from Section 2 - Fetal disease
Published online by Cambridge University Press: 05 February 2013
Introduction
Red cell alloimmunization, with its resultant fetal anemia, continues to be a cause of perinatal morbidity and mortality. Recent decades have seen major advances in the understanding and management of the condition and it is the aim of this chapter to review this. In particular, the role of direct fetal therapy for fetal anemia will be described, which has been one of the success stories of fetal medicine.
Red cell alloimmunization in pregnancy
There is a risk of red cell alloimmunization in any pregnancy where the mother is exposed to fetal red cells that possess antigens for which her own red cells are negative. The underlying mechanism for this exposure during pregnancy is fetomaternal hemorrhage (FMH). As a result, the mother mounts an immune response that is initially composed of IgM antibodies – large molecules that do not cross the placenta. Later, IgG antibodies are produced that are able to cross the placenta. This represents the primary immune response. A second exposure to the foreign antigens, for example in the next pregnancy, results in the secondary immune response and a rapid production of IgG antibodies which cross the placenta and cause fetal red cell hemolysis. The risk and severity of alloimmunization increases with each subsequent pregnancy that is positive for the relevant red cell antigen.
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