Iodine induced goiter

Iodine-induced goiter Iodine-induced hypothyroidism Fetus and neonate... 

Another important group, the National IDD Advisory Committee (NIDDAC) chaired by Professor Chen Zupei, has played a crucial role in the national program. Under the leadership of the MOH, NIDDAC provides scientific and technical guidefines, standards and recommendations. It also provides evidence for poficy development (IDD Newsletter, 1998). Since 1993 NIDDAC has re-evaluated and standardized the measmement of thyroid gland size by palpation and ultrasound standardized urinary iodine testing methods. It has also evaluated the technical aspects and the application of neonatal TSH in IDD monitoring, iodine excess and excessive dietary iodine-induced goiter, and the role of iodized oil in the prevention and control of IDD and iodine-induced hyperthyroidism (Chen, 2002). 

Many of the inhabitants of Hokkaido, a Japanese island, consume large quantities of an iodine-rich seaweed (Kombu) daily, delivering up to 200mg iodine daily (34). Approximately 10 percent of these subjects have goiter but rarely hypothyroidism. Endemic iodine-induced goiter has also been observed in a majority of school children... 

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). 

In older patients with goiter due to iodine deficiency there is a risk of provoking hyperthyroidism by increasing iodine intake (p. 247) During chronic maximal stimulation, thyroid follicles can become independent of TSH stimulation ( autonomic tissue"). If the iodine supply is increased, thyroid hormone production increases while TSH secretion decreases due to feedback inhibition. The activity of autonomic tissue, however, persists at a high level thyroxine is released in excess, resulting in iodine-induced hyperthyroidism. 

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). 

Because of reports of severe hyperthyroidism after the introduction of iodized salt in two severely iodine-deficient African counties (Zimbabwe and the Democratic Republic of the Congo), a multicenter study has been conducted in seven countries in the region to evaluate whether the occurrence of iodine-induced hyperthyroidism after the introduction of iodized salt was a generalized phenomenon or corresponded to specific local circumstances in the two affected countries (46). Iodine deficiency had been successfully eliminated in all of the areas investigated and the prevalence of goiter had fallen markedly. However, it was clear that some areas were now exposed to iodine excess as a result of poor monitoring of the quality of iodized salt and of the iodine intake of the population. In these areas, iodine-induced hyperthyroidism occurred only when iodized salt had been recently introduced. 

Adults goiter with its complications, hypothyroidism, impaired mental functions, iodine-induced hyperthyroidism (Hetzel and Wellby 1997). 

It has been known that excessive iodine intake results in goiter, hypothyroidism, or hyperthyroidism in humans (Institute of Medicine, 2001). The biological basis for iodine-induced hyperthyroidism (IIH) appears most often to be mutational events in thyroid cells that lead to autonomy of function. When the mass of cells with such an event becomes sufficient, and the iodine supply is increased, the subject may become thyrotoxic. These changes may occur in localized foci within the gland or... 

The incidence of iodine-induced hyperthyroidism is dependent on the iodine dose and the prevalence of goiter and, in connection with this, the occurrence of autonomies. 

Goiter with its compiications iodine-induced hyperthyroidism (iiH)... 

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. 

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. 

The main use of antithyroid drugs in toxic adenoma and toxic multinodular goiter is therefore to attain a euthyroid state before the patient may undergo other modes of therapy. Another use is to block iodine uptake prior to the exposure to radiographic contrast agents in patients at risk of iodine-induced hyperthyroidism. 

In 1928 Plummer proposed two origins of thyrotoxicosis a diffuse hyperplasia responding to iodine intake, or alternatively arising in nodular goiter. In 1973, it was first suggested by Vidor et al. (1973) that pre-existing thyroid autonomy plays a crucial role in the pathogenesis of iodine-induced hyperthyroidism (IIH). 

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... 

AIT can be categorized into two subtypes, which are termed type 1 and type 2 (Table 96.5). Type 1 AIT is primarily iodine-induced hyperthyroidism that develops in patients with underlying thyroid disease, such as nontoxic multinodular goiter or Graves disease. Synthesis and release of thyroid hormones are increased in type 1 AIT. In contrast, type 2 AIT is a destructive thyroiditis that occurs in persons with no apparent thyroid disease (Basaria and Cooper, 2005 Ursella et al, 2005). Type 1 AIT is more prevalent in iodine-deficient regions and type 2 AIT is more prevalent in iodine-sufficient regions (Daniels, 2001). Thus, type 1 AIT is rare in Japan where dietary iodine intake is high (Sato et al, 1999). 

Table 97.1 Causes of iodine-induced hypothyroidism or goiter...

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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