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Iodine excess and hyperthyroidism.

Abstract

150 microg iodine are daily required for thyroid hormone synthesis. The thyroid gland has intrinsic mechanisms that maintain normal thyroid function even in the presence of iodine excess. Large quantities of iodide are present in drugs, antiseptics, contrast media and food preservatives. Iodine induced hyperthyroidism is frequently observed in patients affected by euthyroid iodine deficient goiter when suddenly exposed to excess iodine. Possibly the presence of autonomous thyroid function permits the synthesis and release of excess quantities of thyroid hormones. The presence of thyroid autoimmunity in patients residing in iodine-insufficient areas who develop iodine-induced hyperthyroidism has not been unanimously observed. In iodine-sufficient areas, iodine-induced hyperthyroidism has been reported in euthyroid patients with previous thyroid diseases. Euthyroid patients previously treated with antithyroid drugs for Graves' disease are prone to develop iodine-induced hyperthyroidism. As well, excess iodine in hyperthyroid Graves' disease patients may reduce the effectiveness of the antithyroid drugs. Occasionally iodine-induced hyperthyroidism has been observed in euthyroid patients with a previous episode of post-partum thyroiditis, amiodarone destructive or type II thyrotoxicosis and recombinant interferon-alpha induced destructive thyrotoxicosis. Amiodarone administration may induce thyrotoxicosis. Two mechanisms are responsible for this condition. One is related to excess iodine released from the drug, approximately 9 mg of iodine following a daily dose of 300 mg amiodarone. This condition is an iodine-induced thyrotoxicosis or type I amiodarone-induced thyrotoxicosis. The other mechanism is due to the amiodarone molecule that induces a destruction of the thyroid follicles with a release of preformed hormones. This condition is called amiodarone-induced destructive thyrotoxicosis or type II thyrotoxicosis. Patients developing type I thyrotoxicosis in general have preexisting nodular goiter whereas those developing type II thyrotoxicosis have a normal thyroid gland. The latter group of patients, after recovering from the destructive process, may develop permanent hypothyroidism as the consequence of fibrosis of the gland.

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  • Authors+Show Affiliations

    ,

    Università di Parma, Cattedra di Endocrinologia, Italy.

    Source

    MeSH

    Amiodarone
    Endemic Diseases
    Environmental Exposure
    Goiter
    Graves Disease
    Hyperthyroidism
    Iodine
    Thyroid Diseases

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't
    Review

    Language

    eng

    PubMed ID

    11396708

    Citation

    Roti, E, and E D. Uberti. "Iodine Excess and Hyperthyroidism." Thyroid : Official Journal of the American Thyroid Association, vol. 11, no. 5, 2001, pp. 493-500.
    Roti E, Uberti ED. Iodine excess and hyperthyroidism. Thyroid. 2001;11(5):493-500.
    Roti, E., & Uberti, E. D. (2001). Iodine excess and hyperthyroidism. Thyroid : Official Journal of the American Thyroid Association, 11(5), pp. 493-500.
    Roti E, Uberti ED. Iodine Excess and Hyperthyroidism. Thyroid. 2001;11(5):493-500. PubMed PMID: 11396708.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Iodine excess and hyperthyroidism. AU - Roti,E, AU - Uberti,E D, PY - 2001/6/9/pubmed PY - 2001/10/12/medline PY - 2001/6/9/entrez SP - 493 EP - 500 JF - Thyroid : official journal of the American Thyroid Association JO - Thyroid VL - 11 IS - 5 N2 - 150 microg iodine are daily required for thyroid hormone synthesis. The thyroid gland has intrinsic mechanisms that maintain normal thyroid function even in the presence of iodine excess. Large quantities of iodide are present in drugs, antiseptics, contrast media and food preservatives. Iodine induced hyperthyroidism is frequently observed in patients affected by euthyroid iodine deficient goiter when suddenly exposed to excess iodine. Possibly the presence of autonomous thyroid function permits the synthesis and release of excess quantities of thyroid hormones. The presence of thyroid autoimmunity in patients residing in iodine-insufficient areas who develop iodine-induced hyperthyroidism has not been unanimously observed. In iodine-sufficient areas, iodine-induced hyperthyroidism has been reported in euthyroid patients with previous thyroid diseases. Euthyroid patients previously treated with antithyroid drugs for Graves' disease are prone to develop iodine-induced hyperthyroidism. As well, excess iodine in hyperthyroid Graves' disease patients may reduce the effectiveness of the antithyroid drugs. Occasionally iodine-induced hyperthyroidism has been observed in euthyroid patients with a previous episode of post-partum thyroiditis, amiodarone destructive or type II thyrotoxicosis and recombinant interferon-alpha induced destructive thyrotoxicosis. Amiodarone administration may induce thyrotoxicosis. Two mechanisms are responsible for this condition. One is related to excess iodine released from the drug, approximately 9 mg of iodine following a daily dose of 300 mg amiodarone. This condition is an iodine-induced thyrotoxicosis or type I amiodarone-induced thyrotoxicosis. The other mechanism is due to the amiodarone molecule that induces a destruction of the thyroid follicles with a release of preformed hormones. This condition is called amiodarone-induced destructive thyrotoxicosis or type II thyrotoxicosis. Patients developing type I thyrotoxicosis in general have preexisting nodular goiter whereas those developing type II thyrotoxicosis have a normal thyroid gland. The latter group of patients, after recovering from the destructive process, may develop permanent hypothyroidism as the consequence of fibrosis of the gland. SN - 1050-7256 UR - https://www.unboundmedicine.com/medline/citation/11396708/full_citation L2 - https://www.liebertpub.com/doi/full/10.1089/105072501300176453?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -