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| {{SK}} Rh (D) disease; rhesus disease | | {{SK}} Rh (D) disease; rhesus disease |
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| == Serology ==
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| During any pregnancy a small amount of the baby's [[blood]] can enter the mother's circulation. If the mother is Rh negative and the baby is Rh positive, the mother produces [[Antibody|antibodies]] (including [[IgG]]) against the [[Rhesus blood group system|Rhesus D]] [[antigen]]s on her baby's [[red blood cell]]s. During this and subsequent pregnancies the IgG is able to pass through the [[placenta]] into the [[fetus]] and if the level of it is sufficient it will cause a Rhesus D positive fetus to develop Rh disease. The mechanism is maternal anti-D IgG passing through the placenta to the fetus causing destruction of fetal red blood cells. Generally Rhesus disease becomes worse with each additional Rhesus incompatible pregnancy.
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| The main and most frequent sensitizing event is child birth (about 86% of sensitized cases), but fetal blood may pass into the maternal circulation earlier during the pregnancy (about 14% of sensitized cases)<ref name=Bowman>{{
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| cite journal |
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| author=Bowman J et al | title=Rh-immunization during pregnancy: antenatal prophylaxis. |
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| journal=Canadian Med Ass Journal | year=1978 | pages=623-627 | volume=118
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| }}</ref>. Sensitizing events during pregnancy include [[miscarriage]], [[therapeutic abortion]], [[amniocentesis]], [[ectopic pregnancy]], abdominal trauma and [[external cephalic version]].
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| The incidence of Rh disease in a population depends on the proportion that are rhesus negative. Many non-caucasian peoples have a very low proportion who are Rhesus negative, so the incidence of Rh disease is very low in these populations. In Caucasian populations about 1 in 10 of all pregnancies are of a Rhesus negative woman with a Rhesus positive baby. It is very rare for the first Rhesus positive baby of a Rhesus negative woman to be affected by Rh disease. The first pregnancy with a Rhesus positive baby is significant for a rhesus negative woman because she can be sensitized to the Rh positive antigen. In Caucasian populations about 13% of Rhesus negative mothers are sensitized by their first pregnancy with a rhesus positive baby. If it were not for modern prevention and treatment, about 5% of the second Rhesus positive infants of Rhesus negative woman, would result in still births or extremely sick babies and many babies who managed to survive would be severely ill. Even higher disease rates would occur in the 3rd and subsequent Rhesus positive infants of rhesus negative woman. By using anti-RhD immunoglobulin ([[Rho(D) Immune Globulin]]) the incidence is massively reduced .
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| Rh disease sensitization is about 10 times more likely to occur if the fetus is ABO compatible with the mother than if the mother and fetus are ABO incompatible.
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| == Prevention ==
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| == Management ==
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| == History of medical advances in Rh disease ==
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Template:DiseaseDisorder infobox
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Synonyms and keywords: Rh (D) disease; rhesus disease
References
- David R. Zimmerman, Rh: The Intimate History of a Disease and Its Conquest Macmillan (1973) ISBN 0-02-633530-1.
- Landsteiner K and Weiner A (1940). An agglutinable factor in human blood recognized by immune sera for rhesus blood. Proceedings of the Society for Experimental Biology and Medicine, 43,223.
- Levine P, Katzin E and Burnham L (1941). Isoimmunization in pregnancy: its possible bearing on the aetiology of erythroblastosis fetalis. Journal of the American Medical Association, 116, 825-7
- Clarke C, Donohoe W, McConnell R, Woodrow J, Finn R, Krevans J et al (1963) Further experimental studies in the prevention of Rh-haemolytic disease. BMJ 979-984
- Freda V, Gorman j, and Pollack W (1964) Successful prevention of experimental Rh sensitization in man with an anti-Rh Gamma 2-globulin antibody preparation: a preliminary report. Transfusion, 4, 26-32
- Wallerstein H (1946). Treatment of severe erythroblastosis by simultaneous removal and replacement of blood of the newborn. Science, 103, 583-4
- Harman C, Bowmanj, Menticoglou S and ManningF (1988). Profound fetal thrombocytopenia in Rhesus diseas: Serious hazard at intravascular transfusion. Lancet 2,741-2
- Clarke CA, Whitfield AGW and Mollison PL (1987) Deaths from Rh haemolytic disease in England and Wales in 1984 and 1985. BMJ 294, 1001
- Levine P and Stetson R E: Intra-group agglutination. J Am Med Assoc, 113: 126,1939
See also
Template:HDN
Template:Certain conditions originating in the perinatal period
de:Rhesus-Inkompatibilität
nl:Resusantagonisme
Template:WikiDoc Sources