Iodine-induced hyperthyroidism treatment

The use of iodine has been held responsible for the increasing frequency of relapse of Graves disease in the USA. Treatment of more severe cases of iodine-induced hyperthyroidism can be difficult, as thyroid synthesis inhibitors are not immediately active and 131I cannot be used because of low thyroid uptake. The carefully supervised combination of perchlorate and methimazole is effective (40), but surgery has also occasionally been advocated. 

A summary of the occurrence and epidemiology of iodine-induced hyperthyroidism has been published (41), based on the authors experience in Tasmania, Zaire, Zimbabwe, and Brazil. Another review has more specifically examined the cardiac features of iodine-induced hyperthyroidism and has emphasized the importance of awareness, monitoring, and treatment of such hyperthyroidism in areas in which iodine supplementation has been recently introduced (42). 

For the prevention or treatment of iodine-induced hyperthyroidism, a thionamide drug may be combined with perchlorate (3 X 300 mg/day for 7—14 days), an iodine uptake blocking agent. 

The direct and immediate treatment result, as opposed to the delayed effect of radioiodine, is another advantage of surgery. The latter may be particularly relevant to patients who require rapid correction of thyrotoxicosis in case of thyroid storm or severe iodine-induced hyperthyroidism. 

Frequency, Pathogenesis, Prevention and Treatment of Iodine-Induced Hyperthyroidism... 

Patients with beta-thalassemia major have an increased risk of primary hypothyroidism. In 23 patients with beta-thalassemia amiodarone was associated with a high risk of overt hypothyroidism (33 versus 3% in controls) (43). This occurred at up to 3 months after starting amiodarone. The risk of subclinical hypothyroidism was similar in the two groups. In one case overt hypothyroidism resolved spontaneously after withdrawal, but the other patients were given thyroxine. After 21-47 months of treatment three patients developed thyrotoxicosis, with remission after withdrawal. There were no cases of hyperthyroidism in the controls. The authors proposed that patients with beta-thalassemia may be more susceptible to iodine-induced hypothyroidism, related to an underlying defect in iodine in the thyroid, perhaps associated with an effect of iron overload. 

The treatment of amiodarone-induced hyperthyroidism is difficult. It often does not respond to conventional therapy with carbimazole, methimazole, or radio-iodine. However, corticosteroids and the combination of methimazole with potassium perchlorate have been reported to be effective (52), even if amiodarone is continued (53). Other regimens that have been used include combinations of corticosteroids with carbimazole (54), corticosteroids and benzylthiouracil (55), or propylthiouracil (SEDA-15, 170). Potassium perchlorate has also been used (SEDA-21, 199). Other forms of treatment that have been successful have been plasma exchange and in very severe cases subtotal thyroidectomy (56) or total thyroidectomy (SEDA-15,170 SEDA-17, 220 57). 

Several studies have evaluated the effects of excessive iodine intake in humans, and antithyroid antibodies and iodine-induced hypo- and hyperthyroidism have been reported following long-term iodine treatment for endemic goitre (Boyages et al., 1989 Kahaly et al., 1997, 1998). 

Endocrine In patients receiving the minimum dose of amiodarone, thyroid abnormalities were observed at a rate between 14% and 18%. The effects on the thyroid gland are variable. Amiodarone may cause abnormal thyroid function detected only by laboratory test as well as clinically manifested thyroid dysfunction. The mechanism of this adverse effect is complex. Amiodarone inhibits the action of deiodinase and decreases peripheral conversion of thyroid hormones. Moreover, it decreases their renal elimination and inhibits their entry to peripheral tissues. The level of T4 increases by 40% within 1-4 months of amiodarone therapy. The deiodinase activity inhibition can be noticed after 3 months of treatment. It leads to an increase in the level of thyroid stimulating hormones. Amiodarone and its metabolite have a direct cytotoxic effect on thyroid follicular cells, which results in destructive thyroiditis. Amiodarone-induced thyroid damage can lead either to hypo- or hyperthyroidism. The latter can be of two types. Type 1 usually occurs in patients with prior thyroid damage. In this type, iodine excess causes excessive synthesis of thyroid hormones whereas in type 2 the inflammatory process is followed by destruction. A destructive thyroiditis leads to the release of hormones from damaged thyroid follicular cells. This mechanism occurs in patients with no history of thyroid disorders [15]. 

The administration of SSKI a few days after for the treatment of hyperthyroid Graves disease and continued for weeks later has been reported to more rapidly ameliorate the symptoms of thyrotoxicosis and to reduce the dose of l necessary to effectively treat the hyperthyroidism (10). However, hypothyroidism not infrequently occurred during iodide therapy and disappeared when iodides were discontinued. Years ago, we reported that the administration of 5 drops SSKI to euthyroid patients treated years earlier with 1 or surgery for Graves disease almost always induced hypothyroidism within weeks (11). The euthyroid state rapidly returned when the iodine was withdrawn. It is likely that these... 

Amiodarone, an anti-arythmic drug containing 37.2 % of organic iodine, may induce hypothyroidism and hyperthyroidism. Dysthyroidism can occur during treatment, but also many months after its discontinuation in patients with underlying thyroid disorders, as well as in subjects with apparently normal glands. We report the case of a patient who developed hypothyroidism followed by hyperthyroidism, related to amiodarone therapy. 

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