Advertisement

Kernicterus pp 43-50 | Cite as

Erythroblastosis Fetalis

  • David W. McCandless
Chapter
Part of the Contemporary Clinical Neuroscience book series (CCNE)

Abstract

Hemolytic disease of the newborn (HDN) is a collective phrase which includes several acquired hemolytic anemias, of which erythroblastosis fetalis is one. The term erythroblastosis fetalis, applies to Rh isoimmunization resulting in hemolysis, but the term focuses on aspects of the disease which are not always specific or present in each case. This chapter will therefore refer to HDN to describe red blood cell hemolytic anemias. In a very general and obvious way, hemolytic anemias in the newborn can be deleterious because they represent an increase in bilirubin formation at a time when the newborn liver may not be enzymatically equipped to conjugate the pigment, facilitating its excretion.

Keywords

Amniotic Fluid Hemolytic Anemia Bilirubin Level Unconjugated Bilirubin Hemolytic Disease 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

References

  1. Altman, K. (1959) Some enzymologic aspects of the human erythrocyte. Am. J. Med. 23:936–951CrossRefGoogle Scholar
  2. Beutler, E. (2006) Disorders of red cells resulting from enzyme abnormalities. In Williams hematology. Lichtman, M., et al. eds. McGraw Hill, New York, NY, pp 603–631Google Scholar
  3. Bevis, D. (1953) The composition of liquor amnii in haemolytic disease of the newborn. J. Obstet. Gynaec. Brit. Emp. 60:244–250PubMedCrossRefGoogle Scholar
  4. Brazie, J., Ibbott, F., and Bowes, W. (1966) Identification of the pigment in amniotic fluid of erythrocytes as bilirubin. J. Pediat. 69:354–358PubMedCrossRefGoogle Scholar
  5. Claireaux, A., Cole, P., and Lathe, G.(1953) Icterus of the brain in the newborn. Lancet 4:1226–1230CrossRefGoogle Scholar
  6. Gardos, G., and Straub, F. (1957) Uber die rolle der ATP in der K-permeabilitat der menschlichen roten blutkorperchen. Acta physiol. Hung. 12:1–12PubMedGoogle Scholar
  7. Hollingsworth, J. (1955) Lifespan of fetal erythrocytes. J. Lab. Clin. Med. 45:469–473PubMedGoogle Scholar
  8. Hyman, C., et al. (1969) CNS abnormalities after neonatal hemolytic disease or hyperbilirubinemia. Am. J. Dis. Child. 117:395–405PubMedGoogle Scholar
  9. Rapoport, S., and Luebering, J. (1950) The formation of 2,3-diphosphoglycerate in rabbit erythrocytes. J. Biol. Chem. 183:507–520Google Scholar
  10. WHO Severe and complicated malaria: A report of the WHO malaria action programme. Trans. R. Soc. Med. Hyg. 80:1–50Google Scholar
  11. Jirsova, V., Jirsa, M., and Janovsky, M. (1958) Importance of the quantitative determination of direct and indirect bilirubin in hemolytic diseasr of the newborn. Acta Pediat. 47:179–186CrossRefGoogle Scholar
  12. Blackfan, K. Diamond, L., and Leister, C. (1944) Atlas of blood in children. The Commonwealth Fund, Oxford University Press, LondonGoogle Scholar
  13. Rapoport, S., and Nieradt, C. (1951) Glycerate-2–3-diphosphatase. J. Biol. Chem. 189:683–691PubMedGoogle Scholar

Copyright information

© Springer Science+Business Media, LLC 2011

Authors and Affiliations

  1. 1.Department of Cell Biology & AnatomyRosalind Franklin University of Medicine & Science, Chicago Medical SchoolNorth ChicagoUSA

Personalised recommendations