Thyroid diseases autoimmune thyroiditis, incidence

There is an increased incidence of late hypothyroidism in patients with autoimmune hyperthyroidism, but the risk increases markedly after extensive thyroid surgery and especially after I treatment. Analysis of the cumulative incidence of hjrpothjroidism shows two phases an early phase of radiation death of thyroid cells, depending on the I dosage and occurring during the first 1-2 years after treatment a second period of a lower (0.5-3.5% per year) but hfe-long risk of developing hypothyroidism for a variety of reasons (natural history of the disease, autoimmune processes) (see Table 1) (12-14). 

In the adult population, the prevalence of overt hypothyroidism is 19 per 1000 women and 1 per 1000 men with annual incidence of overt hypothyroidism is 4 per 1000 women and 0.6 per 1000 men. Subclinical hypothyroidism is also more common in women, the incidence increases with age, with up to 10% of women older than 60 years having an increased thyroid-stimulating hormone concentration. Subclinical hypothyroidism is more common in people who have been treated for hyperthyroidism with radioactive iodine or surgery, and in those with organ-specific autoimmune diseases, such as pernicious anaemia, type 1 diabetes mellitus, or Addison s disease. 

The immunological predisposition to thyroid disorders has been studied in 17 of 439 Japanese patients who had symptomatic autoimmune thyroid disorders during interferon alfa treatment (521). There was a significantly higher incidence of the human leukocyte antigen (HLA)-A2 hap-lotype compared with the general Japanese population (88 versus 41%), suggesting that HLA-A2 is a possible additional risk factor for the development of interferon alfa-induced autoimmune thyroid disease. 

Two studies have provided insights into the incidence and risk factors of the immune-mediated comphcations of interferon alfa in patients with chronic myeloid leukemia. In the first study, 13 of 46 patients had autoimmune manifestations consisting of a combination of autoimmune thyroiditis in four, a direct antiglobulin test without hemolysis in eight, cryoagglutinins in one, Raynaud s phenomenon in two, and chronic autoimmune hepatitis in one (343). Overall, six patients had chnically symptomatic manifestations after a median of 15 months of treatment. In the second study, there were autoimmune diseases in seven of 76 patients after a median of 19 months of treatment, including hypothyroidism in one, immune-mediated hemolysis in two, systemic lupus erythematosus in two, Raynaud s phenomenon in one, and mixed connective tissue disease in one (344). In... 

Models of rheumatoid arthritis (RA) were object to l,25(OH)2D3 treatment, providing additional support for the high potential of the hormone for the treatment of Thl-mediated diseases. As an example, in rat adjuvant arthritis l,25(OH)2D3 improved the inhibiting effect of cyclosporine A on arthritis onset as well as on arthritis aggravation [142]. The incidence and severity of type II collagen-induced arthritis was reduced in rats or mice orally treated with 25-(OH)2-D3, the 1,25 (OH)2D3 analog MC 1288 or l,25(OH)2D3 [143-145], l,25(OH)2D3 has further proven to be therapeutically effective in animal models of autoimmune thyroiditis [146], allogeneic transplantation [66, 147,148], rat Heymann nephritis [149] and autoimmune prostatitis [80]. Results from l,25(OH)2D3-related studies in animal models are summarized in Table 10.3. 

Many specific autoimmune diseases are relatively rare, with an estimated incidence of less than 5 per 100 000 persons per year or an estimated prevalence of less than 20 per 100 000 (Table 7). Other diseases (e.g. rheumatoid arthritis, Graves disease, thyroiditis) are quite common, affecting 1% or more of the population (Cotch et al., 1996 Boberg et al., 1998 Cooper et al., 1998 Marie et al., 1999 Boisseau-Garsaud et al., 2000 Watts et al., 2000 Pillemer et al., 2001 Doran et al., 2002 Kalb et al., 2002 Lovas Husebye, 2002 Feld Heathcote, 2003 Gonzalez-Gay et al., 2003 Mayes et al., 2003 Bogliun Beghi, 2004 Cuadrado et al., 2004). 

Data pertaining to co-morbidity of autoimmune diseases in humans are surprisingly sparse. Few studies are population-based, and few are of sufficient size to address potentially important biological associations, given the relative rarity of many diseases (Scofield, 1996). A recent unpublished review of co-morbidity of rheumatoid arthritis, diabetes mellitus type 1, multiple sclerosis, Crohn disease, and autoimmune thyroid disease found evidence of an increased incidence of autoimmune thyroid disease in patients with rheumatoid arthritis and in autoimmune diabetes (E. Somers, unpublished data). 

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). 

Teng et al. (2006) explored the effect of iodine intake on thyroid diseases in China. Baseline characteristics of three populations were estabfished in three communities in 1999 and then again 5 years later. The communities had different levels of iodine nutrition mild deficiency more than adequate and excessive intake. Salt iodization had been implemented in China in 1996. In the general population, median UI increased from 165 pg/1 in 1995 to approximately 300 pg/1 in 1999. The concern was with oversupplementation of iodine to a level that is more than adequate, in a region in which iodine intake was previously mildly deficient, which in turn may accelerate the development of subclinical hypothyroidism to overt hypothyroidism. High levels of iodine intake may increase the incidence and prevalence of autoimmune thyroiditis, making it imperative to tailor supplementation needs to each region. 

In general, the incidence of autoimmune thyroid disease is not strikingly different among the various areas in Japan. Similarly, postpartum thyroiditis, which can be considered as a good index to compare the incidence of autoimmune thyroid.disorder in a population, is present with the same frequency in different Japanese areas. Finally, concerning hyperthyroidism in relation to high iodine intake, I must say that I have never seen a single case of Jod-Basedow in Japan. 

So probably a higher intake of iodine in Denmark would reduce the incidence of multinodular toxic goitre in elderly subjects. On the other hand a risk would be an increase in the incidence of Graves disease among young subjects. There are evidence to support that high iodine intake may promote other types of autoimmune thyroid disease as well (5). 

Recently evidence is accumulating that iodine is a modulating factor in the development of thyroid autoimmune reactivity. In humans, iodine deficiency as well as iodine excess can lead to goitre formation and/or lymphocytic thyroiditis. Affected patients show a variety of thyroid reactive autoantibodies in the circulation. In experimental animal models of thyroid autoimmunity, viz the BB rat and the OS chicken, the incidence of lymphocytic thyroiditis is enhanced by an excessive dietary iodine intake, whereas iodine restriction ameliorates the disease. 

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