Hypothyroid, goiter, from iodine deficiency

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. 

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. 

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. 

Iodine is a trace element essential for the synthesis of thyroid hormones. Iodine deficiency is well-recognized as a cause of goiter, but the most serious consequence is cretinism. Apart from neurological and motor abnormalities, some of the ocular features of hypothyroidism described subsequently may occur. 

The earliest and potentially most damaging result of iodine deficiency is neonatal hypothyroidism and cretinism. The wide prevalence of cretinism in the Himalayan and sub-Himalayan belt has been shown by several authors, starting from the turn of the last century. Studies of iodine metabolism in the Himalayan goiter zones of India and Nepal (Karmarkar et ai, 1974) showed (a) markedly increased avidity of the thyroid to radioiodine (b) reduced excretion of stable iodine in urine (c) extremely low levels of iodine in the drinking water (d) normal or reduced protein-bound iodine in plasma and (e) low inorganic iodide concentration in plasma. These findings are compatible with the hypothesis that environmental deficiency of iodine is the primary factor responsible for endemic goiter in these areas. 

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. 

The same results were found from other studies a study in Poland enrolled 35000 patients who had received fine-needle aspiration biopsy of the thyroid from 1985 to 1999, and statistical analysis indicated that the incidence of AIT rose from 1.5 to 5.7% after USI since 1992 (Slowinska-Klencka et al, 2002). Kahaly et al. (1997) reported that after supplementing iodine 200pg/l to patients with endemic thyroid goiter (MUI, from 30pg/l, rose to 213pg/l), the incidence of iodine-induced hypothyroidism and AIT increased. It was reported from Greece and Sri Lanka that there was an obvious increase in the incidence of AIT in children after iodine supplementation was implemented in areas with deficient iodine intake (Zois et al, 2003 Premawardhana et al, 2000). 

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