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RH Blood Group System
Medical Technology ((MLS))
Our Lady of Fatima University
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RH Blood Group System Historical Perspective 1939 -1940 ’s Two significant discoveries were made ● Levine and Stetson described a hemolytic transfusion reaction in an obstetrical patient ● After transfusion, the recipient (obstetric patient) demonstrated the classic symptoms of an acute hemolytic transfusion reaction ● Subsequently, an antibody was isolated from the mother’s serum that reacted both at 37C and at 20C with the father’s RBCs ● It was postulated that the fetus and the father possessed a common factor that the mother lacked ● While the mother carried the fetus, she was exposed to this factor and subsequently built an antibody that reacted against the transfused RBCs from the father, which resulted in the hemolytic transfusion reaction A year later, Landsteiner and Wiener ● Reported on an antibody made by guinea pigs and rabbits when they were transfused with rhesus monkey RBCs ● This antibody, which agglutinated 85 percent of human RBCs, was named RH ● Another investigation by Levine and coworkers demonstrated that the agglutinin that had caused the hemolytic transfusion reaction and the antibody described by Landsteiner and Wiener appeared to define the same blood group - Many years later it was recognized that the two antibodies were different - However, the name Rh was retained for the human produced antibody, and the anti rhesus antibody formed by the animals was renamed anti LW in honor of those first reporting it Rh ● Continued investigation showed additional blood group factors associated with the original agglutinin ● Mid 1940 ’s five antigens made up the Rh system ● Today the Rh blood group system is made up of nearly 50 different specificities Nomenclatures of the Rh System Fischer Race (DCE) ● Based on the theory that the antigen of the systems were produced by the three closely linked set of alleles, each gene was responsible for producing a product (or an antigen) on the red cell membrane Wiener (Rh-Hr) ● Postulated that the gene responsible for defining Rh are actually produced an agglutinogen that contains a series of blood factors, in which each factor is an antigen recognized by an antibody Rosenfield (Alpha Numeric) ● Number is assigned to each antigen of the Rh system in order of its discovery ISBT nomenclature uses 6 number designation FISCHER RACE (DCE) ● According to the Fisher Race proposal, each person inherits a set of Rh genes from each parent ● Rh genes are expressed as Codominant - each inherited gene expresses its corresponding antigen on the RBC ● The combination of maternal and paternal haplotypes determines one’s genotype - Dictates one’s phenotype (the antigens expressed on the RBC that can be detected serologically) ● An individual’s Rh phenotype is reported as DCE rather than CDE because Fisher postulated that the C/c locus lies between D/d and E/e loci This information is based on frequencies of the various gene combinations FISHER RACE (DCE) ● Inherit 3 genes ● Each genes codes for Ag
d gene - amorph WIENER (Rh-Hr) ● Inherit 1 gene ● Codes for agglutinogen ( 3 Blood Factors) Rh-Hr TERMINOLOGY OF WIENER ROSENFIELD Nomenclature ● In the early 1960 s Rosenfield and associates proposed a system that assigns a number to each antigen of the Rh system in order of its discovery or recognized relationship to the Rh system ● No genetic basis ● Only indicates presence or absence of Rh Ags Sample Problem: 1. Convert R2 R2 to Fischer Race? DcE/DcE 2. Which of the following could be the possible genotype of a patient, which has a product of Anti c? A. R o R o B. R o R 1 C. R 1 R 2 D. R 1 R 1 ANSWER ● This is the same as DCe/DCe in Fischer Race nomenclature, the patient doesn’t have “ c”(small c) antigen, so when the patient is exposed to RBC that has “ c”(small c) antigen, the patient will produced antibodies to small c (Anti c) this patient can also be triggered to produced Anti E (capital E) Weak D: Variations of the Rh0(D) Antigen Expression ● When Rh positive RBC samples are typed for the D antigen, they are expected to react strongly (macroscopically) with anti D reagents - However, with certain RBCs the testing must be carried through the antiglobulin phase of testing to demonstrate the presence of the D antigen - RBCs carrying the weaker D antigen have historically been referred to as having the “Du” type - Now they are referred to as expressing weak D and are considered Rh positive ● Three different mechanisms have been described
IgG immunoglobulins must attach to an RBC in close proximity ● RBC destruction is EXTRAVASCULAR
- when an Rh antibody coats the RBCs, intravascular, complement mediated hemolysis does not occur
- RBC destruction resulting from Rh antibodies is primarily extravascular ● Causes HDN Breakdown of RBC: Intravascular and Extravascular Hemolysis Clinical Considerations ● Transfusion Reactions a. Rh antigens are highly immunogenic
- The D antigen is the most immunogenic antigen outside the ABO system b. Rh mediated hemolytic transfusion reactions
- Extravascular hemolysis ● HDN
- Rh negative female
- Rh positive father
- Rh positive infants Rh Antigen Typing ● Reagent: anti D ● Rh (+) D antigen is present ● Rh (-) D antigen is absent ● If in Rh typing the result is negative → TEST FOR PRESENCE OF WEAKLY ANTIGEN .(IAT) IN EMERGENCY CASES If the patient is Rh (-) transfuse Rh (+) if no past immunization Coombs’ Test ● Direct Antiglobulin test
- HDN
- HTR
- AIHA ● Indirect Antiglobulin test
- Cross matching
- Antibody detection
- Antibody identification
- RBC Antigen phenotyping AHG REAGENTS ● Polyspecific AHG
- Anti IgG and Anti C3b or Anti C3d ● Monospecific AHG
- Anti IgG or Anti C3b or Anti C3d For Test to be Valid for Negative AHG test ● Group O RBCs sensitized with IgG are added ● Valid if : There is agglutination ● Invalid if There’s no agglutination Rh Immune Globulin (RHOGAM) Application ● Given to pregnant women that is capable of producing anti D when exposed to D positive RBCs ● This principle has been used to prevent immunization to D antigen by the use of high titer RhIg ● During pregnancy and delivery, mixing of fetal and maternal blood occurs ● If the mother is Rh negative and the fetus is Rh positive, the mother has up to a 9 percent chance of being stimulated to form anti D ● Before delivery, the risk of sensitization is 1 to 1 percent of susceptible women, indicating that a significant amount of fetal RBCs can enter the maternal circulation during pregnancy
- HOWEVER, THE GREATEST RISK OF IMMUNIZATION TO Rh IS AT DELIVERY
Dosage Availability MINI OR MICRODOSE RHOGAM ● Contains 50 μg anti D ● protect up to 5 ml D+ WB or 2 ml D+ RBCs ● given to the first 12 weeks of pregnancy (Rh negative) for abortions and ectopic pregnancies, miscarriage FULL DOSE RHOGAM ● contain 300 μg anti D ● protect up to 30 ml of whole blood or 15 ml of RBC’s ● Given after 12 weeks of pregnancy (Rh negative) for abortions and ectopic pregnancies, miscarriage 120 μg dose Rhogam ● is advised after 34 th weeks’ gestation when amniocentesis is performed or in the event of obstetric complication or following termination of pregnancy Antepartum dose 300 μg anti D IM or IV) ● Should be given to nonimmunized D negative females at 28 th weeks’ gestation Postpartum dosage ● a postpartum blood sample is drawn from the mother - The sample will be subjected for screening test for fetomaternal hemorrhage (FMH) A. if POSITIVE FMH must be quantified using the Kleihauer Betke test B. If NEGATIVE the mother should receive a full dose of RhIg within 72 hours of delivery - ADDITIONALY, if the newborn is tested D positive - the mother should receive a full dose of RhIg unless she has demonstrated previous active immunization to the D antigen Determination how many Vials should be injected to D negative women after delivery Kleihauer Betke test Hemoglobin F determination ● Alkali Denaturation Test: - Betke Test - Singer Test ● Acid Elution Test: Kleihauer Betke test
RH Blood Group System
Course: Medical Technology ((MLS))
University: Our Lady of Fatima University
