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6 - Hemolytic disease of the fetus and newborn
- from Section II - Erythrocyte disorders
- Edited by Pedro de Alarcón, Eric Werner, Robert D. Christensen
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- Book:
- Neonatal Hematology
- Published online:
- 05 February 2013
- Print publication:
- 10 January 2013, pp 65-90
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Summary
Introduction
Hemolytic disease of the fetus and newborn (HDFN) is the immune-mediated destruction of fetal red blood cells by maternal antibody. HDFN results when the fetal red blood cells express a paternally inherited red blood cell antigen not present on maternal red blood cells. The spectrum of illness ranges from clinically insignificant to the most severe form of a critically ill, anemic, hydropic, and jaundiced infant who may have subcutaneous edema, ascites, pleural effusions, and pericardial effusions.
There is no agreement when HDFN was first recognized. As reviewed by Stockman, Rosse suggested that the marriage of Catherine of Aragon and Henry VIII illustrates the natural history of HDFN (1). Catherine had five children, three boys and one girl dying in utero with only one surviving girl, Mary I, Tudor Queen of England. A clearer description of the disorder came in 1607 with the description of a twin-birth by a French midwife who delivered a hydropic dead child and a twin that died of jaundice – what we now recognize as kernicterus (2). It was the pivotal paper by Dr. Louis K. Diamond in 1932 that clearly identified the development of the maternal antibody in response to the incompatibility of the fetal red cells with maternal red cells even though the Rhesus red cell antigen had not yet been identified. Parallel to the understanding of HDFN, Landsteiner began the process of identification of the red cell antigens at the start of the 20th century, first with the identification of the ABO system and then with the identification of the Rh system (3). He described the development of antibodies against rhesus monkey red cells in rabbits. He suggested that this was a new antigen distinct from the ABO system and called it the Rhesus antigen. This name is now well established in spite of the early controversy, since the antigen identified was a simian antigen related to but not the same as the human antigen.
6 - Hemolytic disease of the fetus and newborn
- Edited by Pedro A. de Alarcón, University of Tennessee, Eric J. Werner
- Foreword by J. Lawrence Naiman, Stanford University School of Medicine, California
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- Book:
- Neonatal Hematology
- Published online:
- 10 August 2009
- Print publication:
- 18 August 2005, pp 91-131
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- Chapter
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Summary
Introduction
The fetus has a special immunological relationship with the mother that prevents rejection despite it being an allogeneic tissue [1–4]. If fetal blood cells enter the maternal circulation, the peaceful coexistence may be disrupted. The clinical problem of maternal antibody-mediated fetal red-blood-cell (RBC) destruction was a powerful stimulus to the acquisition of knowledge of the RBC antigen systems [5]. The triumphs of Landsteiner, Wiener, Levine, Darrow, Diamond, Chown, Liley, Clarke, Freda, Bowman and many others were among the great accomplishments of twentieth-century medicine [6]. Additionally, the assessment and management of hemolytic disease of the newborn (HDN) was a stimulus to progress in perinatal care in the second half of the twentieth century, including advances in fetal monitoring, in utero intervention, Cesarian section, neonatal resuscitation, and neonatal intensive care [7, 8]. A study of the interactions of RBC antigens with the maternal immune system and the fetal response to anemia can provide tremendous insight into systems of fundamental importance to neonatal health and disease.
The term “hemolytic disease of the newborn” was chosen to replace the term “erythroblastosis fetalis” when the mechanism of fetal anemia and neonatal jaundice was determined [9]. It was intended to name the maternal antibody-mediated fetal hemolytic disease, which, in these investigators' subjects, was the dominant etiology of fetal hemolysis and is a major cause of HDN worldwide. RhD continues to be the most commonly identified antigenic stimulus to HDN [10]. RhD-negative mothers give birth to RhD-positive fetuses in about 9% of European-ancestry pregnancies.