title: The effects of syphilis on endocrine function of the fetoplacental unit.
abstract: Several pregnancy complications that are thought to cause chronic intrauterine stress have been found to lead to inappropriate fetal development and reductions in estrogen production. In the current study we sought to evaluate the fetoplacental unit in pregnancies complicated by maternal syphilis (n = 37), with and without fetal infection. Maternal 17 beta-estradiol and estriol levels were reduced during the third trimester in women with syphilis when compared with those in women with uncomplicated pregnancies. Serum progesterone levels were within normal limits or else were increased in women with syphilis. When compared with data in age- and weight-matched control infants of women having no pregnancy complications, umbilical cord serum levels of dehydroepiandrosterone sulfate, the major fetal adrenal precursor of placental estrogens, were subnormal (897 +/- 597 ng/ml, mean +/- SD) in 12 newborn infants with congenital syphilis (33.9 +/- 4.2 weeks' gestation, birth weight 2020 +/- 719 gm); such infants also had excessive serum levels of cholesterol (103 +/- 37 mg/dl). Dehydroepiandrosterone sulfate (1883 +/- 907 ng/ml) and cholesterol (58.1 +/- 13.9 mg/dl) levels were within normal limits in 19 uninfected infants of women with syphilis (38.6 +/- 2.4 weeks' gestation, birth weight 2861 +/- 660 gm). Cortisol levels were increased and estriol levels were decreased in both groups of neonates of women with syphilis compared with those in control neonates. These findings are suggestive that estrogen production often is reduced in pregnancies complicated by syphilis; the reduction in estriol appears to be largely due to reduced fetal adrenal dehydroepiandrosterone sulfate production. The reduction in 17 beta-estradiol levels may be due to alterations in maternal precursor synthesis. Although placental progesterone formation appears to be normal in women with syphilis, a deficiency in placental aromatase activity also is possible.
authors.affiliation: Department of Obstetrics and Gynecology, University of Alabama, Birmingham 35294.
authors.forename: C R
authors.initials: CR
authors.lastname: Parker
authors.forename: G D
authors.initials: GD
authors.lastname: Wendel
mesh_terms: D002784:Cholesterol / Q000097:blood; D003687:Dehydroepiandrosterone / Q000031:analogs & derivatives / Q000097:blood; D019314:Dehydroepiandrosterone Sulfate; D004702:Endocrine Glands / Q000503:physiopathology*; D004964:Estriol / Q000097:blood; D004967:Estrogens / Q000097:blood; D005260:Female; D005333:Fetus / Q000502:physiology*; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007231:Infant, Newborn / Q000097:blood; D010920:Placenta / Q000503:physiopathology*; D011247:Pregnancy; D011251:Pregnancy Complications, Infectious; D011374:Progesterone / Q000097:blood; D013587:Syphilis / Q000097:blood / Q000503:physiopathology*; D013590:Syphilis, Congenital / Q000097:blood
chemical_list: D004967:Estrogens; D003687:Dehydroepiandrosterone; D011374:Progesterone; D019314:Dehydroepiandrosterone Sulfate; D002784:Cholesterol; D004964:Estriol; D006854:Hydrocortisone