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At least 325 records · Page 18Linked to original sources
PubMed1999

Amniotic fluid nitric oxide metabolites, cyclic guanosine 3',5' monophosphate and dimethylarginine in alloimmunized pregnancies.

OBJECTIVE: To determine the relationship between gestational age or the Liley index (the severity of fetal hemolysis) and the amniotic fluid total nitrite (NOx), cyclic guanosine 3',5 'monophosphate (cGMP) and dimethylarginine (DMA) concentrations. We hypothesized that the concentrations of these components change because of fetal growth or adaptation to fetal anemia. STUDY DESIGN: Amniotic fluids (n=64) were obtained between 23 and 37 weeks from fifty-three patients at risk for alloimmunization. Amniotic fluids from the pregnancies with a Liley index=1 were considered as controls (n=17). Creatinine (C, microMol) was determined with the Jaffé reagent, nitrite (NOx, microMol) with the Griess reagent, cGMP (nMol) by an enzyme immunoassay and DMA (microMol) after HPLC. Multiple regression analysis was used for separating the effects of growth and the estimated degree of anemia. RESULTS: The concentration of NOx, cGMP and DMA was not related to the Liley index or whether or not the fetuses needed blood transfusions. The concentrations of creatinine (C), NOx and cGMP increased during pregnancy (in weeks;W) (C=-69.2+6.28W; r2=0.532; P<0.0001, NOx=-17.6+1.29W; r2=0.106; P=0.01, cGMP=-20.9+1.05W; r2=0.414; P<0.0001). The DMA concentration (3.8+/-0.8(SD) and the NOx/creatinine ratio (181+/-110 mM/M) did not change with gestational age. The cGMP/creatinine ratios (microM/M) increased (cGMP/C=-41.8+4.31W; r2=0.134; P=0.007) whereas the DMA/creatinine ratio (mM/M) declined during pregnancy (DMA/C=73.1-1.34W; r2=0.278; P=0.0002). Consequently, the NOx/DMA and cGMP/DMA ratios increased (NOx/DMA=-6.96+0.43W; r2=0.105; P=0.02, cGMP/DMA=-5.9+0.29W; r2=0.391; P<0.0001). CONCLUSIONS: The concentrations in amniotic fluid of cGMP and NOX, but not of DMA increase during gestation. The cGMP/creatinine ratio increases also whereas that of DMA decreases. The changes in products of the NO-cGMP pathway are independent of mild to moderate fetal hemolysis and may result from fetal growth as well as from reduced inhibition of NO synthase by DMA. Gestational age related effects should be taken into account when analyzing nitric oxide metabolites in amniotic fluids.

Amniocentesis↗
PubMed2001

Basis of hematopoietic defects in platelet-derived growth factor (PDGF)-B and PDGF beta-receptor null mice.

Platelet-derived growth factor (PDGF)-B and PDGF beta-receptor (PDGFR beta) deficiency in mice is embryonic lethal and results in cardiovascular, renal, placental, and hematologic disorders. The hematologic disorders are described, and a correlation with hepatic hypocellularity is demonstrated. To explore possible causes, the colony-forming activity of fetal liver cells in vitro was assessed, and hematopoietic chimeras were demonstrated by the transplantation of mutant fetal liver cells into lethally irradiated recipients. It was found that mutant colony formation is equivalent to that of wild-type controls. Hematopoietic chimeras reconstituted with PDGF-B(-/-), PDGFR beta(-/-), or wild-type fetal liver cells show complete engraftment (greater than 98%) with donor granulocytes, monocytes, B cells, and T cells and display none of the cardiovascular or hematologic abnormalities seen in mutants. In mouse embryos, PDGF-B is expressed by vascular endothelial cells and megakaryocytes. After birth, expression is seen in macrophages and neurons. This study demonstrates that hematopoietic PDGF-B or PDGFR beta expression is not required for hematopoiesis or integrity of the cardiovascular system. It is argued that metabolic stress arising from mutant defects in the placenta, heart, or blood vessels may lead to impaired liver growth and decreased production of blood cells. The chimera models in this study will serve as valuable tools to test the role of PDGF in inflammatory and immune responses. (Blood. 2001;97:1990-1998)

Anemia↗
PubMed1999

Increased erythrocyte deformability in fetal erythropoiesis and in erythrocytes deficient in glucose-6-phosphate dehydrogenase and other glycolytic enzymes.

Erythrocyte deformability was determined in more than 500 clinical samples, and was found to be elevated in conditions in which fetal-like red cells are produced: aplastic anemia (3/3 cases), myelodysplastic syndromes, polycythemias, sickle cell anemia during treatment with hydroxyurea, paroxysmal nocturnal hemoglobinuria, and recovery from B12 deficiency. Elevated deformability was observed in neonatal erythrocytes, and during recovery from transient erythroblastopenia of childhood, when fetal-like red cells are known to be produced. Increased deformability appears to be a feature of fetal and fetal-like red cells. Forty-eight cases of enzymatically verified glucose-6-phosphate (G-6-PD) deficiency were also examined. Thirty out of 32 G-6-PD(A-) individuals, including both heterozygotes and hemizygotes, exhibited increased deformability during the steady state. In contrast, G-6-PD(Med) hemizygotes had normal deformability. Increased deformability was also found in G-6-PD(Huron) (n=3), G-6-PD(Wayne) (n=4), triose phosphate isomerase deficiency (n=2), and pyruvate kinase deficiency (n=2). An elevated osmoscan was found in more than 90% of female G-6-PD heterozygotes, affording a simple screening test for heterozygotes. Deformability remained high during hemolytic episodes, when older enzyme deficient cells are removed from the circulation. In four cases of G-6-PD deficiency with normal deformability, evidence for co-existing hereditary spherocytosis was found. The combination of conditions with opposing effects on deformability resulted in nearly normal deformability. Because increased red cell deformability is a feature of fetal erythrocytes, these results suggest that the red cells in many cases of glycolytic enzyme deficiency are fetal-like.

Anemia, Sickle Cell↗
PubMed1989

Fetal growth and fetal glucose and C-peptide levels in relation to the degree of anemia in fetuses affected by rhesus iso-immunization.

Fetal growth rate was determined by measuring the fetal biparietal diameter at 63 two-week time points during the second trimester in 14 patients with severe Rhesus isoimmunization. Growth rate was found to be related to the fetal hemoglobin concentration which was determined at the end of each 2-week period. Fetuses with a hemoglobin concentration of less than 30% of the normal value had a significantly decreased growth rate (p less than 0.01). These fetuses had also reduced C-peptide (p less than 0.05) and increased glucose levels (p less than 0.1) compared with less anemic fetuses. The physiological background to impaired fetal growth in cases of severe fetal anamia at Rhesus iso-immunization is discussed.

Anemia↗
PubMed2001

Outcome of infants receiving in-utero transfusions for haemolytic disease.

AIMS: To review the outcome of infants who received in-utero transfusion (IUT) at National Women's Hospital (NWH). Specifically to determine postnatal exchange and top-up transfusion requirements, to examine perinatal factors useful for predicting this and review neurodevelopmental status of recipients. METHODS: A review was undertaken of infants delivered at NWH between 1991 and 2000, who had received one or more IUT for haemolytc disease. The mean gestational age at birth was 34 weeks and birth weight 2298 g. The median number of IUT was four (range 1-9). The mean gestational age at the first IUT was 25 weeks and at last IUT was 31 weeks. RESULTS: All 37 infants survived to discharge. Postnatal exchange transfusion was required in ten and top up transfusion in 27 infants. Late transfusion (>3 weeks) was required in 21 infants. Follow-up information on 36 infants revealed one born prematurely following death of a co-twin had cerebral palsy and developmental delay. No other infant had audiology or neurodevelopmental abnormality. CONCLUSIONS: This review helps to confirm the good outcome following IUT although some infants continue to require transfusions for up to four months after birth.

Birth Weight↗