We hypothesized that the origins of abruption may extend to the stages of placental implantation; however, there are no reliable markers to predict its development. Based on this hypothesis, we sought to evaluate whether first-trimester and second-trimester serum analytes predict placental abruption.
We performed a secondary analysis of data of 35,307 women (250 abruption cases) enrolled in the First and Second Trimester Evaluation of Risk cohort (1999–2003), a multicenter, prospective cohort study. Percentiles (based on multiples of the median) of first-trimester (pregnancy-associated plasma protein A and total and free β-hCG) and second-trimester (maternal serum alpha-fetoprotein, unconjugated estriol, and inhibin-A) serum analytes were examined in relation to abruption. Associations are based on risk ratio (RR) and 95% confidence interval (CI).
Women with an abnormally low pregnancy-associated plasma protein A (fifth percentile or less) were at increased risk of abruption compared with those without abruption (9.6% compared with 5.3%; RR 1.9, 95% CI, 1.2–2.8). Maternal serum alpha-fetoprotein 95th percentile or greater was more common among abruption (9.6%) than nonabruption (5.1%) pregnancies (RR 1.9, 95% CI 1.3–3.0). Inhibin-A fifth percentile or less (8.0% compared with 5.1%; RR 1.8, 95% CI 1.1–2.9), and 95th percentile or greater (9.6% compared with 5.0%; RR 2.0, 95% CI 1.3–3.1) were associated with abruption. Women with all three abnormal pregnancy-associated plasma protein A, maternal serum alpha-fetoprotein, and inhibin-A analytes were at 8.8-fold (95% CI 2.3–34.3) risk of abruption. No associations were seen with other analytes.
These data provide support for our hypothesis that the origins of placental abruption may extend to the early stages of pregnancy.
Supplemental Digital Content is Available in the Text.The origins of placental abruption may extend to the early stages of pregnancy.
Department of Obstetrics and Gynecology, College of Physicians and Surgeons, and the Department of Epidemiology, Joseph L. Mailman School of Public Health, Columbia University, New York, New York; West Windsor-Plainsboro High School North, Plainsboro, New Jersey; and the Department of Obstetrics and Gynecology, Winthrop-University Hospital, Mineola, New York.
Corresponding author: Cande V. Ananth, PhD, MPH, Department of Obstetrics and Gynecology, College of Physicians and Surgeons, Columbia University, 622 West 168th Street, New York, NY 10032; email: email@example.com.
The FASTER prospective cohort study was funded by the Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD38625), National Institutes of Health.
Financial Disclosure The authors did not report any potential conflicts of interest.
For a list of members and institutions who participated in the First and Second Trimester Evaluation of Risk (FASTER) study, see Appendix 1 online at http://links.lww.com/AOG/A923.
Each author has indicated that he or she has met the journal's requirements for authorship.