ABO subgroups Flashcards
ABO subgroups represent:
Phenotypes showing weaker and variable serologic reactivity with anti-A, anti-B, and anti-A,B reagents
Cause of ABO subgroups:
Result of less effective enzymes that convert H antigens to A or B antigens
Key difference in ABO subgroups:
Amount of antigen present on the red blood cell membrane
Phenotype A1: Antigens present and population frequency
Antigens: A, A1; Frequency: 80%
Phenotype A2: Antigens present and population frequency
Antigens: A; Frequency: 20%
Reactivity of A1 individuals with anti-A (B sera) and anti-A1 lectin
Positive for both anti-A and anti-A1 lectin
Reactivity of A2 individuals with anti-A (B sera)
Positive for anti-A only
Frequency of anti-A1 formation in A2 individuals
1-8%
Frequency of anti-A1 formation in A2B individuals
0.25
Anti-H lectin reactivity comparison: A1 vs A2 RBCs
A2 shows increased reactivity with anti-H lectin compared to A1
Weak A subgroup characteristics: Antigen sites per RBC
Decreased number of A antigen sites per RBC
Weak A subgroup characteristics: Agglutination with human anti-A, B
Variable degrees of agglutination
Weak A subgroup characteristics: Detectability of H antigen
Strong reactions with anti-H due to variability in detectability
Weak A subgroup characterization methods
Secretor studies, adsorption studies, and molecular testing
Subgroups of A showing mixed-field reactions
A3, Ax, Aend
Subgroups of A with no reaction with anti-A and anti-AB
Am, Ay, Ael
Subgroup of B with mixed-field agglutination with anti-B and/or anti-A,B
B3
Subgroup of B with agglutination only with anti-A,B (weak/none with anti-B)
Bx
Subgroup of B with no agglutination with anti-B and anti-A,B
Bm, Bel
Subgroup of B with secretors demonstrating quantities of B substance in saliva
Bel
Subgroup of B with secretors containing only H substance and no B substance in saliva
Bel
Year and location of first reported H-deficient case (Bombay phenotype)
1952, Bombay, India
Phenotype lacking ABH antigen expression, typing as hh antigen
Bombay phenotype
Consequence of no H antigens being formed in Bombay phenotype
No A nor B antigens are formed; phenotypes as blood group O
Serum composition in Bombay phenotype
Anti-A, anti-B, anti-AB, and anti-H
Blood compatibility for transfusion in Bombay phenotype
Only from another Bombay (Oh)
Genotype of classic Bombay phenotype
hh/sese
Genotype of para Bombay phenotype
hh/Se
Genotype of H-partially deficient variant
hh/se
Glycosyltransferase activity in para Bombay phenotype
A and/or B transferase
Glycosyltransferase activity in H-partially deficient variant
A and/or B transferase
Antibodies present in classic Bombay phenotype
Anti-A, Anti-B, Anti-H
Antibodies present in para Bombay phenotype
Weak Anti-H, Anti-A/B
Antibodies present in H-partially deficient variant
Anti-H, Anti-A/B
Source of group-specific substances (Ernest Witebsky) for A and B antigens
A: Hog stomach
B: Horse stomach
Common ABO discrepancy involving defects in reverse typing
Group I: Missing or weakly reacting antibodies
may be due to age, medications, and other health conditions
ABO discrepancy detected in forward typing due to missing or weakly reacting antigens
Group II
ABO discrepancy detected in both forward and reverse typing due to protein or plasma abnormalities
Group III
ABO discrepancy in reverse typing caused by miscellaneous issues
Group IV
Group II discrepancy due to weakened antigens neutralized by blood group-specific soluble substances (BGSS)
Subgroups of A(B), leukemias, acquired B phenomenon
Reaction seen in acquired B phenomenon with Anti-B clone ES4
Positive reaction
Reagent treatment to re-acetylate surface molecules and reduce anti-B reactivity in acquired B phenomenon
Acetic anhydride treatment
Anti-B pH range for reduced reactivity in acquired B phenomenon
pH >8.5 or <6.0
Substance used to neutralize anti-sera in acquired B phenomenon
Blood group-specific soluble substance (BGSS)
Group I discrepancies are common in these populations or conditions
Newborns, elderly patients, hypogammaglobulinemia, agammaglobulinemia, patients receiving plasma transfusion or exchange transfusion
Rare Group I discrepancy caused by two cell populations in one individual
Chimerism
Group II discrepancies can occur due to these conditions
Leukemia, Hodgkin’s disease, A/B subgroups, acquired B phenomenon, antibodies to low-incidence antigens
Group III discrepancy is caused by these conditions
Elevated globulin levels (e.g., multiple myeloma, Waldenstrom’s macroglobulinemia, advanced Hodgkin’s lymphoma), elevated fibrinogen, plasma expanders (dextran, polyvinylpyrrolidone), Wharton’s jelly in cord blood
ABO discrepancy seen with elevated levels of fibrinogen or plasma expanders
Group III
Group IV discrepancy causes
Cold reactive autoantibodies, more than one ABO group due to RBC transfusion or bone marrow transplant (BMT), unexpected alloantibodies, unexpected ABO isoagglutinins
Group IV discrepancy involving inherited genetic variation of the ABO group
Cis-AB
Definition of Cis-AB
Inheritance of both A and B genes from one parent on the same chromosome, with an O gene inherited from the other parent
Group III discrepancy commonly seen in this type of blood sample
Cord blood contaminated with Wharton’s jelly
Cold reactive autoantibodies causing ABO discrepancies are categorized as
Group IV
Discrepancy in a patient with both RBC transfusion and bone marrow transplant presenting multiple ABO groups
Group IV
Unexpected ABO isoagglutinins are a feature of which discrepancy group
Group IV
