Bonini
authors.forename: C
authors.initials: C
authors.lastname: Manfredi
authors.forename: S
authors.initials: S
authors.lastname: Berti
authors.forename: M
authors.initials: M
authors.lastname: Ravani
authors.forename: C
authors.initials: C
authors.lastname: Palmieri
authors.forename: A
authors.initials: A
authors.lastname: Carpi
authors.forename: A
authors.initials: A
authors.lastname: Biagini
authors.forename: I J
authors.initials: IJ
authors.lastname: Chopra
mesh_terms: D000368:Aged; D000638:Amiodarone / Q000009:adverse effects* / Q000627:therapeutic use; D001145:Arrhythmias, Cardiac / Q000188:drug therapy*; D005260:Female; D006801:Humans; D007700:Kinetics; D008297:Male; D008875:Middle Aged; D013959:Thyroid Diseases / Q000139:chemically induced* / Q000503:physiopathology; D013961:Thyroid Gland / Q000503:physiopathology; D013972:Thyrotropin / Q000097:blood; D013974:Thyroxine / Q000097:blood; D014284:Triiodothyronine / Q000097:blood; D014285:Triiodothyronine, Reverse / Q000097:blood
chemical_list: D014284:Triiodothyronine; D014285:Triiodothyronine, Reverse; D013972:Thyrotropin; D000638:Amiodarone; D013974:Thyroxine