Newborn Red Cells Research Articles

Rare combination of alloantibodies causing hemolytic disease of the newborn – Challenge for identification

Abstract Hemolytic disease of the newborn (HDN) refers to the destruction of the fetal and newborn red cells by maternal red cell antibodies specific for paternally inherited antigens on fetal red cells or erythroid precursors.[1] ABO-incompatibility is the most common cause of HDN. Rh-negative mothers can be alloimmunized with Rh-positive fetus. Prophylactic Rh immunoglobulin use has greatly reduced the HDN due to Rh incompatibility. Alloimmunization can also occur due to other clinically significant minor blood group antigens such as E, c, C, k, KP(a), Js(a), Js(b), Jk(a), Jk(b), Fy(a), Fy(b), S, s, and U. Multiple alloantibodies in mothers’ blood can pose a difficult challenge for identification and finding compatible blood for exchange transfusion. We report a case of HDN due to multiple antibodies and a rare combination of anti-c and anti-Jkb, challenges associated with the identification, confirmation, and finding of compatible blood units.

Fetal Cytokine Balance, Erythropoietin and Thalassemia but Not Placental Malaria Contribute to Fetal Anemia Risk in Tanzania.

Fetal anemia is common in malaria-endemic areas and a risk factor for anemia as well as mortality during infancy. Placental malaria (PM) and red cell abnormalities have been proposed as possible etiologies, but the relationship between PM and fetal anemia has varied in earlier studies, and the role of red cell abnormalities has not been studied in malaria-endemic areas. In a Tanzanian birth cohort study designed to elucidate the pathogenesis of severe malaria in young infants, we performed a cross-sectional analysis of risk factors for fetal anemia. We determined PM status, newborn red cell abnormalities, and maternal and cord blood levels of iron regulatory proteins, erythropoietin (EPO), cytokines and cytokine receptors. We examined the relationship between these factors and fetal anemia. Fetal anemia was present in 46.2% of the neonates but was not related to PM. Maternal iron deficiency was common (81.6%), most frequent in multigravidae, and interacted with parity to modify risk of fetal anemia, but it was not directly related to risk. Among offspring of iron-deficient women, the odds of fetal anemia increased with fetal α+-thalassemia, as well as these patterns of cord blood cytokines: increased cord IL-6, decreased TNF-RI, and decreased sTfR. The EPO response to fetal anemia was low or absent and EPO levels were significantly decreased in newborns with the most severe anemia. This study from an area of high malaria transmission provides evidence that 1) fetal α+-thalassemia and cytokine balance, but not PM at delivery, are related to fetal anemia; 2) maternal iron deficiency increases the risk that other factors may cause fetal anemia; and 3) fetal anemia has a multifactorial etiology that may require a variety of interventions, although measures that reduce maternal iron deficiency may be generally beneficial.

Anti-Holley detected in a primary immune response

Abstract Anti-Holley (Hy) has been reported as an IgG antibody occurring in previously transfused or multiparous black patients. In this case anti- Hy was identified in a 16-year-old black, primigravida female admitted at 32 weeks gestation because of premature rupture of the membranes. On admission, her blood type was determined to be A2B, D-positive and an antibody screen was negative. A second antibody screen, performed 4 days later, was positive in all three cells. Anti-Hy was subsequently identified. The antibody was reactive at room temperature, 37°C, and in the antiglobulin phase. IgG and IgM components of anti-Hy were demonstrated in the maternal serum, documenting a primary immune response. This resulted in serologic findings not previously described for anti-Hy. A direct antiglobulin test on the newborn red cells was negative and there was no clinical evidence of hemolytic disease of the newborn (HDN). A monocyte monolayer assay performed with maternal serum yielded negative results. Recent scientific information has resulted in the placement of Hy in the Dombrock blood group system. Alloantibodies to Dombrock system antigens have not been associated with severe HDN. Immunohematology 1996;12:62–65.

Storage-induced changes in human newborn red cells.

Fetal red cells are well suited for intrauterine life; however, little is known about their response to postnatal environments. The purpose of this work was to investigate the metabolic and membrane changes affecting newborn red cells during their exposure to storage in citrate-phosphate-dextrose (CPD) and citrate-phosphate-dextrose-adenine (CPDA-1). The findings suggest that newborn red cells are affected more by storage than are adult cells. These accelerated storage changes in the red cells of newborns may be related indirectly to the rapid adenosine triphosphate (ATP) decline. As is the case with adult red cells, fetal cells withstand storage in CPDA-1 better than in CPD. The storage lesion in these cells was partly reversible, as in adult cells, by incubation with adenosine. It was therefore concluded that newborn red cells obtained from placentas and stored for several weeks in CPD or CPDA-1 media or other media that improve the metabolic profile of these cells may be acceptable for transfusion.

Li Cold Agglutinin: A Further Antibody Recognizing Sialic Acid-Dependent Antigens Fully Expressed on Newborn Erythrocytes

The cold agglutinin anti-Li recognizes a sialic acid-dependent antigen fully expressed only on newborn red cells. Although it resembles anti-i in all aspects except for its nonreactivity with neuraminidase-treated red cells, it is entirely different from anti-i, since sialic acid is not involved in i antigenic determinants.

Red cells of newborn rats have low bisphosphoglyceromutase and high pyruvate kinase activities in association with low 2,3-bisphosphoglycerate

2,3-Bisphosphoglycerate is a physiologically important regulator of red cell oxygen affinity during mammalian development. The rat has no fetal hemoglobin, but the newborn red cell has low 2,3-bisphosphoglycerate and high ATP concentrations, and high oxygen affinity. This report shows that red cell bisphosphoglyceromutase activity increases from near zero in the newborn rat to very high levels by four weeks of age. This increase roughly parallels the increase in red cell 2,3-bisphosphoglycerate concentration. Red cell pyruvate kinase activity declines ten-fold from birth to four weeks of age. This decrease is associated with a changeover in red cell populations from larger to smaller cells. The glycolytic rate is at least 50% higher in newborn than adult rat red cells. The data suggest that high pyruvate kinase activity and glycolytic rate contribute to the high ATP concentration in newborn rat red cells, but that their low 2,3-bisphosphoglycerate concentration is due primarily to low bisphosphoglyceromutase activity.