Abstract
The current study aimed to identify correlative and regressive dependencies between the water iodine concentration and the levels of TSH (thyroid-stimulating hormone), thyroglobulin antibodies (TgAbs), and thyroid peroxidase (TPOAb) in the serum of 168 in patients (34 men and 134 women) with a hypothyroid form of Hashimoto’s thyroiditis who use water from the supply network and individual wells. Based on the water iodine concentration, low and moderate degrees of iodine endemia in the location of the patients were determined. In the groups of men and women using water from different water supply sources, there were direct correlations between the water iodine concentrations and the TgAbs and TPOAb titers as well as an inverse dependence between iodine and TSH levels. Multivariate regressive analysis indicated that TgAb and TSH in the group of women using water from a supply network and TPOAb titers in the group of women using well water were independent factors associated with water iodine concentrations. Statistically significant correlations and regressive dependencies between the water iodine concentrations and the biomarkers of the thyroid status of the patients indicate the risk of Hashimoto’s thyroiditis progression, especially among women with additional iodine intake.
Highlights
Hashimoto’s thyroiditis (HT) is one of the most prevalent autoimmune diseases leading to the formation of anti-thyroid antibodies that attack the thyroid tissue, causing lymphocytemediated cell-damaging process and leading to the destruction of follicular cells and progressive fibrosis [11, 30]
The pathogenetic mechanisms leading to the development of autoimmune thyroid disease are based on several different factors [36]
It is well established that 20% of etiology is attributed to environmental factors and physiological states [2, 41]
Summary
Hashimoto’s thyroiditis (HT) is one of the most prevalent autoimmune diseases leading to the formation of anti-thyroid antibodies that attack the thyroid tissue, causing lymphocytemediated cell-damaging process and leading to the destruction of follicular cells and progressive fibrosis [11, 30]. The current diagnosis of Hashimoto’s disease is based on clinical symptoms correlated with laboratory results showing elevated thyroid-stimulating hormone (TSH) with normal to low thyroxin levels [29]. The role of anti-thyroid peroxidase (antiTPO) antibodies in the pathogenesis of autoimmune thyroid disease (AITD) is negligible. Arciszewski Str. 22b, 76-200 Słupsk, Poland 3 Lviv Medical Institute, Lviv, Ukraine noted in human studies between the severity of the disease and the level of anti-TPO antibody concentration in serum [45]. The pathogenetic mechanisms leading to the development of autoimmune thyroid disease are based on several different factors [36]. The contribution of each factor varies from patient to patient, and there are no clear genotype-phenotype correlations [21]
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