This study aimed to establish a method of screening for pregnancy hypertension by a combination of maternal variables, including mean arterial pressure, uterine artery pulsatility index, pregnancy-associated plasma protein-A, and placental growth factor in early pregnancy. The base-cohort population constituted of 7797 singleton pregnancies, including 34 case subjects who developed preeclampsia (PE) requiring delivery before 34 weeks (early PE) and 123 with late PE, 136 with gestational hypertension, and 7504 cases subjects (96.3%) who were unaffected by PE or gestational hypertension. Maternal history, uterine artery pulsatility index, mean arterial pressure, and pregnancy-associated plasma protein-A were recorded in all of the cases in the base cohort, but placental growth factor was measured only in the case-control population of 209 cases who developed hypertensive disorders and 418 controls. In each case the measured mean arterial pressure, uterine artery pulsatility index, pregnancy-associated plasma protein-A, and placental growth factor were converted to a multiple of the expected median (MoM) after correction for maternal characteristics found to affect the measurements in the unaffected group. Early PE and late PE were associated with increased mean arterial pressure (1.15 MoM and 1.08 MoM) and uterine artery pulsatility index (1.53 MoM and 1.23 MoM) and decreased pregnancy-associated plasma protein-A (0.53 MoM and 0.93 MoM) and placental growth factor (0.61 MoM and 0.83 MoM). Logistic regression analysis was used to derive algorithms for the prediction of hypertensive disorders. It was estimated that, with the algorithm for early PE, 93.1%, 35.7%, and 18.3% of early PE, late PE, and gestational hypertension, respectively, could be detected with a 5% false-positive rate and that 1 in 5 pregnancies classified as being screen positive would develop pregnancy hypertension. This method of screening is far superior to the traditional approach, which relies entirely on maternal history.

Objective: To examine the association between maternal age and a wide range of adverse pregnancy outcomes after adjustment for confounding factors in obstetric history and maternal characteristics.Methods: This was a retrospective study in women with singleton pregnancies attending the first routine hospital visit at 11 + 0 to 13 + 6 weeks' gestation. Data on maternal characteristics, and medical and obstetric history were collected and pregnancy outcomes ascertained. Maternal age was studied, both as a continuous and as a categorical variable. Regression analysis was performed to examine the association between maternal age and adverse pregnancy outcome including pre‐eclampsia, gestational hypertension, gestational diabetes mellitus (GDM), preterm delivery, small‐for‐gestational age (SGA) neonate, large‐for‐gestational age (LGA) neonate, miscarriage, stillbirth and elective and emergency Cesarean section.Results: The study population included 76 158 singleton pregnancies with a live fetus at 11 + 0 to 13 + 6 weeks. After adjusting for potential maternal and pregnancy confounding variables, advanced maternal age (defined as ≥ 40 years) was associated with increased risk of miscarriage (odds ratio (OR), 2.32 (95% CI, 1.83–2.93); P < 0.001), pre‐eclampsia (OR, 1.49 (95% CI, 1.22–1.82); P < 0.001), GDM (OR, 1.88 (95% CI, 1.55–2.29); P < 0.001), SGA (OR, 1.46 (95% CI, 1.27–1.69); P < 0.001) and Cesarean section (OR, 1.95 (95% CI, 1.77–2.14); P < 0.001), but not with stillbirth, gestational hypertension, spontaneous preterm delivery or LGA.Conclusions: Maternal age should be combined with other maternal characteristics and obstetric history when calculating an individualized adjusted risk for adverse pregnancy complications. Advanced maternal age is a risk factor for miscarriage, pre‐eclampsia, SGA, GDM and Cesarean section, but not for stillbirth, gestational hypertension, spontaneous preterm delivery or LGA. Copyright © 2013 ISUOG. Published by John Wiley & Sons Ltd.

Objective: To determine the performance of screening for pre‐eclampsia (PET) by maternal characteristics and uterine artery pulsatility index (PI) at 11 + 0 to 13 + 6 weeks' gestation.Methods: In women with singleton pregnancies attending for routine care at 11 + 0 to 13 + 6 weeks' gestation we recorded maternal variables and measured the uterine artery PI. We identified 107 cases that subsequently developed PET and 5041 that were unaffected by PET, gestational hypertension or delivery of newborns with birth weight below the 10^th centile. A multivariate Gaussian model was fitted to the distribution of log multiples of the median (MoM) PI in the PET and unaffected groups. Likelihood ratios for log MoM PI were computed and used together with maternal variables to produce patient‐specific risks for each case. Predicted detection rates (DR) and false‐positive rates (FPR) were calculated by taking the proportions with risks above a given risk threshold.Results: In the unaffected group log MoM PI was influenced by maternal ethnic origin, body mass index, previous history of PET and fetal crown–rump length. In the prediction of PET significant contributions were provided by log MoM PI, ethnic origin, body mass index and previous and family history of PET. For an FPR of 10% the DRs of all PET and PET leading to delivery before 34 weeks' gestation by log MoM PI and maternal variables were 61.7% and 81.8%, respectively.Conclusion: Maternal variables together with uterine artery PI at 11 + 0 to 13 + 6 weeks' gestation provide sensitive prediction of the development of PET, especially of severe early‐onset PET. Copyright © 2007 ISUOG. Published by John Wiley & Sons, Ltd.

A beneficial consequence of screening for trisomy 21 is the early diagnosis of trisomies 18 and 13. Our objective was to examine the performance of first-trimester screening for trisomies 21, 18 and 13 by maternal age, fetal nuchal translucency (NT) thickness, fetal heart rate (FHR) and maternal serum-free β-hCG and pregnancy-associated plasma protein-A (PAPP-A). Prospective screening for trisomy 21 by maternal age, fetal NT, free β-hCG and PAPP-A at 11⁺⁰–13⁺⁶ weeks in singleton pregnancies, including 56 376 normal cases, 395 with trisomy 21, 122 with trisomy 18 and 61 with trisomy 13. Risk algorithms were developed for the calculation of patient-specific risks for each of the three trisomies based on maternal age, NT, FHR, free β-hCG and PAPP-A. Detection (DR) and false positive rates (FPR) were calculated and adjusted according to the maternal age distribution of pregnancies in England and Wales in 2000–2002. The DR and FPR were 90% and 3%, respectively, for trisomy 21, 91% and 0.2% for trisomy 18 and 87% and 0.2% for trisomy 13. When screen positivity was defined by an FPR of 3% on the risk for trisomy 21 in conjunction with an FPR of 0.2% on the maximum of the risks for trisomies 13 and 18, the overall FPR was 3.1% and the DRs of trisomies 21, 18 and 13 were 91%, 97% and 94%, respectively. As a side effect of first-trimester screening for trisomy 21, ∼95% of trisomy 13 and 18 fetuses can be detected with an 0.1% increase in the FPR.

Objectives: To examine the relationship between low maternal serum pregnancy‐associated plasma protein‐A (PAPP‐A) and uterine artery pulsatility index (UtA‐PI) at 11 + 0 to 13 + 6 weeks with subsequent development of pre‐eclampsia (PE).Methods: UtA‐PI and serum PAPP‐A were measured in women attending for routine care at 11 + 0 to 13 + 6 weeks of gestation. In the population, 156 (1.9%) women developed PE, including 32 (0.4%) in whom delivery was before 34 weeks (early PE) and 124 (1.5%) with delivery at 34 weeks or more (late PE); 7895 (98.1%) women had no PE. Regression analysis was used to examine which of the factors amongst maternal characteristics, log PAPP‐A multiples of the median (MoM) and log UtA‐PI MoM contributed to the prediction of PE.Results: The median PAPP‐A MoM was 1.002 (interquartile range (IQR), 0.685–1.411) in the unaffected group, 0.555 (IQR, 0.463–0.922) in early PE and 0.911 (IQR, 0.580–1.247) in late PE. Serum PAPP‐A was below the 5^th centile in 21.9% of early PE and 6.5% of late PE cases. The PAPP‐A‐related patient‐specific risk for PE was strongly influenced by maternal characteristics. There was a significant association between log UtA‐PI MoM and log PAPP‐A MoM (P = 0.001), and the detection rate of screening for PE by maternal variables and UtA‐PI was not improved by inclusion of PAPP‐A. Regression analysis was used to establish tables that allow modification of the maternal history and PAPP‐A‐related patient‐specific risk for PE by the measurement of UtA‐PI.Conclusions: Low PAPP‐A is a marker for subsequent development of PE. The PAPP‐A‐related patient‐specific risk for PE can be modified by the measurement of UtA‐PI. Copyright © 2008 ISUOG. Published by John Wiley & Sons, Ltd.