This is a discussion on Rh D Immunoglobulin within the Ask a Professional forum; I am a midwifery student in NZ and wondering if anyone out there could give ...
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Rh D Immunoglobulin
I am a midwifery student in NZ and wondering if anyone out there could give me a technical description of HOW the Rh D Immunoglobulin (anti-D as we affectionately call it) actually works? Am doing an assignment on the drug and have to cover pharmacodynamics and pharmacokinetics also.
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Without getting too technical, about 90% of humans have an antigen called the rhesus (rh) antigen on the surface of their red blood cells; only about 10% of the population do not have this antigen. The latter are called Rh-negative blood type. The Rh factor becomes a problem when an Rh-negative woman is pregnant with an Rh-positive child. During childbirth some of the baby's blood can leak from the placenta and come into contact with the mother's blood. Her immune system will then begin to mount a response to the Rh antigen by producing antibodies that destroy any red blood cells that carry the Rh antigen. (This response usually begins within 72 hours of exposure.) Thus, all future pregnancies are at risk if the fetus is rh-positive, since antibodies from the mother's blood can cross the placenta and enter the baby's bloodstream.
When an Rh-negative mother is suspected of having been exposed to Rh-positive blood, she may agree to be given a rhesus-immunoglobulin (RhIG) injection (sometimes known as anti-D). These antibodies quickly attack any leaked Rh-positive red blood cells from the baby and destroy them before they have time to sensitize the mother. This effectively eliminates the danger to the next baby, since no antibodies against Rh-positive blood have been produced by the mother's immune system. This anti-D immunoglobulin (a common brand name is RhoGam) is produced in a serum extracted from plasma, hence is a blood fraction. Its use would be a matter of individual conscience for those with religious objections to blood transfusion. Last edited by Informaticus; 07-27-2008 at 04:56 PM. |
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The exact mechanism by which an immune response to rh anigens is mounted is still not fully understood and there is more than one hypothesis offered as explanation, as illustrated by the article whose abstract appears below.
It is not the purpose of this website to present highly technical data on bioscience, and there are many other resources on the Internet that accomplish that purpose. May I suggest that you start by typing some of the keywords listed at the end of the abstract into a search engine. I am sure you will find what you are looking for that way. Best wishes. Immunology Letters Volume 82, Issues 1-2, 3 June 2002, Pages 67-73 Copyright © 2002 Elsevier Science B.V. All rights reserved. On the mechanism of tolerance to the Rh D antigen mediated by passive anti-D (Rh D prophylaxis) Belinda M. Kumpel International Blood Group Reference Laboratory, Bristol Institute of Transfusion Sciences, Southmead Road, Bristol BS10 5ND, UK Available online 15 February 2002. References and further reading may be available for this article. To view references and further reading you must purchase this article. Abstract Anti-D prophylaxis is the most successful clinical application of antibody-mediated immune suppression. Passive IgG anti-D is given to Rh D-negative women to prevent immunisation to foetal Rh D-positive red blood cells (RBC) and subsequent haemolytic disease of the newborn. Despite its widespread use and efficacy, the mechanism of action of this therapy is unproven. The known facts about the antigen, antibody response, dose of anti-D, RBC clearance and effects of the passive anti-D on subsequent primary and secondary immune responses are discussed in relation to recent information on ways by which immune responses may be suppressed. Most Rh D antigen sites on RBC are not bound by passive anti-D, and thus epitope masking (which may occur in experimental murine models using xenogeneic RBC) is not the reason why anti-D responses are prevented by administration of prophylactic anti-D. It is hypothesised that although clearance and destruction of the antigenic RBC may be a contributing factor in preventing immunisation, down-regulation of antigen-specific B cells through co-ligation of B cell receptors and inhibitory IgG Fc receptors must also occur. Author Keywords: Anti-D; Rh D antigen; Haemolytic disease of the newborn; Monoclonal antibodies; Antibody-mediated immune suppression; Red blood cells; B cells; IgG Fc receptors Abbreviations: HDN, haemolytic disease of the newborn; AMIS, antibody-mediated immune suppression; RBC, red blood cells; SRBC, sheep red blood cells; BCR, B cell receptor; FcγR, IgG Fc receptor; FMH, foeto-maternal haemorrhage |
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