Abstract
The pathogenesis of erythroblastosis fetalis in man seems to be well known and understood (Wiener and Wexler, 1950; Wiener, 1961). In the classic case, an Rh-negative pregnant woman becomes sensitized to the Rh factor, usually as a result of transplacental leakage of fetal Rh-positive blood into her circulation. The resulting maternal Rh antibodies readily pass through the placenta into the fetal circulation and then coat the red cells of the fetus, leading to their destruction and giving rise to manifestations of hemolytic disease. In the most severe cases, there is stillbirth or hydropic or macerated fetus with marked hepatosplenomegaly; less severely affected offspring are liveborn with pronounced jaundice (icterus gravis) which may lead to kernicterus, causing severe mental retardation. The mildest manifestation is hemolytic anemia. As can be expected, the severity of the manifestations is usually correlated with the degree of sensitization of the mother, i.e., the higher the titer of the maternal antibodies, the greater the stillbirth rate.
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© 1979 Plenum Press, New York
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Socha, W.W., Moor-Jankowski, J. (1979). Serological Materno-Fetal Incompatibility in Nonhuman Primates. In: Ruppenthal, G.C., Reese, D.J. (eds) Nursery Care of Nonhuman Primates. Advances in Primatology. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-3477-4_4
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DOI: https://doi.org/10.1007/978-1-4684-3477-4_4
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