THYROID AUTOIMMUNITY AND FEMALE GENDER

Citation
L. Chiovato et al., THYROID AUTOIMMUNITY AND FEMALE GENDER, Journal of endocrinological investigation, 16(5), 1993, pp. 384-391
Citations number
44
Categorie Soggetti
Endocrynology & Metabolism
ISSN journal
03914097
Volume
16
Issue
5
Year of publication
1993
Pages
384 - 391
Database
ISI
SICI code
0391-4097(1993)16:5<384:TAAFG>2.0.ZU;2-Y
Abstract
Sexual dimorphism exists in regard to the immune response between wome n and men, and it accounts for the greater prevalence of thyroid autoi mmunity in women. Similarly to the human situation a sex-related susce ptibility to autoimmune thyroiditis is evident in animal models. A dir ect influence of genes on sex chromosomes (X or Y) on the immune respo nse has been postulated in some models of autoimmune thyroiditis in ra ts. On the other hand sex hormones have been implicated to explain the majority of sex differences in the autoimmune response against the th yroid. A state of immune suppression during pregnancy influences the c linical course of autoimmune thyroid diseases, in that a typical ameli oration during pregnancy is accompanied by aggravation following deliv ery. This immmunologic rebound phenomenon may also underly the post pa rtum thyroid dysfunction in otherwise healthy women with a genetic pre disposition to autoimmune thyroid disease. Thyroid autoimmunity also i nterferes with the female reproductive function. Hypothyroidism and le ss frequently hyperthyroidism due to thyroid autoimmune disorders may produce menstrual dysfunction, anovulation and eventually infertility. Maternal hyper-or hypothyroidism can affect the outcome of pregnancy, producing a higher incidence of miscarriages, maternal complications, and congenital malformations. Untreated maternal hypothyroidism produ ced by Hashimoto's disease during pregnancy can impair the neurologica l development of the fetus due to a reduced availability of maternal t hyroxine during early gestation. More specifically, fetal and/or neona tal hypo- or hyperthyroidism produced by the transplacental passage of maternal thyroid autoantibodies can impair growth and neuropsychologi cal development of affected children.