Study of the autoimmune reactions of the thyroid disorders in pregnant women suffering from miscarriage and relation gene expression of HLA DR3

This doctoral dissertation aimed to investigate the relationship between autoimmune reactions associated with thyroid disorders and the expression of the HLA DR3 gene in pregnant women who experienced miscarriage. The study was conducted between 2024 and 2025, involving 130 women who had miscarriages during the first trimester and 20 healthy pregnant women as the control group. Participants were categorized into hypothyroidism, subclinical hypothyroidism, hyperthyroidism, and subclinical hyperthyroidism groups for comparison. Thyroid function parameters (TSH, T3, T4, FT3, FT4), antithyroid autoantibodies (anti-TPO, anti-TG, TSH receptor antibody), and HLA DRB3 gene expression were analyzed using PCR amplification and gel electrophoresis. The electrophoresis results confirmed successful amplification of the HLA DRB3 gene with a clear 801 bp band. The findings demonstrated significant differences in thyroid hormone levels between the miscarriage groups and the control group. In the subclinical hypothyroidism group, the mean TSH level reached 4.09 mIU/L compared to 1.00 mIU/L in the control group. Women with hyperthyroidism exhibited the highest mean T3 and FT3 levels (4.97 nmol/mL and 7.03 pmol/L, respectively). The hyperthyroid group also showed markedly increased T4 values (189.11 pmol/L), while the hypothyroid group had significantly decreased free T4 levels (9.02 pmol/L). Analysis of autoimmune markers revealed elevated anti-TPO (29.88 IU/L) and anti-TG (34.0 IU/L) levels in the hypothyroidism group compared with controls. The subclinical hypothyroidism group showed a remarkable increase in thyroglobulin (TG) concentration, reaching 55.0 ng/ml. The expression of the HLA DRB3 gene indicated that autoimmune responses may be genetically influenced. In conclusion, thyroid dysfunction and autoimmune reactions were found to be closely associated with pregnancy loss, and HLA DR3 gene expression appears to play a key role in this pathophysiological process.