Autoimmune thyroid disease is much more common in women than in men. One intriguing explanation for this disparity is fetal-to-maternal cell traicking (Greer, 201l). Fetal cells are known to enter maternal circulation during pregnancy. When fetal lymphocytes enter maternal circulation, they can live for more than 20 years. Stem cell interchange can lead to engraftment in several maternal tissues and is termed etal microchimerism. In some cases, this may involve the thyroid gland (Bianchi, 2003; Boddy, 2015; Khosrotehrani, 2004). A high prevalence of Y-chromosome-positive cells has been identiied using luorescence in situ hybridization (FISH) in the thyroid glands of women with Hashimoto thyroiditis-60 percent, or with Graves disease-40 percent (Renne, 2004). In another study of women giving birth to a male fetus, Lepez and colleagues (201l) identiied signiicantly more circulating male mononuclear cells in those with Hashimoto thyroiditis. Ironically, such micro chimerism may have a protective role for autoimmune thyroid disorders (Cirello, 2015).
TABLE 58-1. Incidence of Overt Hyperthyroidism in Pregnancy
Vaidya (2007)a United Kingdom 0.7%
Lazarus (2007)b United Kingdom 1.7%
Casey (2006r United States 0.4%
Andersen (201n6r,d Denmark 0.4-0.7% aScreened irl the first trimester. bScreened at 9-15 weeks. (Screened before 20 weeks.
dDiagnosed in early versus later pregnancy.
The incidence of thyrotoxicosis or hyperthyroidism in pregnancy is varied and complicates between 2 and 17 per 1000 births when gestational-age appropriate TSH threshold values are used (Table
Because normal pregnancy simulates some clinical findings similar to thyroxine excess, clinically mild thyrotoxicosis may be diicult to diagnose. Suggestive indings include tachycardia that exceeds that usually seen with normal pregnancy, thyromegaly, exophthalmos, and failure to gain weight despite adequate food intake. Laboratory testing is confirmatory. TSH levels are markedly depressed, while serum free T4 (IT4) levels are elevated Qameson, 2015). Rarely, hyperthyroidism is caused by abnormally high serum triiodothyronine (T 3) levels-so-called Trtoxicosis.
he overwhelming cause of thyrotoxicosis in pregnancy is Graves disease, an organ-speciic autoimmune process associated with thyroid-stimulating TSH-receptor antibodies as previously discussed'(De Leo, 2016). Because these antibodies are specific to Graves hyperthyroidism, such assays have been proposed for diagnosis, management, and prognosis in pregnancies complicated by hyperthyroidism (Barbesino, 2013). At Parkland Hospital, these receptor antibody assays are generally reserved for cases in which fetal thyrotoxicosis is suspected. With Graves disease, during the course of pregnancy, hyperthyroid symptoms may initially worsen because ofhCG stimulation but then subsequently diminish with drops in receptor antibody titers in the second half of pregnancy (Mestman, 2012; Sarkhail, 2016). Amino and coworkers (2003) have found that levels of blocking antibodies also decline during pregnancy.