Thyrotoxicosis drug-induced

Amiodarone may induce thyrotoxicosis (2% to 3% of patients) or hypothyroidism. It interferes with type I 5 -deiodinase, leading to reduced conversion of T4 to T3, and iodide release from the drug may contribute to iodine excess. Amiodarone also causes a destructive thyroiditis with loss of thyroglobulin and thyroid hormones. 

In addition, the metabohsm of OCAs results in the release of large amounts of E into the circulation. As described for KI, I released from OCAs may have effects at the thyroid gland and if used alone to treat hyperthyroidism, OCAs carry the same potential to induce increased secretion of thyroid hormone and exacerbation of thyrotoxicosis. When an OCA is used in the treatment of hyperthyroidism, large doses of antithyroid agents are usually administered concomitantly. However, the combination of OCAs and antithyroid drugs may cause resistance to the antithyroid drugs with time, presumably because of the elevation in intrathyroidal 1 content. Thus, it is recommended that the use of OCAs be reserved for short-term treatment of patients with severe thyrotoxicosis and significant comorbidity (e.g., myocardial infarction, sepsis, stroke) for rapid control of plasma Tj concentrations. 

Potassium perchlorate is a thyrostatic drug that is still used (in a dose of 1000 mg/day or more) as an alternative to the thionamides, especially in cases of allergy. It has also been used to treat the iodine-induced form of thyrotoxicosis, such as type 1 hyperthyroidism due to amio-darone (qv). 

The antithyroid effect of lithium has occasionally been used to benefit patients. In a case of amiodarone-induced thyrotoxicosis that did not respond to antithyroid drugs and glucocorticoids, low-dose lithium normalized thyroid function (62). 

That amiodarone can potentiate the action of warfarin by inhibiting its metabolism is well known (SEDA-11, 156). However, potentiation of the action of warfarin has been attributed to amiodarone-induced thyrotoxicosis (264). A metabolic interaction in this case was unlikely, because the patient had taken both drugs together for 2 years before the increase in response to warfarin, coincident with the emergence of thyrotoxicosis. 

Hyperthyroidism and toxicity Iodine-induced hyperthyroidism A mild increase in the incidence of hyperthyroidism worldwide has been described following iodized salt programs (Connolly et al. 1970, Stewart et al. 1971, Bauch 1985, Koutras etal. 1999, Joseph 1989, Meng etal. 1989, Lobbers etal. 1989, Pickardt 1989). Joseph et al. (1980) reported that iodine intakes of < 100 xg per day pose no risk for patients with autonomous tissue due to iodine deficiency critical amounts are between 100 and 200 jg I per day. The absence of iodine deficiency in the Japanese population accounts for the absence of iodine-induced thyrotoxicosis (Nagataki 1987). Hyperthyroidism is easily controlled with antithyroid drugs. 

The treatment of type 1 AIT is more difficult than that of other forms of iodine-induced thyrotoxicosis. Discontinuation of amiodarone therapy is usually recommended in patients with type 1 AIT, as long as other anti-arrhythmic drugs are available. However, withdrawal of amiodarone is often difficult because of underlying severe heart disease. High doses of antithyroid drugs have been used to treat type 1 AIT. Combined therapy with antithyroid drugs and potassium perchlorate is recommended in patients who fail to respond to antithyroid drugs alone after 2—3 months of treatment (Basaria and Cooper,... 

Presentation Atrial fibrillation can be induced by amiodarone-induced thyrotoxicosis even some time after drug withdrawal, as has been described in a patient who had taken oral amiodarone for 2.5 years for ventricular dysrhythmias, in whom it had been withdrawn 6 months before [37 ]. 

Kurt IH, Yigit T, Karademir BM. Atrial flbrillation due to late amiodarone-induced thyrotoxicosis. Clin Drug Invest 2008 28 (8) 527-31. 

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