Iodine induced thyroid autoimmunity

Kahaly GJ, Dienes HP, Beyer J, Hommel G. Iodine induces thyroid autoimmunity in patients with endemic goitre a randomised, double-blind, placebo-controlled trial. Eur J Endocrinol 1998 139(3) 290-7. 

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). 

Excessive/rlsk of adverse health consequences such as Iodine-Induced hyperthyroidism, autoimmune thyroid disease... 

Excessive Risk of adverse health consequences (iodine-induced hyperthyroidism, autoimmune thyroid diseases)... 

IODINE-INDUCED THYROIDITIS IN GOITROUS AUTOIMMUNE PRONE NON OBESE DIABETIC MICE... 

The autoimmune prone BB-DP rat, on the other hand, more easily developed AITD under the influence of a diet rich in iodine, depending on the previous state of the thyroid (Ruwhof and Drexhage, 2001). In severe ID, those animals had less severe lymphocytic thyroiditis and the production ofTg-Ab was depressed, probably as part of a general lowering of thyroid autoimmunity induced by severe ID. The results obtained with these different strains of rats may be viewed as a model for the individual heterogeneity in response to changes in iodine intake. 

A sudden increase in iodine intake in an iodine-deficient population may induce enhanced thyroid autoimmunity (Harach and Williams, 1995). Both cellular immune response with histological signs of thyroiditis and humoral immune response with circulating thyroid autoantibodies may be increased. It seems as if at least a part of this autoimmunity is reversible, and that the prevalence of antibodies will decrease to a lower level over time if the higher iodine intake is continued (Mazziotti et al., 2003 Zimmermann et al., 2003), or decrease in a relatively short time period if the iodine intake is reduced to the basefine level (Kahaly et al.y 1998). 

A number of mechanisms have been suggested to explain the association between thyroid autoimmunity and the level of iodine intake. A sudden shift from very low to high iodine intake may induce damage to the thyroid tissue by free radicals (Li and Boyages, 1994). Also, enhancement of the autoimmunogenic properties of thyroglobuhn by increased iodination may play a role (Saboori et ai, 1998 Sundick et al., 1987). Apart from these two mechanisms, no other model has been put forward that satisfactorily explains the association between excessive iodine intake and the generation of thyroid autoimmunity. 

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). 

Previously published reports have described both sub-clinical and overt thyroid dysfunction as a result of excess iodine ingestion. Moreover, iodine-induced hypothyroidism is not rare, at least in iodine-replete areas. The possible underlying mechanisms of this impairment consist of both the inhibition of thyroid function by excess iodine and the iodine-induced enhancement of thyroid autoimmunity. On the basis that an excess iodine intake may cause hypothyroidism, several study results support iodine restriction for the treatment of hypothyroidism. The success rate of dietary iodine restriction alone, without thyroid hormone replacement, is reported to be approximately 50-80% in patients with primary hypothyroidism due to Hashimotos thyroiditis and other causes. Relatively mild hypothyroidism, high radioactive iodine uptake and uptake, increased free plasma iodine and... 

The possible underlying mechanisms of excess iodine-induced hypothyroidism consist of both the inhibition of thyroid function by excess iodine and the iodine-induced enhancement of thyroid autoimmunity. 

The therapeutic dosage of iodine is in the range of 100— 200 tg/day. Side-effects of low doses are rare and minor, consisting mainly of iodine-induced acne. Contraindications for the use of iodine are all states of subclinical or overt hyperthyroidism, thyroid autoimmune diseases and the rare dermatological disease Dermatitis herpetiformis Duhring. 

Chronic excessive iodine induced the onset of autoimmune thyroiditis in NOD.H-2 mice, and the degree of lymphocytes infiltration showed a positive correlation with the dosage and the duration of iodine supplementation... 

Iodine-induced thyrotoxicosis in apparently normal thyroid glands has been reported in two patients after exposure to 2—10 mg iodine daily for 2—12 months before thyrotoxicosis was diagnosed. Although the pathogenesis of this kind of IIH remains obscure, the positive family history for thyroid disease in both patients may indicate a latent abnormality of their thyroid glands (Skare and Frey, 1980). Moreover, 10 further cases of iodine-induced thyrotoxicosis in apparently normal thyroid glands have been reported (Savoie et al, 1975). In contrast, a more-than-adequate or excessive iodine intake may lead to hypothyroidism and autoimmune thyroiditis, as shown in China in areas with more than adequate and excessive iodine consumption (Teng et al., 2006). 

What we would like to know more precisely is the duration of the preventive effect of a single injection of iodized oil in women on the incidence of cretinism in the offspring. More information is also needed on the possible adverse effects of iodized oil. The possibility that this therapy could induce a Wolff-Chaikoff effect in the fetus has been raised (85) but never conclusively demonstrated. The hypothesis has also been proposed (86), but never confirmed, that an acute increase in iodine supply could trigger thyroid autoimmunity. 

Yes, I agree with you. Both in the obese strain chicken and in the BB Worcester rat, the animals do not develop lymphocytic thyroiditis if you keep them on a low iodine diet. About 30-40 % of them will develop autoimmune changes in the thyroid gland if you keep them on a regular diet. If you give them a high iodine diet, every animal will develop iodine-induced lymphocytic thyroiditis. 

No obvious apoptosis was identified, no matter whether autoimmune thyroiditis were induced or not by excessive iodine supplementation. 

Unfortunately, some euthyroid patients with underlying thyroid disease, some euthyroid patients with no evidence of previous or current thyroid disorders, and the fetus and neonate do not adapt to excess iodine intake and may develop either hypothyroidism or hyperthyroidism. Furthermore, excess iodine ingestion-induces lymphocytic thyroiditis in the diabetes prone BB/Wor rat (7), the obese strain chicken (8) and the Buffalo rat (9), and may be related to the apparent rise in the prevalence of Hashimoto s thyroiditis in populations residing in iodine sufficient regions. It is beyond the scope of this review to discuss the role of iodine as a pathogen in the induction of autoimmune thyroiditis in these animals and man. 

Along the line of the discussion between Dr. Laurberg and Dr. Braverman, I would like to mention that we have actually confirmed the experiments of Dr. Braverman in the BB rat, there is a continuum in the appearance of autoimmune thyroiditis when going from low to high iodine contents of the food. However, the opposite is true with the Wistar rat high iodine in the food seems to protect this strain of rat from autoimmune thyroiditis. Therefore, these data suggest that genetic predisposition to autoimmunity plays an important role in these effects induced by iodine. 

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