Browsing by Author "Lockwood, Charles J. (7102516684)"

There is little information available concerning the ontologic development of the human hypothalamic-pituitary-adrenal (HPA) axis nor of the potential interactions among fetal, maternal and placental-derived HPA axis hormones. This study evaluated levels of these hormones in matched maternal and fetal pairs during the second half of uncomplicated pregnancies. Immunoassays were used to measure serum concentrations of corticotropin-releasing hormone (CRH), adrenocorticotropin (ACTH) and cortisol in 104 matched fetal and maternal blood samples. Fetal specimens were obtained by percutaneous umbilical blood sampling (PUBS) between 18 and 40 weeks in patients whose pregnancies resulted in healthy, term infants. Correlations among these hormones, and the effect of gestational age were assessed. Maternal CRH concentrations [median (range)l [1.10 ng/ml (0.15 to 23.69)] were significantly greater than fetal values [0.35 ng/ml (0.07 to 1.0)]. Levels of maternal CRH (r = 0.73; p < 0.001) but not fetal CRH (r = 0.01; p = 0.98) correlated with gestational age. Maternal ACTH decreased (r = -0.21; p = 0.04) while fetal ACTH increased (r = 0.35; p < 0.003) with gestational age. Both maternal (r = 0.45; p < 0.001) and fetal (r = 0.57; p < 0.001) cortisol levels increased with gestational age. Maternal serum CRH values correlated best with fetal cortisol (r = 0.40; p = 0.0002) and correlated modestly with maternal cortisol (r = 0.28; p = 0.01), fetal ACTH (r = 0.24; p = 0.03) and fetal CRH (r = 0.23; p = 0.04); but not with maternal ACTH (r = -0.12; p = 0.3). Maternal CRH concentrations increase in the third trimester and correlate with rising fetal cortisol levels.

Objective: To measure fetal and maternal plasma homocysteine (Hcy) concentrations in uncomplicated pregnancies. Methods: Paired maternal venous and fetal umbilical cord blood (n = 81) samples were evaluated for plasma Hcy and vitamin B12 levels, in addition to eight neonatal umbilical cord blood samples obtained immediately following delivery. Results: Both fetal and maternal Hcy concentrations were positively correlated with advancing gestational age (ρ = 0.44, p < 0.0001; and ρ = 0.27, p < 0.05, respectively). Fetal plasma Hcy concentrations [2.2 μmol/l (IQR: 2.0-3.2)] were significantly lower than both neonatal umbilical vein [5.0 μmol/l (IQR: 4.4-6.5); p < 0.001] and maternal plasma Hcy levels [4.4 μmo/l (IQR: 3.4-5.4); p < 0.001]. In addition, Hcy values at term were higher in the umbilical vein compared with the umbilical artery [5.0 μmol/l (IQR: 3.4-5.4) versus 4.2 μmol/l (IQR: 3.7-5.5), respectively; p = 0.016]. Significant correlation was noted and between fetal and maternal Hcy levels (ρ = 0.50, p < 0.0001), while fetal Hcy was negatively correlated with maternal B12 concentrations (ρ = -0.32, p < 0.001). Conclusions: Fetal Hcy levels were significantly lower than maternal and neonatal levels and correlated with gestational age across the second half of pregnancy. © 2014 Informa UK Ltd. All rights reserved.

Apolipoprotein B is elevated in growth-retarded compared with normally grown fetuses, demonstrating a link between low birth weight and risk of subsequent atherosclerosis. Increased apolipoprotein B levels and an elevated apolipoprotein B to A-I ratio are predictors of atherogenesis. Elevated apolipoprotein B levels in young adults have been linked to atherosclerosis in later life, whereas impaired fetal growth has been linked to higher than normal apolipoprotein B levels in adulthood. We conducted this research to test the hypothesis that circulating apolipoprotein A-I and B concentrations differ in growth-retarded compared with normal fetuses. Fetal umbilical plasma samples were obtained at diagnostic cordocenteses in 18 growth-retarded and 23 normally grown fetuses. Levels of apolipoprotein A-I and B were measured by turbidimetric assay. There were no differences in median (range) plasma apolipoprotein A-I concentrations between growth-retarded and normal fetuses [0.61 (0.30-1.42) vs. 0.60 (0.30-1.63) g/L, respectively; P = 0.94]. In contrast, we found significantly higher plasma apolipoprotein B levels in growthretarded vs. normal fetuses [0.62 (0.37-1.84) vs. 0.40 (0.16-1.47) g/L, respectively; P < 0.001]. Moreover, the ratio of apolipoprotein B to A-I was significantly higher in growth-retarded than in normal fetuses [1.00 (0.38-2.42) vs. 0.53 (0.31-1.80); P = 0.005]. Levels of apolipoprotein B are elevated in growth-retarded fetuses, suggesting a linkage between low birth weight and adult-onset atherosclerosis.

Apolipoprotein B is elevated in growth-retarded compared with normally grown fetuses, demonstrating a link between low birth weight and risk of subsequent atherosclerosis. Increased apolipoprotein B levels and an elevated apolipoprotein B to A-I ratio are predictors of atherogenesis. Elevated apolipoprotein B levels in young adults have been linked to atherosclerosis in later life, whereas impaired fetal growth has been linked to higher than normal apolipoprotein B levels in adulthood. We conducted this research to test the hypothesis that circulating apolipoprotein A-I and B concentrations differ in growth-retarded compared with normal fetuses. Fetal umbilical plasma samples were obtained at diagnostic cordocenteses in 18 growth-retarded and 23 normally grown fetuses. Levels of apolipoprotein A-I and B were measured by turbidimetric assay. There were no differences in median (range) plasma apolipoprotein A-I concentrations between growth-retarded and normal fetuses [0.61 (0.30-1.42) vs. 0.60 (0.30-1.63) g/L, respectively; P = 0.94]. In contrast, we found significantly higher plasma apolipoprotein B levels in growthretarded vs. normal fetuses [0.62 (0.37-1.84) vs. 0.40 (0.16-1.47) g/L, respectively; P < 0.001]. Moreover, the ratio of apolipoprotein B to A-I was significantly higher in growth-retarded than in normal fetuses [1.00 (0.38-2.42) vs. 0.53 (0.31-1.80); P = 0.005]. Levels of apolipoprotein B are elevated in growth-retarded fetuses, suggesting a linkage between low birth weight and adult-onset atherosclerosis.

[No abstract available]

Objective: To determine if intrauterine intravascular fetal transfusion affects fetal umbilical venous endothelin levels. Methods: Endothelin concentrations were measured by radioimmunoassay in fetal umbilical venous blood obtained immediately before and after 36 fetal transfusions performed for Rh alloimmune hemolytic anemia. Umbilical venous pressures also were recorded before and after transfusion. Results: The mean (± standard deviation [SD]) gestational age at transfusion was 27.0 ± 4.6 weeks, whereas the initial and post-transfusion hematocrits were 23.3 ± 8.5% and 41.8 ± 6.3%, respectively. Post-transfusion endothelin levels correlated significantly with the volume of transfused blood (r = .41; P = .03) and with post-transfusion increases in umbilical vein pressure (r = .86; P < .001). Among fetuses undergoing initial transfusion, there were significant differences between mean (± SD) pre- and post-transfusion endothelin levels [3.6 (± 2.2) pg/mL versus 6.3 (± 4.0) pg/mL, respectively; P = .02]. In contrast, among fetuses undergoing a repeat fetal transfusion, no differences in mean (± SD) pre-versus post-transfusion endothelin levels were observed [3.8 (± 1.8) pg/mL versus 2.2 (± 1.77) pg/mL, respectively; P = .3)]. Step- wise multiple regression analysis identified order of transfusion as a significant predictor of change in endothelin levels from pre- to post- transfusion measurements (adjusted r2 = .26; P = .003). Conclusion: Rapid expansion of fetal intravascular volume by intravenous transfusion of packed red blood cells with a high hematocrit enhances fetal endothelin levels in those fetuses undergoing initial but not subsequent transfusions.