Goiters iodine supplementation

It is difficult to define the normal range of iodine intake in humans, and despite efforts to provide iodine supplementation in many geographic areas of the world, endemic iodine deficiency and attendant goiter remain a world health problem (147). Exposure to excess iodine may sometimes lead to the development of thyroid disease. This unusual type of iodide-induced goiter has been found, for example, in 10% of the population of a Japanese island where fishermen and their families consume large quantities of an iodine-rich seaweed and have an iodine intake as high as 200 mg/d (148). 

Deficiency of iodine, a component of thyroid hormones, may result in goiter formation (see Chap. 73). However, not everyone with an iodine-deficient diet will develop a goiter. Thyroxine (T4) and triiodothyronine (T3) can be used to assess iodine status (see Table 135-8). Intravenous iodine supplements typically are not necessary except during long-term parenteral nutrition with minimal enteral intake. Iodine needs generally are met by cutaneous absorption of iodine from germicides (e.g., povidone-iodine) used in catheter care or consumption of iodized salt. " Use of povidone-iodine wiU likely decrease with the increased use of chlorhexidine for catheter care, and the need for iodine supplementation must be individualized. Iodine excess is rarely a clinical concern when thyroid function is normal. 

The most serious and common complication of salt iodization is the development of iodine-induced hyperthyroidism (IIH), which affects mainly older people with nodular goiter another possibifity is the aggravation or even the induction of autoimmune thyroiditis. IIH has been reported in almost all iodine supplementation programs in countries with history of severe ID (Stanbury et ai, 1998). However, IIH can occur following iodine supplementation in areas with previous sufficient iodine intake Galofre et al. (1994) the authors have reported increased incidence of both nodular and Graves hyperthyroidism. Also, increased iodine intake is associated with increased incidence of thyroid autoimmune diseases (Papanastasiou et al, 2000 Zois etai, 2003) (Figure 73.4). 

The beneficial effects of iodine supplementation in the prevention and control of developed thyroid abnormalities due to iodine deficiency have been discussed so far in this chapter. However, supplementation with excess iodine, including the improvement of a previous iodine-deficient state, may cause thyroid dysfunctions, viz., iodine-induced hypothyroidism/iodide goiter in susceptible subjects (Roti and Vagenakis, 2000) and iodine-induced hyperthyroidism (IIH) especially in individuals over 40 years of age and who have been iodine deficient for a long period in the past (Vidor et ai, 1973). It may also increase the ratio of papillary/follicular carcinomas (Slowinska-Klencka et ai, 2002). In other words, both low and excess intake of iodine is related to further risk of thyroid disease. Although a daily intake of up to 1000 pg/day by a normal adult individual is quite safe (WHO, 1994), the upper limit is much lower in a population that has been exposed to iodine deficiency in the past. Therefore, to prevent IDD, the recommended iodine requirement in an adult individual is fixed within a narrow range of 150 rg/day (Knudsen et ai, 2000). Iodine supplementation under certain conditions in certain populations causes adverse effects, e.g., iodide goiter and iodine-induced hypothyroidism, IIH, iodine-induced thyroiditis and thyroid cancer. 

In 1966, iodized oil was injected in residents of Papua New Guinea, where the severity of endemic goiter and cretinism was high. A follow-up study showed that cretinism disappeared almost completely from the offspring of mothers who received iodized oil. The effect of iodine supplementation on the survival of the fetus and on their brain development was established. 

Excess iodine supplementation, however, is related to the further risk of thyroid disease. Occurrence of iodine-induced hypothyroidism and iodide-goiter, IIH and iodine-induced thyroiditis are the consequence of excess iodine supplementation in certain populations who were iodine deficient till 40 years or more of age. 

Iodine supplementation programs have limitations, because they do not always result in complete eradication and prevention of endemic goiter and associated disorders in all areas, because of the interference of... 

Chronic excessive iodine supplementation could cause goiter or retention of colloid in the thyroid. 

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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