Maternal serum markers, characteristics and morbidly adherent placenta in women with previa



To examine associations with morbidly adherent placenta (MAP) among women with placenta previa.

Study Design:

Women with MAP (cases) and previa alone (controls) were identified from a cohort of 236 714 singleton pregnancies with both first and second trimester prenatal screening, and live birth and hospital discharge records; pregnancies with aneuploidies and neural tube or abdominal wall defects were excluded. Logistic binomial regression was used to compare cases with controls.


In all, 37 cases with MAP and 699 controls with previa alone were included. Risk for MAP was increased among multiparous women with pregnancy-associated plasma protein-A (PAPP-A) 95th percentile (2.63 multiple of the median (MoM); adjusted OR (aOR) 8.7, 95% confidence interval (CI) 2.8 to 27.4), maternal-serum alpha fetoprotein (MS-AFP) 95th percentile (1.79 MoM; aOR 2.8, 95% CI 1.0 to 8.0), and 1 and 2 prior cesarean deliveries (CDs; aORs 4.4, 95% CI 1.5 to 13.6 and 18.4, 95% CI 5.9 to 57.5, respectively).


Elevated PAPP-A, elevated MS-AFP and prior CDs are associated with MAP among women with previa.


Morbidly adherent placenta (MAP), including placenta accreta, increta and percreta, is characterized by failure of the placenta to separate at delivery, with potential for significant perinatal and maternal morbidity and mortality.1 Once rare, with an average reported occurrence of 1 in 7000 deliveries during the century preceding 1972,2, 3 placenta accreta occurrence has risen steadily4 to 1 in 533 between the years 1982 and 2002.5 This ~13-fold increase parallels the increase in cesarean delivery (CD).1 When prior CD is combined with placenta previa, the risk for accreta increases with each prior CD, from 11 to 40%, 61 and 67% for one, two, three and four prior CDs, respectively.6

While multiple risk factors for MAP have been described7, 8, 9, 10, 11, 12, 13, 14, 15 mechanisms of accreta development remain opaque and pre-delivery prediction is limited. Proposed mechanisms of accreta include excessive trophoblast invasion into the myometrium,16, 17 deficient decidua enabling placental implantation onto the myometrium,18 suggested by increased accreta risk with previa alone,19 and a combination of both.20, 21

Antenatal diagnosis of accreta is critical, as it can reduce maternal morbidity by enabling for a scheduled delivery22 by a multidisciplinary team in a tertiary care center.23 Ultrasound identifies many, but not all, women with MAP, and without significant benefit from magnetic resonance imaging.24, 25 Elevated serum markers second trimester maternal-serum alpha fetoprotein (MS-AFP)26, 27, 28, 29 and beta-human chorionic gonadotropin28, 29 have been associated with MAP. Low first trimester pregnancy-associated plasma protein-A (PAPP-A), a zinc metalloproteinase implicated in local proliferation,30 is associated with adverse pregnancy outcomes related to poor placental invasion;31, 32, 33 its overexpression could plausibly be associated with abundant placental invasion and MAP. While not thought to be associated with adverse obstetrical outcomes,34 elevated PAPP-A was recently reported among women with accreta in a small, retrospective study.35

Our objective was to examine the strength of the associations between routinely collected first and second trimester maternal serum markers and maternal and obstetric characteristics with MAP among a large population-based cohort of women with placenta previa to aid in pre-delivery prediction of MAP.


Our study sample was drawn from all singleton pregnancies undergoing first and second trimester prenatal serum screening through the California Prenatal Screening Program with expected delivery between December 2009 and May 2010. Women were included if they also had linked live birth and hospital discharge records in a birth cohort database maintained by the Office of Statewide Health Planning and Development, a diagnosis of placenta previa based on ICD-9 codes (ICD-9 641.0 or 641.1) or linked records, and underwent cesarean delivery (CD). Women were considered to have MAP if they had ICD-9 codes for both placenta previa and retained placenta (ICD-9 666.0, 666.2 and/or 667.1). Women were excluded if their fetuses had chromosomal abnormalities or neural tube or abdominal wall defects.

Maternal serum analytes included first trimester PAPP-A and total human chorionic gonadotropin (hCG), collected between 10 weeks 0 days and 13 weeks 6 days gestation, and second trimester MS-AFP, hCG, unconjugated estriol (uE3) and dimeric inhibin A (INH), collected between 15 weeks 0 days and 20 weeks 0 days gestation. All analytes were measured on automated equipment (Auto DELFIA, Perkin-Elmer Life Sciences, Waltham, MA, USA and Applied Biosystems, Brea, CA, USA) and results were entered directly into the State’s database. All analyte multiple of the median (MoM) values were adjusted for gestational age, maternal weight, race/ethnicity, smoking status and pre-existing diabetes. Biomarker MoM percentiles were calculated based on the entire screened population (n=236 714).

Maternal and obstetric variables including body mass index (BMI), parity, prior CD, history of prior preterm birth and interpregnancy interval (IPI) were obtained from the linked live birth and hospital discharge records. BMI was calculated using height and pre-pregnancy weight. IPI was calculated from the date of the previous live birth (month and year) to the conception of the index pregnancy. Procedures and labor and delivery complications were obtained from live birth and hospital discharge records, and birth weight and gestational age at delivery were obtained from GDSP (Genetic Disease Screening Program) prenatal and newborn screening records.

Analyses utilized logistic binomial regression methods to estimate odds ratios (ORs, Tables 1 and 2). To measure associations between serum markers or maternal characteristics and MAP, calculations were performed with the following pre-defined referent groupings: biomarker MoMs between the 6th and 94th percentile, White race/ethnicity, maternal age 18 to 34 years, normal BMI (18.5 to 24.9), non-diabetic, non-smoker and parity=1. Among women with parity 2, referent groups included those without a prior preterm birth and an IPI of 24 to 59 months. Final models were built using backwards stepwise logistic regression populated with maternal characteristics and biomarkers with crude OR findings P<0.10, and were stratified by parity after current birth =1 and 2. (Table 3) The predictive performance of variables (isolated and co-occurring) found to be significantly associated with MAP was also calculated.

Table 1 Maternal characteristics: placenta previa with and without MAP, n=736
Table 2 Maternal serum markers: placenta previa with and without MAP, n=736
Table 3 Predictors of MAP among multiparous womena with parity 2 after current birth (n=470)

All analyses were conducted using Statistical Analysis Software (SAS) version 9.3 (Cary, NC, USA) and were based on data received by the screening program as of 31 March 2013. The study was approved by the Committee for the Protection of Human Subjects within the Health and Human Services Agency of the State of California.


Thirty-seven women with previa and MAP and 699 women with previa alone were identified from a population of 236 714 women (Figure 1) and included in this analysis. Maternal and obstetric demographics and characteristics are shown in Table 1. The greatest proportion of the population was Hispanic (45.9%), age 18 to 34 years (51.6%), of normal weight (52.2%), non-diabetic (88.6%), non-smoking (98.6%) and multiparous (63.9%). Of multiparous women, 46% had a prior CD and 37% had an IPI of 24 to 59 months. Women with MAP were more likely to be 35 years old (OR 2.0, 95% CI 1.0 to 4.1, P<0.05), overweight (OR 2.2, 95% CI 1.0 to 4.9, P<0.05) or obese (OR 2.7, 95% CI 1.1 to 6.7), diabetic (OR 2.3, 95% CI 1.0 to 5.1) and multiparous (OR 2.5, 95% CI 1.1 to 5.8). Among multiparous women, prior CD was a risk for MAP (OR 6.4, 95% CI 2.4 to 17.1), and risk increased with increasing numbers of prior CDs (OR 3.7, 95% CI 1.3 to 10.9 for 1 prior; OR 15.0, 95% CI 5.2 to 43.8 for 2 prior). Racial/ethnic differences were not observed.

Figure 1

Overview of sample selection.

Maternal serum analyte values are shown in Table 2. PAPP-A 95th percentile and MS-AFP 95th percentile were associated with MAP (PAPP-A MoM 2.63, OR 3.4, 95% CI 1.3 to 8.6; MS-AFP 1.79 MoM, OR 3.2, 95% CI 1.3 to 7.7) while hCG (first and second trimester), uE3 and INH were not. Analyte values were based on the entire screened population. Analyte values for the entire screened population were similar to those of the included population, at 5th and 95th percentiles, as follows: PAPP-A: 0.38 and 2.63 vs. 0.39 and 2.56; hCG: 0.50 and 2.00 vs. 0.51 and 1.95; AFP: 0.60 and 1.79 vs. 0.60 and 1.67; hCG: 0.41 and 2.28 vs. 0.41 and 2.16; uE3: 0.63 and 1.40 vs. 0.63 and 1.42; and INH: 0.54 and 2.14 vs. 0.54 and 1.99.

When final logistic models were created, stratified by parity and adjusted with maternal characteristics and biomarkers that had crude OR findings of P<0.10 (Table 1), no significant risk factors for MAP were identified for nulliparous women. For multiparous women, risk for MAP increased nearly ninefold when PAPP-A MoM was 95th percentile (aOR 8.7, 95% CI 2.8 to 27.4) and nearly threefold when MS-AFP MoM was 95th percentile (aOR 2.8, 95% CI 1.01 to 8.0) (Table 3).

Prior CD independently increased the risk for MAP (1 prior: aOR 4.4, 95% CI 1.5 to 13.6), with the strongest risk found among women with 2 prior CDs (aOR 18.4, 95% CI 5.9 to 57.5). Maternal age, weight and diabetes were no longer independently associated with MAP in the final logistic models. MAP occurred among 1.8% of multiparous women without a prior CD and with normal serum analytes. With one prior CD, MAP occurred among 5.2% (relative risk 2.8, 95% CI 0.8 to 9.4) when serum analytes were normal versus 42.9% (relative risk 23.5, 95% CI 6.4 to 85.6) when PAPP-A was also elevated. Among women with 2 two prior CDs, MAP occurred among 16.3% (relative risk 18.9, 95% CI 2.8 to 28.5) when serum analytes were normal versus 66.7% when PAPP-A was also elevated (relative risk 36.3, 95% CI 10.4 to 128.4) and 50% when MS-AFP was elevated (relative risk 27.4, 95% CI 8.3 to 90.2). The positive and negative predictive values for MAP in the setting of two prior CDs were 16.3 and 94.8; in the setting of 2 prior CDs and PAPP-A95th percentile, 66.7 and 94.0; and in the setting of 2 prior CDs and MS-AFP 95th percentile, 50.0 and 94.4.

Of the 699 women diagnosed with previa alone, 9 (1.3%) underwent cesarean hysterectomy and 244 (34.9%) experienced hemorrhage. Of the 37 women diagnosed with MAP, 23 (62.2%) underwent cesarean hysterectomy and 32 (86.5%) experienced hemorrhage. There were no maternal or neonatal deaths.


We found that among multiparous women with placenta previa, first trimester PAPP-A values greater than 2.63 MoM conferred a nearly 9-fold increased risk of MAP overall independent of prior CDs, and a 23- and 36-fold increased risk for MAP in the setting of one and two prior CDs, respectively. As expected, prior CD and elevated MS-AFP were associated independently with MAP.

Advanced prediction of accreta is important to optimize outcomes through scheduled preterm delivery23 in a tertiary care center.36 Among women with previa, elevated PAPP- A should be considered, in addition to risk factors such as elevated MS-AFP and prior CD, to help identify women at increased risk for MAP. The high specificities and negative predictive values of these risk factors may also help stratify high-risk women who are less likely to have MAP. While elevated PAPP-A, as well as MS-AFP, should be validated prospectively before becoming a part of standard assessment of MAP risk, our data support the value of examining maternal serum analytes to inform risk of MAP among multiparous women. Why maternal serum biomarkers and other risk factors were not predictive of MAP among nulliparous women with previa is less clear, and may be a function of the lower prevalence of MAP among nulliparous women and a relatively small sample size (n=7) in our study cohort.

PAPP-A is novel zinc metalloproteinase produced by placental syncytiotrophoblasts, secreted into the maternal circulation in increasing concentrations until term;37 its function is not well understood.30 PAPP-A is responsible for proteolysis of IGF from IGFBP-4,38 implying a role in growth. Low PAPP-A has been associated with poor placental invasion with placental insufficiency, intrauterine growth restriction, preeclampsia, stillbirth, abruption and premature birth.32, 39, 40 Elevated PAPP-A could plausibly be implicated in excessive placental invasion. Desai et al.35 recently reported higher median PAPP-A values among 16 women with accreta (1.68 MoM) compared with 82 women with previa alone (0.98 MoM); PAPP-A values of 3 MoM and above were associated with an unadjusted 4-fold increased risk accreta. We adjusted for potential confounding variables and found much higher associations between PAPP-A and MAP among multiparous women. This also suggests a role for excessive trophoblast invasion as a mechanism for accreta. Whether PAPP-A levels continue to rise disproportionately in the second and third trimesters among women with MAP is one area for future investigation.

Elevated maternal serum AFP in the setting of a non-anomalous fetus has previously been shown to be associated with placenta accreta26, 27, 28, 29 potentially due to placental impairment, with breakdown of the fetal–maternal–placental interface.29, 41 We similarly found an association between elevated MS-AFP and placenta accreta. Women with AFP greater 1.79 MoM, the 95th percentile, independently experienced a nearly 3-fold increased risk for placenta accreta.

The incidence of MAP in our study was far lower than the 1/533 incidence of accreta reported in the general population.5 There are several possible explanations. Our study was based on a large data set that relied on medical billing codes for the diagnosis of MAP; we lacked access to surgical or pathologic records for confirmation. Without an ICD-9 code for placenta accreta, we took a conservative approach to ensure that cases would be expected to carry a diagnosis of MAP. We excluded women who were not delivered by CD and women who did not have a previa, and included women with a code for adherent placenta. Our approach appears to have resulted in our missing some cases of accreta, which may limit the generalizability of our findings. However, we created a study cohort that experienced significant pathology related to MAP, as 87% hemorrhaged. We excluded pregnancies affected by neural tube defects, abdominal wall defects and aneuploidy, but due to constraints of coding were unable to exclude more rare conditions potentially associated with elevated MS-AFP such as urogenital malformations. Given the rare nature of these conditions, this lack of exclusion is unlikely to have altered our results.

Despite its limitations, our uniquely large, linked data set allowed us to explore maternal serum markers and maternal characteristics among women with placenta previa to identify the relatively novel associations of increased PAPP-A with MAP. Women with placenta previa and prior CD should undergo careful ultrasound examination for signs for accreta. When PAPP-A is elevated in a multiparous woman with placenta previa, a careful ultrasound examination of the placental-uterine interface should also be considered. Future research should explore the combination of ultrasound examination with maternal serum biomarkers to predict placenta accreta.


  1. 1

    Committee on Obstetric Practice. Committee opinion No. 529: placenta accreta. American College of Obstetricians and Gynecologists. Obstet Gynecol 2012; 120: 207–211.

  2. 2

    Breen JL, Neubecker R, Gregori CA, Franklin JE . Placenta accreta, increta, and percreta. A survey of 40 cases. Obstet Gynecol 1977; 49 (1): pp43–pp47.

    Google Scholar 

  3. 3

    Wortman AC, Alexander JM . Placenta accreta, increta, and percreta. Obstet Gynecol Clin North Am 2013; 40 (1): 137–154.

    Article  Google Scholar 

  4. 4

    Pridjian G, Hibbard JU, Moawad AH . Cesarean: changing the trends. Obstet Gynecol 1991; 77: 195–200.

    CAS  Article  Google Scholar 

  5. 5

    Wu S, Kocherginsky M, Hibbard JU . Abnormal placentation: 20-year analysis. Am J Obstet Gynecol 2005; 192: 1458–1461.

    Article  Google Scholar 

  6. 6

    Silver RM, Landon MB, Rouse DJ, Leveno KJ, Spong CY, Thom EA et al. Maternal morbidity associated with multiple repeat cesarean deliveries. National Institute of Child Health and Human Development MFMU. Obstet Gynecol 2006; 107: 1226–1232.

    Article  Google Scholar 

  7. 7

    Fox H . Placenta accreta, 1945-1969. Obstet Gynecol Surv 1972; 27: 475–490.

    Article  Google Scholar 

  8. 8

    Jacques SM, Qureshi F, Trent VS, Ramirez NC . Placenta accreta: mild cases diagnosed by placental examination. Int J Gynecol Pathol 1996; 15: 28–33.

    CAS  Article  Google Scholar 

  9. 9

    Al-Serehi A, Mhoyan A, Brown M, Benirschke K, Hull A, Pretorius DH . Placenta accreta: an association with fibroids and Asherman syndrome. J Ultrasound Med 2008; 27 (11): 1623–1628.

    Article  Google Scholar 

  10. 10

    Sharp HT . Endometrial ablation: postoperative complications. Am J Obstet Gynecol 2012; 207 (4): 242–247.

    Article  Google Scholar 

  11. 11

    Hamar BD1, Wolff EF, Kodaman PH, Marcovici I . Premature rupture of membranes, placenta increta, and hysterectomy in a pregnancy following endometrial ablation. J Perinatol 2006; 26 (2): 135–137.

    CAS  Article  Google Scholar 

  12. 12

    Pron G, Mocarski E, Bennet J, Vilos G, Common A, Vanderburgh L Ontario UFE Collaborative Group et al. Pregnancy after uterine artery embolization for leiomata: the Ontario multicenter trial. Obstet Gynecol 2005; 105 (1): 67–76.

    Article  Google Scholar 

  13. 13

    Miller DA, Chollet JA, Goodwin TM . Clinical risk factors for placenta previa-placenta accreta. Am J Obstet Gynecol 1997; 177: 210–214.

    CAS  Article  Google Scholar 

  14. 14

    Clark SL, Koonings PP, Phelan JP . Placenta previa/accreta and prior cesarean section. Obstet Gynecol 1985; 66: 89–92.

    CAS  PubMed  PubMed Central  Google Scholar 

  15. 15

    Wax JR, Seiler A, Horowitz S, Ingardia CJ . Interpregnancy interval as a risk factor for placenta accreta. Conn Med 2000; 64 (11): 659–661.

    CAS  PubMed  Google Scholar 

  16. 16

    Kim KR, Jun SY, Kim JY, Ro JY . Implantation site intermediate trophoblasts in placenta cretas. Mod Pathol 2004; 17: 1483–1490.

    Article  Google Scholar 

  17. 17

    Stanek J, Drummond Z . Occult placenta accreta: the missing link in the diagnosis of abnormal placentation. Pediatr Dev Pathol 2007; 10: 266–273.

    Article  Google Scholar 

  18. 18

    Miller WG . A clinical and pathological study of placenta accrete. J Obstet Gynaecol Br Emp 1959; 66: 353–364.

    Article  Google Scholar 

  19. 19

    Bowman ZS, Eller AG, Bardsley TR, Greene T, Varner MW, Silver RM . Risk Factors for Placenta Accreta: A Large Prospective Cohort. Am J Perinatol 2013; 31 (9): 799–804.

    Article  Google Scholar 

  20. 20

    Wehrum MJ, Buhimschi IA, Salafia C, Thung S, Bahtiyar MO, Werner EF et al. Accreta complicating complete placenta previa is characterized by reduced systemic levels of vascular endothelial growth factor and by epithelial-to-mesenchymal transition of the invasive trophoblast. Am J Obstet Gynecol 2011; 204 (5): 411 e1-411.

    Article  Google Scholar 

  21. 21

    Tantbirojn P, Crum CP, Parast MM . Pathophysiology of placenta creta: the role of decidua and extravillous trophoblast. Placenta 2008; 29: 639–645.

    CAS  Article  Google Scholar 

  22. 22

    Warshak CR, Ramos GA, Eskander R, Scioscia AL, Mattrey RF, Benirschke K et al. Effect of predelivery diagnosis in 99 consecutive cases of placenta accreta. Obstet Gynecol 2010; 115 (1): 65–69.

    Article  Google Scholar 

  23. 23

    Eller AG, Porter TF, Soisson P, Silver RM . Optimal management strategies for placenta accreta. BJOG 2009; 116 (5): 648–654.

    CAS  Article  Google Scholar 

  24. 24

    D'Antonio F, Iacovella C, Palacios-Jaraquemada J, Bruno CH, Manzoli L, Bhide A . Prenatal identification of invasive placentation using magnetic resonance imaging (MRI): a systematic review and meta-analysis. Ultrasound Obstet Gynecol 2014; 44 (1): 8–16.

    CAS  Article  Google Scholar 

  25. 25

    D'Antonio F1, Iacovella C, Bhide A . Prenatal identification of invasive placentation using ultrasound: systematic review and meta-analysis. Ultrasound Obstet Gynecol 2013; 42 (5): 509–517.

    CAS  Article  Google Scholar 

  26. 26

    Kupferminc MJ, Tamura RK, Wigton TR, Glassenber R, Socol ML . Placenta accreta is associated with elevated maternal serum alpha-fetoprotein. Obstet Gynecol 1993; 82 (2): 266–269.

    CAS  PubMed  Google Scholar 

  27. 27

    Zelop C, Nadel A, Frigoletto FD Jr, Pauker S, MacMillan M, Benacerraf BR . Placenta accreta/percreta/increta: a cause of elevated maternal serum alpha-fetoprotein. Obstet Gynecol 1992; 80 (4): 693–694.

    CAS  PubMed  Google Scholar 

  28. 28

    Dreux S, Salomon LJ, Muller F, Goffinet F, Oury JF ABA Study GroupSentilhes L. Second- trimester maternal serum markers and placenta accreta. Prenat Diagn 2012; 32 (10): 1010–1012.

    CAS  Article  Google Scholar 

  29. 29

    Hung TH, Shau WY, Hsieh CC, Chiu TH, Hsu JJ, Hsieh TT . Risk factors for placenta accreta. Obstet Gynecol 1999; 93 (4): 545–550.

    CAS  PubMed  Google Scholar 

  30. 30

    Conover CA . Key questions and answers about pregnancy-associated plasma protein-A. Trends Endocrinol Metab 2012; 235 (5): 242–249.

    Article  Google Scholar 

  31. 31

    Dugoff L, Hobbins JC, Malone FD, Porter TF, Luthy D, Comstock CH et al. First-trimester maternal serum PAPP-A and free-beta subunit human chorionic gonadotropin concentrations and nuchal translucency are associated with obstetric complications: a population-based screening study (the FASTER Trial). Am J Obstet Gynecol 2004; 191 (4): 1446–1451.

    CAS  Article  Google Scholar 

  32. 32

    Jelliffe-Pawlowski LL, Shaw GM, Currier RJ, Stevenson DK, Baer RJ, O'Brodovich HM et al. Association of early-preterm birth with abnormal levels of routinely collected first- and second- trimester biomarkers. Am J Obstet Gynecol 2013; 208 (6): 492.

    Article  Google Scholar 

  33. 33

    Goetzinger KR, Cahill AG, Macones GA, Odibo AO . Association of first-trimester low PAPP-A levels with preterm birth. Prenat Diagn 2010; 30: 309–313.

    CAS  PubMed  Google Scholar 

  34. 34

    Gagnon A, Wilson RD . Obstetrical complications associated with abnormal maternal serum markers analytes. J Obstet Gynaecol Can 2008; 30 (10): 918–932.

    Article  Google Scholar 

  35. 35

    Desai N, Krantz D, Roman A, Fleischer A, Boulis S, Rochelson B . Elevated first trimester PAPP-A is associated with increased risk of placenta accrete. Prenat Diagn 2014; 34: 159–162.

    CAS  Article  Google Scholar 

  36. 36

    Robinson BK, Grobman WA . Effectiveness of timing strategies for delivery of individuals with placenta previa and accreta. Obstet Gynecol 2010; 116: 835–842.

    Article  Google Scholar 

  37. 37

    Folkersen J, Grudzinskas JG, Hindersson P, Teisner B, Westergaard JG . Pregnancy-associated plasma protein-A: circulating levels during normal pregnancy. Am J Obstet Gynecol 1981; 139: 910–914.

    CAS  Article  Google Scholar 

  38. 38

    Lawrence JB, Oxvig C, Overgaard MT, Sottrup-Jensen L, Gleich GJ, Hays LG et al. The insulin-like growth factor (IGF) –dependent binding protein-4 protease secreted by human fibroblasts is pregnancy-associated plasma protein-A. Proc Natl Acad Sci USA 1999; 96: 3149–3153.

    CAS  Article  Google Scholar 

  39. 39

    Smith GCS, Stenhouse EJ, Crossley JA, Aitken DA, Cameron AD, Connor JM . Early pregnancy levels of pregnancy-associated plasma protein A and the risk for intrauterine growth restriction, premature birth, preeclampsia and stillbirth. J Clin Endocrinol Metab 2002; 87: 1762–1767.

    CAS  Article  Google Scholar 

  40. 40

    Blumenfeld YJ, Baer RJ, Druzin ML, El-Sayed YY, Lyell DJ, Faucett AM, Shaw GM, Currier RJ, Jelliffe-Pawlowski LL . Association between maternal characteristics, abnormal serum aneuploidy analytes, and placental abruption. Am J Obstet Gynecol 2014; 211 (2): 144.

    Article  Google Scholar 

  41. 41

    Berkeley AS, Killackey MA, Cederqvist LL . Elevated maternal serum alpha-fetoprotein levels with breakdown in fetal-maternal-placental barrier. Am J Obstet Gynecol 1983; 146: 859–861.

    CAS  Article  Google Scholar 

Download references


This study was supported by California Genetic Disease Screening Program (GDSP) and California Office of Statewide Health Planning and Development, Richmond CA. Dr Lyell received support from the Arline and Pete Harman, Children's Health Research Institute fund at Lucile Packard Children's Hospital at Stanford. This study was presented at the Society for Maternal-Fetal Medicine Annual Meeting on 6 February 2014 in New Orleans, LA.

Author information



Corresponding author

Correspondence to D J Lyell.

Ethics declarations

Competing interests

The authors declare no conflict of interest.

Rights and permissions

Reprints and Permissions

About this article

Verify currency and authenticity via CrossMark

Cite this article

Lyell, D., Faucett, A., Baer, R. et al. Maternal serum markers, characteristics and morbidly adherent placenta in women with previa. J Perinatol 35, 570–574 (2015).

Download citation

Further reading