ABO Blood Group
ABO Blood Group
ABO Blood Group
Importance of
ABO system
ABO compatibility between donor cell and patient serum is the essential foundation of pre-transfusion testing It is the only system with expected antibodies Whether they are IgG or IgM, ABO antibodies can activate complement readily
This means that incompatibilities can cause life threatening situations (transfusion reactions)
ABO antigens
Biochemical & Genetic Considerations
Genes at three separate loci control the occurrence and location of ABO antigens. The presence or absence of the A, B, and H antigens is controlled by the H and ABO genes. The presence or absence of the ABH antigens on the red blood cell membrane is controlled by the H gene. The presence or absence of the ABH antigens in secretions is indirectly controlled by the Se gene. H Antigen The H gene codes for an enzyme that adds the sugar fucose to the terminal sugar of a precursor substance (PS) The precursor substance (proteins and lipids) is formed on an oligosaccharide chain (the basic structure)
There are two potential precursors substances for ABH antigens Type I and Type II Both are comprised of identical sugars but the linkage of the terminal sugars differs in the two types Type I precursor has a terminal galactose linked to a subterminal N-acetylgluosamine in a 1-3 linkage These same sugars combine in a 1-4 linkage in type II precursor ABH Ags on red cells are derived from Type II chains whereas the ABH Ags in plasma are made from both types I & II precursors
Glucose
Precursor Substance (stays the same) Galactose N acetylglucosamine Galactose
Glucose
H antigen
H antigen
The H antigen is the foundation upon which A and B antigens are built A and B genes code for enzymes that add a sugar to the H antigen
A and B Antigen
The A gene codes for an enzyme (transferase) that adds N-acetylgalactosamine to the terminal sugar of the H antigen N-acetylgalactosaminyltransferase The B gene codes for an enzyme that adds Dgalactose to the terminal sugar of the H antigen D-galactosyltransferase.
Glucose
Galactose N-acetylglucosamine Galactose Fucose N-acetylgalactosamine
Glucose Galactose
N-acetylglucosamine
Galactose Fucose Galactose
Genetics
The H antigen is found on the RBC when you have the Hh or HH genotype, but NOT from the hh genotype The A antigen is found on the RBC when you have the Hh, HH, and A/A, A/O, or A/B genotypes The B antigen is found on the RBC when you have the Hh, HH, and B/B, B/O, or A/B genotypes. The O allele Why do Group O individuals have more H antigen than the other groups? The O gene is a silent allele. It does not alter the structure of the H substance.that means more H antigen sites.
A Group O A Group O
A
Group A Group A A
Most of the H antigen sites in a Group A individual have been converted to the A antigen
Bombay Phenotype (Oh) Inheritance of hh The h gene is an amorph and results in little or no production of L-fucosyltransferase Very rare
The hh causes NO H antigen to be produced Results in RBCs with no H, A, or B antigen (patient types as O) Bombay RBCs are NOT agglutinated with anti-A, anti-B, or anti-H (no antigens present) Bombay serum has strong anti-A, anti-B and anti-H, agglutinating ALL ABO blood groups
Another Bombay
Group O RBCs cannot be given because they still have the H antigen You have to transfuse the patient with blood that contains NO H antigen
ABO Antibodies
ABO antibodies
RBC Phenotype Frequency (%) Serum Ab
A
B
43
9
Anti-B
Anti-A
AB
O
4
44
-------Anti-A,B
ABO antibodies
Anti-A Anti-B
Complement can be activated with ABO antibodies (mostly IgM, some IgG) High titer: react strongly (4+)
Anti-A, Anti-B, Anti-A,B Clinically Significant Yes Thermal range 4 - 37 Transfusion Reactions Abs class IgM, less IgG HDNB Yes
Extravascular
Yes
Intravascular
Yes
Rh Genetics: The genes that control the system are autosomal codominant located on the short arm of chromosome 1.
Rh Positive Rh Negative
D antigen 85% d antigen 15% C antigen 70% c antigen 80% E antigen 30% e antigen 98%
Rh Deleted Red cells that express no Ags at the C & E loci (D) Number of D Ags greatly increase Anti-D IgG Abs can agglutinate these cells RH null: individual that appears to have no Rh antigens ( , , ) Must use autologous blood products
Rh antibodies
Result from the exposure to Rh antigens IgG form Bind at 37C Form agglutination in IAT phase
Rh Abs
Clinically Significant Yes Thermal range 4 - 37 Abs class IgG HDNB Yes
Usually related to D antigen exposure and the formation of anti-D Usually results from D negative female and D positive male producing and offspring. The baby will probably be D positive. 1st pregnancy not effected, the 2nd pregnancy and on will be effected-results in still birth, severe jaundice, anemia related to HDN. To prevent this occurrence the female is administered RH-IG.
Rh factor
First pregnancy
Anti-Rh+ antibodies
During the mothers next pregnancy, Rh antibodies can cross the placenta and endanger the fetus.
Weak D Phenotype
Most D positive rbcs react macroscopically with Reagent anti-D at immediate spin These patients are referred to as Rh positive Reacting from 1+ to 3+ or greater HOWEVER, some D-positive rbcs DO NOT react (do NOT agglutinate) at Immediate Spin using Reagent Anti-D. These require further testing (37oC and/or AHG) to determine the D status of the patient. Variants of D: Weak expression of the Rh system on the RBC, (Du)
Cross-matching involves mixing a sample of the recipient's serum with a sample of the donor's red blood cells and checking if the mixture agglutinates ,or forms clumps. If agglutination is not obvious by direct vision, blood bank technicians usually check for agglutination with a microscope .If agglutination occurs, that particular donor's blood cannot be transfused to that particular recipient .
Put 10 of anti A on one side of a slide and put 10 of anti B on the other side
Put 10 of blood tested in each side and mix the blood with the reagent added. results: +A & + B = AB
+A & - B = A
-A&+B=B -A & - B = O