Short-course antenatal zidovudine reduces both cervicovaginal human immunodeficiency virus type 1 RNA levels and risk of perinatal transmission. Bangkok Collaborative Perinatal HIV Transmission Study Group.
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Human immunodeficiency virus (HIV) levels in cervicovaginal lavage (CVL) and plasma samples were evaluated in relation to perinatal transmission in a randomized placebo-controlled trial of brief antenatal zidovudine treatment. Samples were collected at 38 weeks' gestation from 310 women and more frequently from a subset of 74 women. At 38 weeks, after a 2-week treatment period, CVL HIV-1 was quantifiable in 23% and 52% of samples in the zidovudine and placebo groups, respectively (P<.001). The perinatal transmission rate was 28.7% among women with quantifiable CVL HIV-1 and high plasma virus levels (>10,000 copies/mL) and 1% among women without quantifiable CVL HIV-1 and with low plasma virus levels (P<.001). A 1-log increase in plasma HIV-1 increased the transmission odds 1.8 and 6.1 times (95% confidence interval, 0.9-3.5 vs. 2.4-15.4) for women with and without quantifiable CVL HIV-1, respectively (P=.03). CVL HIV-1 is an independent risk factor for perinatal HIV-1 transmission. (+info)
Lack of human leukocyte antigen-G expression in extravillous trophoblasts is associated with pre-eclampsia.
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Pre-eclampsia, a common complication of first pregnancies, is thought to result from a poorly perfused placenta and may reflect an abnormal maternal immune reaction to the hemiallogenic fetus. Human leukocyte antigen (HLA)-G, a major histocompatibility tissue-specific antigen expressed in extravillous trophoblast cells (fetal-derived), may protect trophoblasts from maternal-fetal immune intolerance and allow these cells to invade the uterus. Through RNA in-situ hybridization analysis, we studied the expression pattern of HLA-G in normal placentae and placentae from pregnancies complicated by severe pre-eclampsia. In normal placenta we found HLA-G expression in the anchoring extravillous trophoblasts with an increasing gradient of expression in the more invasive cells. However, in nine out of 10 pre-eclamptic placentae HLA-G expression was absent or reduced. We conclude that HLA-G is normally expressed in invasive trophoblasts and HLA-G expression is defective in most pre-eclamptic placentae. We propose that trophoblasts lacking HLA-G are vulnerable to attack by the maternal immune system. These defective trophoblasts will be unable to invade the maternal spiral arteries effectively, thereby developing vessels which cannot adequately nourish the developing placenta. This poorly perfused placenta may initiate the systemic cascade of events associated with pre-eclampsia. (+info)
Is a third-trimester antibody screen in Rh+ women necessary?
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OBJECTIVE: To determine the need for routine third-trimester antibody screening in Rh+ women. STUDY DESIGN: An analytic case-control study. METHODS: We identified Rh+ pregnant women who had received prenatal care and retrospectively analyzed their laboratory data. Patients were grouped into those with a positive third-trimester antibody screen (cases) and those with a negative third-trimester screen (controls). Because entry into a group was decided by the investigators, it could not be randomized. We reviewed the maternal medical records for antibody identification and final pregnancy outcome. We also reviewed the neonatal medical records for evidence of direct Coombs-positive cord blood, anemia, need for transfusion or phototherapy, other medical complications, and death. RESULTS: Using a computerized laboratory database from 2 teaching hospitals, we identified 10,581 obstetric patients who underwent routine first- and third-trimester antibody screening between 1988 and 1997. Of these, 1233 patients were Rh- and 9348 were Rh+. Among the Rh+ patients, 178 (1.9%) had 1 or more atypical antibodies at the first-trimester screen, and 53 (0.6%) had a positive third-trimester antibody screen despite a negative first-trimester screen. Although 6 of these 53 patients (0.06% of the study population) had clinically relevant antibodies for hemolytic disease of the new-born, no significant neonatal sequelae occurred among these 6 patients. CONCLUSION: Based on the patient and hospital records studied, a repeat third-trimester antibody screen for Rh+ patients is clinically and economically unjustified. Eliminating this laboratory test from clinical practice will not adversely affect pregnancy outcomes and will decrease the costs of prenatal care. (+info)
Plasma acid-base regulation above and below ventilatory threshold in late gestation.
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Stewart's physicochemical approach was used to study the effects of pregnancy on acid-base regulation in arterialized blood. Responses of 15 healthy pregnant women (PG; gestational age, 37.1 +/- 0.2 wk) were compared with those of 15 nonpregnant controls (CG) at rest and during cycling at 70 and 110% of the ventilatory threshold (T(vent)). Hydrogen ion concentration ([H(+)]) was lower in the PG vs. CG at rest and during exercise (P < 0.05 at rest and 70% T(vent)). Exercise-induced changes in [H(+)] were similar between groups. Lower resting [H(+)] values in the PG vs. CG resulted from lower values for arterialized PCO(2) (Pa(CO(2))) and total weak acid ([A](tot)), which were partly offset by a lower strong-ion difference ([SID]). Reductions in [A](tot) and [SID] at rest were primarily the result of reductions in albumin [Alb] and sodium [Na(+)], respectively. In the transition from rest to 70% T(vent), small increases in Pa(CO(2)) and [A](tot) contributed to moderate increases in [H(+)] in both groups, however [SID] increased in the PG and decreased in the CG (P < 0.05 between groups). In the transition from rest to 110% T(vent), decreases in [SID] made a significantly greater contribution to changes in [H(+)] in the CG vs. PG. Exercise-induced increases in [H(+)] are similar in the pregnant vs. nonpregnant state, but there is a reduced contribution of [SID] both above and below T(vent) during pregnancy. (+info)
Effect of vitamin A status at the end of term pregnancy on the saturation of retinol binding protein with retinol.
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BACKGROUND: Vitamin A (retinol), which is required for normal fetal development and successful gestation, circulates in the blood bound to a specific protein, the retinol binding protein (RBP). Little is known about the transport and metabolism of this complex protein or about retinol status during normal human pregnancy. OBJECTIVE: The aim of this study was to assess retinol status and transport modalities of retinol in well-nourished women with normal pregnancies, a population poorly investigated compared with pathologic and malnourished pregnant women. DESIGN: The maternal blood and cord blood concentrations of retinol, vitamin E, beta-carotene, RBP, and transthyretin of pregnant French women at term (n = 27) were measured and compared with values from a nonpregnant control group (n = 27). In addition, holo-RBP (retinol bound), apo-RBP (retinol free), and total protein were assessed in both groups to enable the hemodilution occurring during pregnancy to be taken into consideration and to evaluate the extent of saturation of RBP with retinol. RESULTS: Healthy pregnant women at term had normal serum circulatory amounts of retinol, vitamin E, binding proteins, and beta-carotene. However, they had less binding of retinol to RBP (holo-RBP: 49.9% in pregnant women, 54.0% in cord blood, and 77.5% in the control group). CONCLUSION: The results of this study suggest that retinol homeostasis and transport are modified during normal human pregnancy. (+info)
Maternal drug abuse and human term placental xenobiotic and steroid metabolizing enzymes in vitro.
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We evaluated the impact of maternal drug abuse at term on human placental cytochrome P450 (CYP)-mediated (Phase I) xenobiotic and steroid-metabolizing activities [aromatase, 7-ethoxyresorufin O-deethylase (EROD), 7-ethoxycoumarin O-deethylase (ECOD), pyrene 1-hydroxylase (P1OH), and testosterone hydroxylase], and androstenedione-forming isomerase, NADPH quinone oxidoreductase (Phase II), UDP-glucuronosyltransferase (UGT), and glutathione S-transferase (GST) activities in vitro. Overall, the formation of androstenedione, P1OH, and testosterone hydroxylase was statistically significant between control and drug-abusing subjects; we observed no significant differences in any other of the phase I and II activities. In placentas from drug-abusing mothers, we found significant correlations between ECOD and P1OH activities (p < 0. 001), but not between ECOD and aromatase or P1OH and EROD activities; we also found significant correlations between blood cotinine and UGT activities (p < 0.01). In contrast, in controls (mothers who did not abuse drugs but did smoke cigarettes), the P1OH activity correlated with ECOD, EROD (p < 0.001), and testosterone hydroxylase (p < 0.001) activities. Our results (wider variation in ECOD activity among tissue from drug-abusing mothers and the significant correlation between P1OH and ECOD activities, but not with aromatase or EROD activities) indicate that maternal drug abuse results in an additive effect in enhancing placental xenobiotic metabolizing enzymes when the mother also smokes cigarettes; this may be due to enhancing a "silent" CYP form, or a new placental CYP form may be activated. The change in the steroid metabolism profile in vitro suggests that maternal drug abuse may alter normal hormonal homeostasis during pregnancy. (+info)
Antenatal visualization of vascular anastomoses in monochorionic twins using color Doppler sonography: the protective function of these anastomoses and the phenomenon of interference beating.
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This report concerns the antenatal visualization and velocimetry of an arterioarterial and a venovenous anastomosis in a monochorionic twin pregnancy using color Doppler sonography. The phenomenon of 'interference beating' occurs when two flow velocity waveforms are superimposed in one blood vessel. This characteristic image can be generated antenatally to confirm the existence of a vascular communication. We were able to reveal these anastomoses postnatally using the dye injection technique. (+info)
Circulating hematopoietic progenitor cells in first trimester fetal blood.
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The yolk sac and aorto-gonad-mesonephros region are well recognized as the principal sites of hematopoiesis in the developing embryo, and the liver is the principal site of hematopoiesis in the fetus. However, little is known about circulating hematopoietic stem and progenitor cells in early fetal life. We investigated the number and characteristics of circulating progenitors in first trimester blood of 64 human fetuses (median gestational age, 10(+4) weeks; range, 7(+6)-13(+6) weeks). CD34+ cells accounted for 5.1 +/- 1.0% of CD45+ cells in first trimester blood, which is significantly more than in term cord blood (0.4 +/- 0.03%; P =.0015). However, the concentration of CD34+ cells (6.6 +/- 2.4 x 10(4)/mL) was similar to that in term cord blood (5.6 +/- 3.9 x 10(4)/mL). The total number of progenitors cultured from unsorted mononuclear cells (MNCs) in first trimester blood was 19.2 +/- 2.1 x 10(3)/mL, which is similar to that in term cord blood (26.4 +/- 5.6 x 10(3)/mL). All lineages were seen: colony-forming unit-GEMM (CFU-GEMM), CFU-GM, BFU-e, BFU-MK, and CFU-MK. Clonogenic assays of CD34+ cells purified from first trimester samples produced mainly two lineages: BFU-e (39.0 +/- 9.6 x 10(3)/mL CD34+ cells) and CFU-GEMM (22.6 +/- 4.7 x 10(3)/mL CD34+ cells). Short-term liquid culture of first trimester blood MNCs in SCF + IL-3 + Flt-3 (stem cell factor + interleukin-3 + Flt-3) increased, by 7-fold, the numbers of CFU-GEMM and induced a dramatic increase in BFU-e (65.6 +/- 12.1-fold). These data show that significant numbers of committed and multipotent progenitors with capacity for expansion circulate in first trimester fetal blood and can be CD34 selected. These cells should be suitable targets for gene transfer and stem cell transplantation and, because fetal hematopoietic progenitors have been demonstrated in the maternal circulation from early gestation, may also be manipulated for noninvasive prenatal diagnosis of major genetic disorders. (Blood. 2000;95:1967-1972) (+info)