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Amiodarone induced thyrotoxicosis (AIT) is a form of hyperthyroidism due to treatment with antiarrhythmic drug, amiodarone. Amiodarone induced thyroid dysfunction more commonly results in hypothyroidism , estimated to occur in 6-32% of patients, whereas hyperthyroidism from amiodarone use is estimated at 1-12%. [ 1 ]
Amiodarone has been used both in the treatment of acute life-threatening arrhythmias as well as the long-term suppression of arrhythmias. [13] Amiodarone is commonly used to treat different types of abnormal heart rhythms, such as atrial arrhythmias (supraventricular arrhythmias) and ventricular arrhythmias.
Amiodarone, some benzodiazepines, cyclosporine, diphenoxylate, indomethacin, itraconazole, propafenone, quinidine, quinine, spironolactone, and verapamil may lead to toxic levels and increased incidence of side effects. [8] Digoxin plasma concentrations may increase while on antimalarial medication hydroxychloroquine. [3]
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The Jod-Basedow effect (also Jod-Basedow syndrome and Jod-Basedow phenomenon) is hyperthyroidism following administration of iodine or iodide, [1] either as a dietary supplement, for iodinated contrast medical imaging, or as a medication (mainly amiodarone).
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Compounds that prolong the action potential: matching the modern classification, with the key drug example being amiodarone, and a surgical example being thyroidectomy. This was not a defining characteristic in an earlier review by Charlier et al. (1968), [ 17 ] but was supported by experimental data presented by Vaughan Williams (1970).
Budiodarone (ATI-2042) is an antiarrhythmic agent and chemical analog of amiodarone that is currently being studied in clinical trials.Amiodarone is considered the most effective antiarrhythmic drug available, [1] [2] [3] but its adverse side effects, including hepatic, pulmonary and thyroid toxicity as well as multiple drug interactions, [4] are discouraging its use.
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