Postpartum Autoimmune Thyroid Syndrome: A Model of Aggravation of Autoimmune Disease

Abstract

Postpartum thyroid dysfunction is rather a common problem during the postpartum period being found in approximately 5% of mothers in the general population. It occurs from subclinical autoimmune thyroiditis that is aggravated after parturition and causes various types of thyroid dysfunction. Immune activity is physiologically suppressed during pregnancy so that the fetus is not rejected, and rebounds above the normal level after parturition. Graves' disease and Hashimoto's thyroiditis also spontaneously ameliorate during pregnancy, and are often aggravated after parturition. The high-risk mothers for postpartum thyroid dysfunction are well screened by antithyroid microsomal antibody (MCAb) and 60% to 70% of MCAb-positive mothers develop postpartum thyroid dysfunction, which is transient in most cases. New onset of Graves' disease may be screened by thyroid-stimulating antibody (TSAb) and 70% of TSAb-positive mothers develop either transient or persistent postpartum Graves' disease that usually occurs 3 to 6 months postpartum. Immune rebound after parturition may cause not only autoimmune thyroid diseases but other autoimmune diseases, which may be investigated with similar strategies to those in postpartum autoimmune thyroid disease. Thus, we found that postpartum onset of rheumatoid arthritis was found in 0.08% of women in the general population and could be partially predicted by measuring rheumatoid factors in early pregnancy. There are several case reports of other autoimmune diseases that develop after delivery; postpartum renal failure or postdelivery hemolytic-uremic syndrome, postpartum idiopathic polymyositis, postpartum syndrome with antiphospholipid antibodies, postpartum autoimmune myocarditis. Many other possible postpartum autoimmune diseases are still unexplored. Puerperal diseases should be carefully examined in relation to autoimmune abnormalities in the affected organs.

Natural history of the transition from euthyroidism to overt autoimmune hypo- or hyperthyroidism: a prospective study

“…The proportion of women who had never been pregnant was lower in the hyperthyroid cases than their controls, that is hyperthyroid cases had experienced pregnancies more often. This is in line with the notion that in the postpartum year the risk of developing Graves' hyperthyroidism is higher (21,22). The use of oral estrogens (oral contraceptive pills) was not related in our study to the occurrence of hypo-or hyperthyroidism, although a few studies in the past indicate a protective effect of estrogens on the development of hyperthyroidism (23,24).…”

Functional modification of CD11c+ liver dendritic cells during liver regeneration after partial hepatectomy in mice

“…Evidence shows that pregnancy is associated with reduced relapse rate of multiple sclerosis, 37,38 rheumatoid arthritis, 39 and autoimmune thyroiditis. 40 Moreover, in murine experimental allergic encephalomyelitis (EAE), an experimental model of multiple sclerosis, estrogen administration reduces disease severity. 21 One interpretation of these results is that estrogen may drive Th2 and suppress Th1 responses, and that this is achieved by multiple interactions with cells of the immune system.…”

Immune Modulation in Multiple Sclerosis Patients Treated with the Pregnancy Hormone Estriol

“…While the etiology of MS is unknown, a Th1-mediated autoimmune component driven by myelin protein-specific, proinflammatory cytokine-secreting T lymphocytes is believed to be involved in the pathogenesis. A beneficial effect of pregnancy on clinical symptoms has been observed in MS and other Th1-mediated autoimmune diseases, including rheumatoid arthritis (RA), psoriasis, uveitis, and thyroiditis (2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20). Interestingly, most of these diseases are characterized by temporary rebound exacerbations postpartum (2, 4, 5, 7-9, 14, 17, 20).…”