Objective: To determine whether serum levels of activin A and inhibin A are
altered in patients before development of preeclampsia.
Methods: Blood samples were collected from patients during the second trime
ster of prenatal care. We identified patients who subsequently developed pr
eeclampsia and matched them with patients who had no evidence of preeclamps
ia during their gestation. Matching criteria included gestational age at bl
ood sampling, gestational age at delivery, and birth weight. Assays were th
en performed to assess the levels of activin A and inhibin A in the control
and study groups. A power calculation determined that 12 patients who subs
equently developed preeclampsia, if matched with controls in a 1:2 ratio, w
ould allow the detection of differences in analyte levels that were 60% as
large as those previously reported between patients already diagnosed with
preeclampsia and matched controls.
Results: Twelve patients with preeclampsia were identified and matched with
24 controls. No differences in serum levels of activin A or inhibin A were
detected between the two groups. Because of the significant overlap of ana
lyte levels between the two groups, no cutpoint that would allow identifica
tion of patients destined to become preeclamptic could be determined.
Conclusion: These data suggest that activin A and inhibin A cannot be used
as markers for later development of preeclampsia in a low-risk population.
(Obstet Gynecol 2000;96:390-4. (C) 2000 by The American College of Obstetri
cians and Gynecologists).