BACKGROUND Visfatin and adiponectin are produced by adipose tissue and have opposite effects on insulin resistance. Circulating concentrations of these biomarkers are altered in type 2 diabetes mellitus. We sought to examine the potential value of maternal serum visfatin and adiponectin concentrations in early pregnancy as potential biomarkers in the prediction of gestational diabetes mellitus (GDM). METHODS This work was a case-control study of 100 women who developed GDM and 300 nondiabetic controls. Maternal serum visfatin and adiponectin were measured between 11 and 13 weeks of gestation. Regression analysis in the nondiabetic group was performed to examine the maternal characteristics affecting the serum concentrations of visfatin and adiponectin. Likelihood ratios for GDM were calculated for visfatin and adiponectin, and performance of screening was assessed by using ROC curve analysis. RESULTS In the GDM group compared with the nondiabetic group, the median maternal serum visfatin concentration was increased (1.34 multiples of the median [MoM], interquartile range [IQR] 0.70–2.87, vs 1.00 MoM, IQR: 0.53–1.92; P = 0.004) and serum adiponectin was decreased (0.66 MoM, IQR 0.50–0.92, vs 1.01, IQR 0.70–1.29; P < 0.0001). In screening for GDM by a combination of maternal factors and serum adiponectin and visfatin, the estimated detection rate was 68.0% (95% CI 58.3–76.3%), at a false-positive rate of 10%. CONCLUSIONS At 11–13 weeks in pregnancies that develop GDM, the serum concentration of adiponectin is decreased and visfatin is increased, and these biomarkers can be combined with maternal factors to provide effective early screening for GDM.

Objective: To assess the value of ductus venosus pulsatility index for veins (DV PIV) in screening for aneuploidies at 11–13 weeks’ gestation. Methods: Fetal DV PIV was measured in singleton pregnancies undergoing first-trimester screening for aneuploidies. In euploid (n = 44,756) and aneuploid (202 cases of trisomy 21, 72 cases of trisomy 18 and 30 cases of trisomy 13) fetuses, DV PIV was best described by a mixture model of distributions. Performance of screening for aneuploidies by DV PIV alone and in combination with fetal nuchal translucency (NT) thickness and serum free β-hCG and PAPP-A was estimated. Results: In euploid pregnancies there was a bimodal distribution of DV PIV with a dominant crown-rump length (CRL)-dependent part, accounting for around 97% of cases in Caucasians and around 93% in Afro-Caribbeans, and a smaller CRL-independent distribution. In aneuploidies the dominant part was the CRL-independent distribution, which accounted for around 85% cases of trisomies 21 and 18 and 70% of cases of trisomy 13. In screening for trisomy 21 by maternal age, NT and biochemistry at a risk cutoff of 1 in 100, the detection rate was 89.7% and false positive rate was 2.74%; with addition of DV PIV, the values were 93.5 and 1.63%, respectively. Conclusions: Measurement of DV PIV improves the performance of first-trimester combined test for aneuploidies.

At 11 to 13 weeks' gestation many fetuses with trisomy 18, trisomy 13 and triploidy have measurable abnormalities in the posterior brain.

Objective: To determine if in fetuses with aneuploidies the diameter of the fourth cerebral ventricle at 11–13 weeks’ gestation is different from euploid fetuses. Methods: The fourth ventricle at 11–13 weeks’ gestation was assessed in 62 cases of trisomy 21, 32 of trisomy 18, 10 of trisomy 13, and 12 of triploidy and compared to 410 normal euploid fetuses. Transvaginal sonography was carried out and 3D brain volumes were acquired. The fetal head was assessed in an axial plane and the diameter of the fourth ventricle was measured. Values in aneuploid and euploid fetuses were compared. Results: The diameter of the fourth ventricle in trisomy 18, trisomy 13 and triploidy, but not in trisomy 21, was significantly higher than in euploid fetuses. In the euploid fetuses the median diameter of the fourth ventricle was 1.9 mm and the 95th percentile was 2.5 mm. The measurements were above the median and the 95th percentile in 25 (78.1%) and 17 (53.1%) cases of trisomy 18, in 10 (100%) and 8 (80.0%) of trisomy 13, and in 10 (83.3%) and 10 (83.3%) of triploidy. Conclusions: In trisomy 18, trisomy 13 and triploidy the diameter of the fourth ventricle at 11–13 weeks’ gestation is increased.

The objective of this study was to determine if the maternal serum levels of visfatin in the first trimester of pregnancy are altered in cases that develop preeclampsia (PE) and whether the levels are related to placental perfusion reflected in uterine artery pulsatility index (PI). Serum visfatin and uterine artery PI were measured at 11(+0)-13(+6) weeks in 80 cases that developed PE and 240 unaffected controls. The median visfatin and uterine artery PI multiple of the unaffected median (MoM) in the outcome groups was compared and the significance of the association between visfatin MoM and uterine artery PI MoM, birth weight percentile and gestation at delivery was determined. In the PE group, compared with controls, there was a significantly higher median visfatin MoM (1.35, interquartile range (IQR): 0.69-2.16 vs 1.00, IQR: 0.55-1.96, P=0.027) and uterine artery PI MoM (1.19, IQR: 0.95-1.44 vs 1.03, IQR: 0.83-1.22, P<0.0001). In the PE group, there was no significant association between serum visfatin MoM and uterine artery PI MoM (P=0.589), gestation at delivery (P=0.763) or birth weight percentile (P=0.646). Serum visfatin levels at 11-13 weeks are increased in women who develop PE by a mechanism unrelated to impaired placental perfusion.