W A Grobman1, E Y Wang. 1. Section of Maternal-Fetal Medicine and Department of Obstetrics and Gynecology, Northwestern Memorial Hospital, Northwestern University Medical School, Chicago, IL, USA.
Abstract
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 trimester of prenatal care. We identified patients who subsequently developed preeclampsia and matched them with patients who had no evidence of preeclampsia during their gestation. Matching criteria included gestational age at blood sampling, gestational age at delivery, and birth weight. Assays were then 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 subsequently developed preeclampsia, if matched with controls in a 1:2 ratio, would 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 analyte levels between the two groups, no cutpoint that would allow identification 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.
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 trimester of prenatal care. We identified patients who subsequently developed preeclampsia and matched them with patients who had no evidence of preeclampsia during their gestation. Matching criteria included gestational age at blood sampling, gestational age at delivery, and birth weight. Assays were then 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 subsequently developed preeclampsia, if matched with controls in a 1:2 ratio, would 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 analyte levels between the two groups, no cutpoint that would allow identification 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.
Authors: E Fitzpatrick; M P Johnson; T D Dyer; S Forrest; K Elliott; J Blangero; S P Brennecke; E K Moses Journal: Mol Hum Reprod Date: 2009-01-06 Impact factor: 4.025