Autoantibodies to thyroglobulin and thyroid peroxidase are common in the euthyroid population and are considered secondary responses and indicative of thyroid inflammation. By contrast, autoantibodies to the TSH receptor are unique to patients with Graves' disease and to some patients with Hashimoto's thyroiditis. Both types of thyroid antibodies are useful clinical markers of autoimmune thyroid disease and are profoundly influenced by the immune suppression of pregnancy and the resulting loss of such suppression in the postpartum period. Here, we review these three types of thyroid antibodies and their antigens and how they relate to pregnancy itself, obstetric and neonatal outcomes, and the postpartum.
In pregnancy, complex physiologic changes in the immune system alters the environment for the "non-self" fetus allowing it to be tolerated in the maternal womb, while the immune system is still able to counteract external pathogens. The interplay of the immune system and the physiologic changes induced by pregnancy on the thyroid induce changes in the natural history of the autoimmune thyroid diseases (AITD). This review discusses the various players in creating this milieu, including the MHC, the T-and B-cells, sex steroids and the possible role of microchimerism. The participants provide a variety of mechanisms that create the clinical scenarios that we see in patients with AITDmost commonly the improvement in Grave's Disease during pregnancy and the rebound in thyroid autoantibodies and recurrence, or new onset, of Graves' and Hashimoto's diseases in the post-partum.
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