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Iodine-induced thyrotoxicosis (IIT) is known since the early days of iodine
therapy for goiter. In the last few decades it has been reported with increased
frequency due to the widespread use of iodine-containing drugs and iodinated
radiographic contrast media. IIT accounts for 0.2-10 % of all cases of
thyrotoxicosis in various series[9]. IIT is more frequently observed in
patients with preexisting thyroid disease such as endemic or nonendemic
nontoxic goiter, Graves' disease or autonomous thyroid nodules, but it
may also occur in patients with no previous thyroid abnormality.
Treatment of ITT is a medical challenge. In this condition all usual forms of treatment of hyperthyroidism have a reduced efficacy, or may not be used at all. Treatment with 131I is not feasible for the low radioiodine uptake and the high stable iodine content of the gland, that will reduce the efficacy of radioiodine. On the other hand, treatment with thionamides (MMI or PTU) has a delayed effect because of the high amounts of preformed thyroid hormones stored in the gland, mainly in goitrous patients. Thus, inhibition of new hormone synthesis by blocking iodine organification requires a longer period of time to control thyrotoxicosis in IIT with respect to the other forms of hyperthyroidism. Thyroid surgery during uncontrolled thyrotoxicosis may be hazardous, especially in patients who have large amounts of stored thyroid hormones with the attendant risk of thyroid storm. The first step in the treatment is withdrawal of iodine substance. Although their effect may be delayed, full doses of thionamides should be administered for the time required to normalize serum thyroid hormone concentrations. This may take as much as 2 to 4 months. Propranolol or other beta-adrenergic antagonist should be added to the treatment regimen until complete control of hyperthyroidism is achieved. Other general supportive measures should be undertaken, as required. Once euthyroidism is achieved, further therapeutic measures will depend on the underlying disease. The above measures will control IIT in most cases, with the exception of those related to amiodarone, and less frequently to other long-lasting iodinated substances. Amiodarone-induced thyrotoxicosis (AIT) represents a special problem because it usually occurs in patients with significant heart disease (severe arrhythmias or ischemic heart disease) requiring the administration of this potent antiarrhythmic drug[9]. Furthermore, because amiodarone is stored in adipose tissue, its metabolic disposition is slow, with the result that the release of iodine will continue for up to several months after it has been withdrawn. In AIT, the use of potassium perchlorate in addition to thionamides has been proven useful[9]. The rationale of this treatment derives from the fact that the increased iodine content of the thyroid is the major cause of poor response to antithyroid drugs. Potassium perchlorate competitively inhibits iodide uptake by the thyroid gland and also induces a release of excess intrathyroid iodide which is still not organified. The dose of potassium perchlorate is 600-1200 mg daily together with full doses of thionamides. In many patients with AIT, this treatment will restore euthyroidism within 6 weeks. Administration of potassium perchlorate for periods longer than 6 weeks should generally be avoided because of its renal and bone marrow toxicity. Unless specifically contraindicated, propranolol should be administered together with other supportive measures, as required. After discontinuation of potassium perchlorate, patients with toxic nodular goiter or underlying Graves' disease require a prolongation of thionamide treatment, followed in general by radioiodine administration for the resolution of their disease. Such vigorous treatment schedule is not required in milder forms of AIT, especially in those with no underlying thyroid disease. In these cases the main pathogenetic factor may well be the direct cytotoxic effect elicited by amiodarone and its derivatives on thyroid cells, resulting in destructive thyroiditis and the subsequent release of preformed thyroid hormones[9]. In keeping with this pathogenic sequence, glucocorticoids have been successfully employed in these cases. In our experience, prednisone at a starting dose of 40 mg/day produces a normalization of serum free T3 in 1to 2 weeks. The absence of preexisting thyroid disease and the finding of very high levels of serum IL-6 are distinctive features of patients with destructive amiodarone-induced thyrotoxicosis, and favor the use of glucocorticoids. A combined regimen of potassium perchlorate, thionamides, and glucocorticoids may be administered to begin with in any patient with severe AIT and high IL-6 serum levels, since thyrotoxicosis may be due to the dual effect of amiodarone. In extremely severe cases, removal of excess thyroid hormones by plasmapheresis has been employed with a transient benefit. |
