Fetal Cord Plasma Research Articles

Fetal cord plasma herpesviruses and preeclampsia: an observational cohort study

A previous study suggested that fetal inheritance of chromosomally integrated human herpesvirus 6 (ici-HHV6) is associated with the hypertensive pregnancy disorder preeclampsia (PE). We aimed to study this question utilizing cord plasma samples (n = 1276) of the Finnish Genetics of Preeclampsia Consortium (FINNPEC) cohort: 539 from a pregnancy with PE and 737 without. We studied these samples and 30 placentas from PE pregnancies by a multiplex qPCR for the DNAs of all nine human herpesviruses. To assess the population prevalence of iciHHV-6, we studied whole-genome sequencing data from blood-derived DNA of 3421 biobank subjects. Any herpes viral DNA was detected in only two (0.37%) PE and one (0.14%) control sample (OR 2.74, 95% CI 0.25–30.4). One PE sample contained iciHHV-6B and another HHV-7 DNA. The control’s DNA was of iciHHV-6B; the fetus having growth restriction and preterm birth without PE diagnosis. Placentas showed no herpesviruses. In the biobank data, 3 of 3421 subjects (0.08%) had low level HHV-6B but no iciHHV-6. While iciHHV-6 proved extremely rare, both fetuses with iciHHV-6B were growth-restricted, preterm, and from a pregnancy with maternal hypertension. Our findings suggest that human herpesviruses are not a significant cause of PE, whereas iciHHV-6 may pose some fetal risk.

Women with gestational diabetes mellitus, controlled for plasma glucose level, exhibit maternal and fetal dyslipidaemia that may warrant treatment

AimsTo compare maternal and fetal cord plasma and lipoprotein triglyceride (TG) concentrations in women with Gestational Diabetes Mellitus (GDM), with hyperglycaemia and hypertriglyceridaemia, and healthy women. MethodsFasted maternal blood at 28.6 ± 3.4 (T1) and 36.2 ± 1.0 (T2) [mean ± S.D] weeks of gestation, and cord blood were collected. Plasma lipoprotein fractions underwent compositional analysis. ResultsPlasma glucose did not differ between GDM and healthy women. T1 maternal plasma TG (2.60 ± 0.89 mmol/l versus 1.71 ± 0.69 mmol/l) and plasma apolipoprotein B (1.30 ± 0.48 g/l versus 0.75 ± 0.40 g/l) were higher in GDM compared to healthy. Maternal plasma TG increased over gestation in both groups. T1 plasma VLDL total protein (38 ± 15 mg/dl versus 25 ± 11 mg/dl), total cholesterol (TC) (30 ± 14 mg/dl versus 16 ± 13 mg/dl) and phospholipid (PL) (43 ± 17 mg/dl versus 26 ± 16 mg/dl) were higher in GDM than healthy, and similarly for IDL, suggesting increased lipoprotein particle number. T1 VLDL-TG enrichment was higher in healthy and increased over gestation in GDM women but decreased in healthy. IDL-TG enrichment (TG/TC) increased over gestation in women with GDM and decreased in healthy. Cord blood VLDL, IDL and LDL from GDM had a two-fold higher TG enrichment than healthy pregnancy. ConclusionIncreased maternal lipoprotein number, but not TG enrichment, in GDM mothers may explain TG enrichment of cord lipoproteins.

464: The kinetics of matrix metalloproteinase-9 inhibition by magnesium sulfate in fetal cord plasma

464: The kinetics of matrix metalloproteinase-9 inhibition by magnesium sulfate in fetal cord plasma

The effect of magnesium sulfate on the activity of matrix metalloproteinase-9 in fetal cord plasma and human umbilical vein endothelial cells

Clinical evidence suggests that magnesium sulfate may reduce the risk of fetal neurologic injury in preterm delivery. Matrix metalloproteinase-9 (MMP-9) levels are elevated in preterm labor patients. There is evidence that MMP-9 may break down the blood-brain barrier in humans, causing cytokine mediated cell injury. Our objective was to determine whether the addition of magnesium sulfate attenuates activity of MMP-9, a complex zinc-dependent enzyme, in fetal cord plasma. We collected cord plasma in 6 term, unlabored patients. Using enzyme-linked immunosorbent assay, we measured the activity of MMP-9 with varying concentrations of magnesium sulfate added in vitro. Results were verified using a human umbilical cord vein endothelial cell (HUVEC) line. Addition of physiologic doses of magnesium sulfate (0.07 mg/mL) resulted in a 25% decrease in active MMP-9 (P = .03). In a HUVEC line, magnesium sulfate resulted in a 32% decrease in MMP-9 activity (P = .00012). The addition of magnesium sulfate attenuated MMP-9 activity in cord plasma and in a HUVEC line.

450: The effect of magnesium sulfate on activity of matrix metalloproteinase -9 in fetal cord plasma and human umbilical cord vein endothelial cells

Clinical epidiomologic evidence suggests that magnesium sulfate used for preterm labor may ameliorate the risks of fetal neurologic injury. The biologic plausibility of this is poorly understood. Matrix metalloproteinases are complex zinc dependent enzymes. Matrix metalloproteinase -9 (MMP9) levels are elevated in preterm labor patients and in patients with preterm amniorrhexis. There is evidence that MMP9 may break down the blood brain barrier in humans, leading to a cytokine mediated cell injury.

Fetal cord plasma lipoprotein status in uncomplicated human pregnancies and in pregnancies complicated by pre-eclampsia and intrauterine growth restriction

Maternal lipids have been studied extensively in pre-eclampsia (PE) and intrauterine growth restriction (IUGR) but little is known about fetal lipids. We hypothesised that the maternal lipid perturbations in PE and IUGR pregnancies would result in similar alterations in the fetal lipid profile. We performed a cross-sectional case control study of maternal and fetal (delivery venous cord blood) lipid and lipoprotein concentrations in third trimester uncomplicated pregnancies ( n = 81) and in pregnancies complicated by PE ( n = 23) or IUGR ( n = 17). In uncomplicated pregnancies, fetal log total cholesterol (TC), log triglyceride (TG) and high-density lipoprotein cholesterol (HDL-C) levels were significantly affected by mode of delivery. Fetal log TC ( r = 0.37, P = 0.02), log TG ( r = 0.34, P = 0.04) and TC/HDL-C ratio ( r = 0.31, P = 0.05) were positively correlated with placental weight. Maternal TC ( r = 0.35, P = 0.03) and LDL levels ( r = 0.36, P = 0.02) were associated with fetal HDL-C levels. Maternal TC was significantly elevated in PE [mean 6.75 (standard deviation 1.14) mmol/L] compared to BMI-matched controls [5.94 (0.89) mmol/L P = 0.04]. In PE, fetal log TC [mean 0.36 (0.23) versus 0.11 (0.15) log mmol/L, P = 0.03], fetal log TG [−0.21 (0.32) versus −0.49 (0.26) log mmol/L, P = 0.02] and fetal TC/HDL-C ratio [3.64 (1.62) versus 1.80 (0.86), P = 0.001] were higher than in controls, after adjustment for mode of delivery. In IUGR, fetal log TG [−0.17 (0.35) versus −0.57 (0.10) log mmol/L, P = 0.01] was higher than controls, after adjustment for mode of delivery. There were no correlations between maternal and fetal lipid levels, or between fetal birth weight and either maternal or fetal lipids in the PE or IUGR groups. We conclude that although fetal lipids do not show a direct correlation with maternal lipids in PE or IUGR, these complications of pregnancy significantly impact upon fetal lipid levels possibly due to increased fetal stress or compromised placental lipid transport. Our findings are potentially pertinent to understanding the future cardiovascular health of the offspring.

Variations in plasma selenium levels as a result of the menstrual cycle and pregnancy in healthy Japanese women.

Plasma levels of selenium (Se) were determined consecutively during a menstrual cycle of six women in three phases (i.e., menses, follicular, and luteal). To detect possible differences in relation to normal pregnancy, plasma levels of Se were also determined in paired samples of maternal and umbilical cord blood from 12 pregnant women. No periodic changes in the plasma Se levels were observed during the menstrual cycle. The intraindividual variation, estimated by coefficients of variation, ranged from 1.9% to 9.9% among the menstrual phases of the subjects. The plasma Se level during pregnancy did not differ significantly from those of nonpregnant women, and those in the second trimester and at delivery were at similar levels (1.58+/-.14 and 1.48+/-.20 mmol/L, respectively). Compared to the levels of maternal Se at delivery, the fetal cord plasma at birth had a significant lower Se level (1.23+/-.34 mmol/L, p<.05).

Fluoride concentration in amniotic fluid and fetal cord and maternal plasma

Fluoride concentrations were determined in plasma of 50 pregnant women, 44 samples of amniotic fluid and fetal cord blood of 29 fetuses at various stages of normal pregnancies, from an area with a relatively low water fluoride (< 0.5 ppm) content. The mean concentrations of fluoride from maternal plasma, cord plasma and amniotic fluid (± S.D.) were 0.033 ± 0.003, 0.028 ± 0.005 and 0.017 ± 0.003 ppm, respectively. Maternal and fetal plasma fluoride concentrations did not differ significantly. In the older age group fetal cord plasma fluoride concentration was significantly lower than maternal plasma levels (0.012 ± 0.08 ppm vs. 0.023 ± 0.001, respectively; p < 0.05). Amniotic fluid fluoride levels were significantly higher at term than in midtrimester pregnancy, 0.017 ± 0.0018 vs. 0.010 ± 0.009 ppm ( P < 0.05), respectively. This higher concentration may imply higher fetal urinary excretion of fluoride at term due to the lower sequestration of fluoride as the process of bone calcification is more complete.

Differences in the carbohydrate moieties of plasma and amniotic fluid fibronectins as revealed by crossed immunoaffinity electrophoresis with concanavalin A.

Human fibronectins isolated from pooled human plasma and amniotic fluid were studied as to differences in their carbohydrate moieties. The chemical analyses showed that amniotic fluid fibronectin is different from adult plasma fibronectin in carbohydrate content and composition while there seems to be no significant differences in amino acid composition. Crossed immunoaffinity electrophoresis with free concanavalin A, as well as rocket immunoelectrophoresis with immobilized concanavalin A intermediate gel, indicated that amniotic fluid fibronectin has little or no reactivity with this lectin while adult plasma fibronectin is strongly reactive. Fetal cord plasma fibronectin apparently interacted with concanavalin A, but its reactivity was weaker than that of adult plasma fibronectin. Fibronectin isolated from ascitic fluid of an ovarian cancer patient which was examined in additional experiments showed much weaker Con A-reactivity than fetal cord plasma fibronectin. These results suggest that fibronectins from various body fluids differ in their carbohydrate structures.

ZINC STATUS OF PREGNANT ALCOHOLIC WOMEN: A DETERMINANT OF FETAL OUTCOME

The zinc status of 25 alcoholic and 25 non-alcoholic pregnant women was measured and correlated with fetal outcome. The volume index of alcohol consumption and the Michigan Alcoholic Screening Test were used to define alcoholic women. The alcoholic women had significantly lower plasma-zinc levels than the non-alcoholic women (50·7 versus 72·2 μg/dl). Fetal cordplasma zinc levels were also lower in the offspring of alcoholic women (65·5 versus 81·3 μg/dl). Manifestation of fetal dysmorphogenesis appears to relate to zinc status.

Comparison of mercury levels in maternal blood, fetal cord blood, and placental tissues

Previous studies have reported that mercury accumulates in cord blood during pregnancy. This study was carried out to determine where in cord blood the mercury accumulates, i.e., in cord erythrocytes, in cord plasma, or in both, and to determine whether the predominant form of mercury which accumulates is methyl or inorganic mercury. From our data it is clear that methyl mercury accumulates in cord erythrocytes: A total of 30% more methyl mercury was found in fetal erythrocytes than in maternal erythrocytes. Also correlation analysis of the methyl mercury levels in maternal and fetal erythrocytes showed a strong correlation (r = 0.87). In regard to inorganic mercury, the highest concentration was found in the placenta, suggesting a barrier role, but a significant correlation (r = 0.62) was also found between the maternal and fetal plasma levels of inorganic mercury. Moreover, the inorganic mercury concentration per gram of plasma was higher in fetal cord plasma than in maternal plasma. Overall, the relative levels of methyl and inorganic mercury reported here varied considerably in maternal and fetal erythrocytes, plasma, and in the placenta, but all of the levels were low (<6 ng Hg/gm of tissue) and in agreement with “total” mercury levels reported by others.