Hypothyroid, goiter, from iodine

Iodine. Of the 10—20 mg of iodine in the adult body, 70—80 wt % is in the thyroid gland (see Thyroid and antithyroid preparations). The essentiahty of iodine, present in all tissues, depends solely on utilisation by the thyroid gland to produce thyroxine [51-48-9] and related compounds. Well-known consequences of faulty thyroid function are hypothyroidism, hyperthyroidism, and goiter. Dietary iodine is obtained from eating seafoods and kelp and from using iodized salt. 

Iodine deficiency affects the socioeconomic development of an afflicted community in other ways than its important physiological manifestations, viz., goiter, hypothyroidism, cretinism, reproductive failure, and child mortality, among others. The socioeconomic retardation of the affected community occurs in two ways. People are mentally slower and less vigorous, so it is harder to educate and motivate them, and thus they are less productive in their work. Besides, iodine deficiency produces more handicapped individuals who depend on others for their care, which in turn diverts the community resources. Secondly, in most of the areas, agriculture is the most important economic activity, and domestic animals suffer from iodine deficiency in much the same way as people do. Therefore, domestic animals are smaller in size and produce less meat, eggs and wool. They also suffer from abortion and are often sterile. 

Extensive work has been performed to assess neonatal thyroid functional status in communities in iodine-deficient parts of the country. KochupiUai et al. (1986) showed that the incidence of neonatal hypothyroidism varied from 7.5% to 13.3% in the highly endemic sub-Himalayan districts of Gonda, Gorakhpur and Deoria. In comparison, the incidence of neonatal hypothyroidism in Delhi was 0.6%, while coastal Kerala, which was not endemic for goiter, had a neonatal hypothyroidism incidence of 0.12%, comparable with the congenital hypothyroidism rates of 0.02—0.05% reported in iodine-sufficient countries. 

Thyroxine (see the model above ) is an aromatic compound and a key hormone that raises metabolic rate. Low levels of thyroxine (hypothyroidism) can lead to obesity, lethargy, and an enlarged thyroid gland (goiter). The thyroid gland makes thyroxine from iodine and tyrosine, which are two essential components of our diet. Most of us obtain iodine from iodized salt, but iodine is also found in products derived from seaweed, like the kelp shown above. An abnormal level of thyroxine is a relatively common malady, however. Fortunately, low levels of thyroxine are easily corrected by hormone supplements. After we study a new class of reaction in this chapter called electrophilic aromatic substitution, we shall return to see how that reaction is related to thyroxine in "The Chemistry of... Iodine Incorporation in Thyroxine Biosynthesis."... 

Goiter and hypothyroidism due to iodine deficiency are major world health problem. Intake of excess iodine, either in food, water or drugs, may also result in disturbances of thyroid function and goiterl>2 Clinical data as well as animal experiences have shown a sharp rise in the incidence of autoimmune thyroiditis when iodine consumption was increased.2>3,4 Administration of iodine or or iodine containing drugs increases the incidence of thyroid autoantibodies in humans without illness as well as in populations with endemic goiter. Hokkaido is located in the northernmost part of Japan. Separated from the main island by the sea, Hokkaido covers an area of 83,511Km2, and its population of 5.3 million is considerably lower than that of the rest of Japan. 

The thyroid gland also regulates its uptake of iodide and thyroid hormone synthesis by intrathyroidal mechanisms that are independent of TSH. These mechanisms are primarily related to the level of iodine in the blood. Large doses of iodine inhibit iodide organification (Wolff-Chaikoff block, see Figure 38-1). In certain disease states (eg, Hashimoto s thyroiditis), this can inhibit thyroid hormone synthesis and result in hypothyroidism. Hyperthyroidism can result from the loss of the Wolff-Chaikoff block in susceptible individuals (eg, multinodular goiter). 

Because of its adverse effects, it is logical to omit iodine from all pharmaceutical formulations whenever possible, and at least clearly label its presence when it is necessary. The adverse effects of iodine include goiter and hypothyroidism (20,22), hyperthyroidism (SEDA-18,176), neutropenia (23), metabolic acidosis (24), and generalized iododerma (17). 

Extensive iodine absorption from povidone-iodine can cause transient hypothyroidism or in patients with latent hypothyroidism the risk of destabilization and thyrotoxic crisis (SEDA-20, 226 SEDA-22, 263). Especially at risk are patients with an autonomous adenoma, localized diffuse autonomy of the thyroid gland, nodular goiter, latent hyperthyroidism of autoimmune origin, or endemic iodine deficiency (51). 

Hypothyroidism (thyroid hormone deficiency) may result from autoimmune disease (Hashimoto s disease) or from deficient synthesis of TSH or TRH (thyroid-stimulating hormone-releasing factor). Because adequate ingestion of iodine is a prerequisite for thyroid hormone synthesis, iodine deficiency also causes hypothyroidism. In children, thyroid hormone deficiency (called cretinism) causes depressed growth and mental retardation. Severe hypothyroidism in adults (myxedema) results in symptoms such as edema (abnormal fluid accumulation) and goiter. Hypothyroidism is usually treated with hormone replacement therapy. 

Fetal TH must come from the maternal circulation before the fetal thyroid gland and pituitary—thyroid axis become functional (gestation day (GD) 17—18 in rats and 90 in humans). Maternal transfer of thyroxine (T4) constitutes a major fraction of fetal TH even after the onset of fetal thyroid secretion, they may contribute to the maintenance of fetal development (Burrow et ai, 1994). Therefore, changes in maternal TH levels have an affirmative effect on fetal TH metabolism. Depending on the dose of iodine, the susceptibility of individuals, and previous conditions of the gland, iodine excess can induce maternal hypothyroidism or hyperthyroidism. In a case reported by Serreaul et al. (2004), an obvious thyroid goiter was found in the fetus after excessive maternal iodine... 

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