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.