During the first pregnancy, the initial exposure to fetal RBCs results in the formation of IgM antibodies, and these do not cross the placental barrier , which is why no effects are seen in first pregnancies for Rh-D mediated disease. However, in subsequent pregnancies, the immune system mounts a memory response when re-exposed, and these antibodies IgG do cross the placenta into fetal circulation. These antibodies are directed against a protein found on the surface of the fetal red blood cells RBCs. The antibody coated fetal red blood cells are destroyed. The resulting anemia has multiple sequelae: [1] [2] [3] 1 The immature hematopoietic system of the fetus is taxed as the liver and spleen attempt to put immature RBCs into circulation erythroblasts, thus the previous name for this disease erythroblastosis fetalis.

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All Rights Reserved. Under the terms of the licence agreement, an individual user may print out a PDF of a single chapter of a title in Oxford Medicine Online for personal use for details see Privacy Policy and Legal Notice. Although effective prophylaxis is available it must be properly used. Postpartum prophylaxis with anti-D immunoglobulin should be given within 72 hours of birth to all RhD-negative women who give birth to a RhD-positive baby, or a baby whose RhD status cannot be determined, irrespective of their ABO status.

Anti-D immunoglobulin should be administered also to all RhDnegative women during pregnancy when there is an increased risk of fetomaternal bleeding. Routine use of anti-D immunoglobulin at 28 or 34 weeks of pregnancy for all Rh-negative women is of value as well, but the costs of such a programme are high and together with the limited supplies of anti-D immunoglobulin may preclude this in some countries. Rhesus iso-immunization has become sufficiently rare, and the treatment sufficiently complex, to warrant regionalization of care for these women and babies.

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1 - Définition – Physiopathologie



Rh disease


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