Iodine deficiency induced hypothyroidism

The first one is the observation that in areas with persisting borderline iodine deficiency, transient hypothyroidism in the newborns and also some anomalies of thyroid func on in pre iant women can still be linked to such an easily preventable factor as iodine deficiency. In some of these areas it is now clear that in screening, for neonatal hypothyroidism, roughly 2 out of 3 newborns rec alled for abnormal thyroid hormone or TSH levels are false positive. Apart from the psycholomcal and economic al costs linked to the rectal proc ess per-se, this transient hypothyroidism might induce around birth, brain maturation retardation of unknown long term... 

The complexity of the interaction between iodine intake and autoimmune thyroid disease has been highlighted by reports of evidence that iodide (compared with thyroxine) induces thyroid autoimmunity in patients with endemic (iodine deficient) goiter (43), while in those with pre-existing thyroid autoimmunity, evidenced by the presence of antithyroid (thyroid peroxidase) antibodies, administration of iodine in an area of mild iodine deficiency led to subclinical or overt hypothyroidism (44). 

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. 

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. 

Amiodarone-induced hyperthyroidism seems to be more common in males than in females and can be found in up to 15% of treated patients, especially in iodine-deficient areas (Kennedy et al, 1989). A comparison between the incidences of thyroid dysfunction in areas with low iodine intake, such as Tuscany (Italy), with that in an iodine-replete area, such as Massachusetts (USA), showed the following distribution hyperthyroidism was more common in Tuscany, with an incidence of 9.6%, than in Massachusetts, with an incidence of 2% (Martino et al, 1984). However, amiodarone-induced hypothyroidism is a more common problem in areas with iodine-repletion 22% incidence in Massachusetts vs. 5% in Tuscany (Martino et al., 1984). Amiodarone-induced hypothyroidism is often found in... 

Iodine is an essential component of thyroid hormones, and iodine deficiency can lead to severe hypothyroidism. On the other hand, excessive iodine intake also results in thyroid dysfunction in certain persons. Coindent described the first case of iodine-induced hyperthyroidism in 1821 (Fradkin and Wolff, 1983), and Hurxthal (1945) reported the first case of iodine-induced hypothyroidism. Ingestion of iodine-rich foods, such as seaweed, can cause hyperthyroidism, and the incidence of hyperthyroidism showed an increase in regions of dietary iodine deficiency after prophylactic iodization of bread or salt. Iodine-containing pharmaceuticals, such as povidone-iodine (PVP-I), radiographic contrast media and amiodarone, are a major source of excessive iodine intake (Wolff, 1969 Fradkin and Wolff, 1983 Markou et aL, 2001 Roti and degli Uberti, 2001). 

The fetus and neonate are both at risk of developing iodine-induced hypothyroidism (Table 96.3). Many cases of such hypothyroidism in fetuses and neonates have been reported, especially in iodine-deficient regions of Europe, but also in iodine-sufficient areas. Iodide goiter in neonates is usually a transient problem. However, tracheal obstruction due to such goiter can be fatal (Markou et al, 2001 Wolff, 1969). Transient hypothyroidism without elevation of thyroid-stimulating hormone (TSH) in extremely... 

Note The fetus and neonate are both at risk of developing iodine-induced hypothyroidism. Many cases of hypothyroidism in newborns have been reported, especially in iodine-deficient regions of Europe, but also in iodine-sufficient areas. 

Iodine is readily absorbed when PVP-I is applied to the skin of a newborn infant, because of high cutaneous permeability, and neonates are very sensitive to iodine overload, as described previously. Topical PVP-I therapy is associated with a significant risk of hypothyroidism in neonates, especially very-low-weight babies (Smerdely et ai, 1989). Many cases of hypothyroidism induced by topical use of PVP-I have been reported in newborn infants, mainly from iodine-deficient regions (Markou et ai, 2001). However, a case of severe hypothyroidism in a neonate was also reported from North America, an iodine-sufficient region (Khashu et al. 2005). A premature infant developed severe hypothyroidism that required L-thyroxine replacement therapy after application of PVP-I for 20 days. 

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). 

Finally, it has been shown experimentally in animals that fetal hypothyroidism induces damage of the inner ear (64-68), which is possibly responsible for the audiogenic seizures reported in the offspring of extremely severely iodine deficient rats (69). 

Hypothyroidism is a relative deficiency in thyroid hormones. It manifests as a slowing down of all body functions or a decrease in metabolic rate. There are many causes for hypothyroidism, including Hashimoto s thyroiditis, drug-induced, radiation and radioactive iodine, dyshormono-genesis, congenital, and secondary causes (pituitary or... 

Development of iodine-induced thyroid dysfunction is influenced by a person s prior iodine intake. Cases of thyrotoxicosis being induced by contrast media are mainly reported in Europe or Australia, where dietary iodine levels are low, as described by Fradkin and Wolff (1983). Except for cases due to amiodarone, the incidence of iodine-induced hyperthyroidism is very low in regions where dietary iodine is adequate (Roti and degfl Uberti, 2001). Neonates treated with PVP-I often develop hypothyroidism in iodine-insufficient regions of Europe, but rarely do so in iodine-sufficient regions of the United States, as described by Brown et al. (1997). Thus, persons who five in areas where iodine is deficient in the diet are at risk of developing thyroid dysfunction induced by iodine-containing pharmaceuticals. 

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