title: [Amiodarone and the thyroid gland].
abstract: Amiodarone is an iodine-rich drug. Its chronic administration may lead to disturbances in thyroid hormone metabolism and/or overt gland dysfunction. It causes an increased in serum fT4, rT3, and TSH concentrations and a decreased serum level of fT3 without thyroid dysfunction. Amiodarone may induce thyrotoxicosis (AIT--Amiodarone-induced thyrotoxicosis) or hypothyroidism (AIH--Amiodarone-induced hypothyroidism) in some persons. AIT occurs more frequently in areas with low iodine intake. The excess iodine contributes to excessive thyroid hormone synthesis-type I AIT or may lead to thyroiditis and a destructive process of thyroid follicular cells, resulting in excess thyroid hormone release-type II AIT. The mixed form of AIT also occurs. Type I AIT should be treated with antithyroid drugs alone or in association with potassium perchlorate, type II AIT benefits from treatment with glucocorticoids, whereas the mixed form of AIT is most effectively treated with a combination of thionamides, potassium perchlorate, and glucocorticoids. AIT often requires thyroidectomy after restoration of euthyroidism or radioiodine therapy, provided that 24-h thyroid radioactive iodine uptake values permit. AIH prevails in areas with high dietary iodine intake. It requires a discontinuation of amiodarone therapy and thyroid hormone (levothyroxine) replacement. It can remit spontaneously. Amiodarone and L-thyroxine therapy is also possible. Baseline thyroid function tests, thyroid antibodies, and imaging examinations such as thyroid ultrasound on initial evaluation and follow-ups every 6 months must be carefully monitored before starting amiodarone therapy.
authors.affiliation: Katedra i Klinika Endokrynologii i Diabetologii, Akademii Medycznej we Wrocławiu, Wrocław. tupikowska@pf.pl
authors.forename: Grazyna
authors.initials: G
authors.lastname: Bednarek-Tupikowska
authors.forename: Alicja
authors.initials: A
authors.lastname: Filus
authors.forename: Justyna
authors.initials: J
authors.lastname: Kuliczkowska
authors.forename: Jarosław
authors.initials: J
authors.lastname: Bugajski
mesh_terms: D000638:Amiodarone / Q000009:adverse effects*; D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000009:adverse effects*; D013956:Antithyroid Agents / Q000627:therapeutic use; D005260:Female; D005938:Glucocorticoids / Q000627:therapeutic use; D006801:Humans; D007037:Hypothyroidism / Q000139:chemically induced* / Q000175:diagnosis; D010472:Perchlorates / Q000627:therapeutic use; D017680:Potassium Compounds / Q000627:therapeutic use; D011247:Pregnancy; D013961:Thyroid Gland / Q000187:drug effects; D013963:Thyroid Hormones / Q000097:blood; D013965:Thyroidectomy; D013966:Thyroiditis / Q000139:chemically induced; D013971:Thyrotoxicosis / Q000139:chemically induced* / Q000175:diagnosis / Q000628:therapy
chemical_list: D000889:Anti-Arrhythmia Agents; D013956:Antithyroid Agents; D005938:Glucocorticoids; D010472:Perchlorates; D017680:Potassium Compounds; D013963:Thyroid Hormones; C009006:potassium perchlorate; D000638:Amiodarone