Thyroid and Pseudothyroid Dysfunction as a Cause That is Promoting the Relapse of Benign Focal Thyroid Pathology.

Several studies deal with learning causes stipulating nodular formations in the thyroid tissue, including those occurring against the ground of metabolic disorders of thyroid hormones. Our study's objective was to determine the peculiarities of thyroid homeostasis disorders in patients suffering from benign nodular thyroid pathology with relapses of the disease and its relapse-free course. For this purpose, 96 female patients suffering from nodular thyroid pathology and 20 without thyroid pathology were examined.

Association of the blood serum cytokines' rate and lymphocytes' apoptosis with polymorphic variants of the BCL-2 (rs17759659), CTLA-4 (rs231775) and APO-1÷FAS (rs2234767) genes in patients with nodular goiters in autoimmune thyroiditis and thyroid adenoma.

The paper analyses results of serum cytokines and lymphocyte apoptosis study in patients with nodular goiter against the background of autoimmune thyroiditis (NGAIT) and thyroid adenoma (TA) based on the cell preparedness to apoptosis (content of lymphocytes carrying apoptosis marker - CD95+-receptor), the number of apoptotic lymphocytes (annexin V+-lymphocytes) and the content of proapoptotic tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β and IL-6, as well as anti-inflammatory IL-4 cytokine in serum, considering the polymorphism of BCL-2 (rs17759659), CTLA-4 (rs231775) and APO-1÷FAS (rs2234767) genes. The results show that under the damaging action of peroxidation products in the thyroid structures, activation of Fas- and caspase-dependent mechanisms of influence on pro- and anti-apoptotic targets, the induced hyperproduction and release of TNF-α from thyroid-stimulated lymphocytes stimulate an additional synthesis of other pro-inflammatory cytokines IL-1β and IL-6, as well as compensatory anti-inflammatory proteins including IL-4. There is a synchronized increase in secretion of the soluble form of TNF-α receptor (sTNFR), which prevents binding the corresponding cytokine to a specific membranous shedding of a number of receptors and separates the apoptotic signals.