ABSTRACT
The link between autoimmune thyroid diseases and reproductive failures, including implantation failure and pregnancy loss, has been attracted a great deal of attention in the last two decades. In this regard, a considerable progress has been achieved in understanding the etiopathogenesis of the adverse pregnancy consequences related to the presence of anti-thyroid antibodies, however, the exact action mechanisms of these antibodies are not fully comprehended. Thyroid peroxidase antibodies (TPOAbs), thyroglobulin antibodies (TgAbs) and TSH receptor antibodies (TRAbs) are the anti-thyroid antibodies which are present in autoimmune thyroid disorder (AITD) patients, such as Hashimoto's thyroiditis. In this condition, the thyroid hormones production, which are essential for normal implantation and pregnancy, are disrupted, and compromise the embryo or fetus development. In addition, a hypothesis suggests that there is underlying generalized immune abnormalities behind the presence of these antibodies. On the other hand, similar immunologic aberrations have been observed in thyroid autoimmunity and reproductive complications, which are postulated to be the proper answer for the scientists who seek for the pathophysiology behind the presence of these antibodies. Elevated inflammatory responses and decreased immunoregulatory actions, seem to be the main interfering pathologic factors in maternal tolerance toward fetus. In addition, cross reactivity of these antibodies with antigenic determinants of egg, embryo and placenta is another suggested mechanism, causing implantation and pregnancy complications. The ability of anti-thyroid antibodies in passing through the placental barrier and affecting the fetal thyroid gland, makes them more threatening for maintenance of a pregnancy.
