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Amiodarone and the Thyroid
Amiodarone is a relatively widely prescribed anti-arrhythmic drug that is most commonly used in the management of refractory tachyarrhythmias such as Supraventricular Tachycardia (SVT) and Atrial Fibrillation (AF). Amiodarone is associated with a range of quite serious adverse effects, meaning that it is usually reserved for use in situations where other treatments are not appropriate.
As the name of the drugs implies, the amiodarone molecule includes a significant proportion of iodine and can exert a significant direct toxic affect upon the thyroid gland. In fact, the molar ratio is involved means that one 200 mg dose of amiodarone contains 6 mg of elemental iodine. This is significant if we consider that an average daily western diet often contains approximately 0.3 mg of iodine. The lipophilic characteristics of the amiodarone molecule mean that it is prone to concentrate preferentially in specific tissues, including the thyroid. Treatment with amiodarone…………
can often cause thyroid dysfunction which may present as either hypothyroidism or hyperthyroidism. In people without thyroid disease the introduction of amiodarone is often associated with a transient increase in the serum concentration of T4 [thyroxine]. The concentration of Thyroid Stimulating Hormone (TSH) will usually rise slightly for people who had normal thyroid function before the introduction of the drug. In many cases after 3-6 months the TSH concentration will normalize and the T4 concentration will remain slightly elevated or at the upper end of the usual reference range.
However, amiodarone is also associated with a range of serious thyroid toxicities – the drug may precipitate significant thyroiditis, particularly for those with underlying thyroid disease. It has been estimated that up to one in five people treated with amiodarone will develop hypothyroidism, emphasizing the importance of monitoring thyroid functioning disease after the introduction of the drug. Amiodarone may also be associated with thyrotoxicosis, resulting in overactivity of the thyroid gland. In particular, amiodarone may cause a destructive thyroiditis that results in increased secretion of thyroid hormones that persists for a period of up to several months and then is followed by a period when hypothyroidism develops in many cases. It is also important to note that some of the manifestations of amiodarone-induced hypothyroidism may be masked because of intrinsic beta blockade associated with the drug. It should be noted that amiodarone has a very long half-life, meaning that even if the drug is stopped it would not be reasonable to expect immediate resolution of the toxicity.
Current recommendations are that thyroid function indices need to be checked at baseline and then repeated every 3 to 4 months during the course of treatment with amiodarone. If thyroid function found to be altered during the course of amiodarone treatment then consideration with treatment with thyroid hormone replacement should be considered. For complex cases referral to an endocrinologist would also be reasonable.
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