| Abstract: | Although iodine prevents goiter, enlarged thyroid glands continue to be detected in subjects, especially children, in spite of adequate iodine ingestion. Iodine may cause goiter in susceptible individuals by inhibiting the organic binding of iodine as is seen in adult asthmatics, neonates born of iodine ingesting mothers and in subjects residing along the littoral of Japan. Myxedema, especially in treated Graves' disease and Hashimoto's disease, may also be precipitated by iodine. On the other hand, iodine given to euthyroid subjects in areas of endemic goiter and to subjects with nontoxic nodular goiter may induce thyrotoxicosis by disclosing diffuse autonomously functioning thyroid tissue. An indirect adverse effect of iodine upon the thyroid gland may be manifested by lymphocyte glandular infiltrates and chronic thyroiditis which were sparse or absent in thyroid glands removed from subjects living in iodine deficient areas before iodine prophylaxis and therapy. Not only has the incidence of thyroiditis increased, but the histologic and clinical distinctions between treated Graves' disease and chronic thyroiditis have become indistinct. Experimentally, chronic thyroiditis has been produced in animals following large doses of iodine. Accumulated evidence supports the concept that iodine contributes to the genesis of chronic thyroiditis. |
