ABO Group Flashcards
When were the ABO blood groups discovered?
1900; located on chromosome #9
ABO and H genes are ….
glycosyltransferases (enzymes)
- add carbohydrates to type-2 paragloboside chain = Precursor Substance
- made of four sugars attached to ceramide (lipid backbone) which is embedded in the RBC membrane
L-fucosyl transferase
- gene = H
- antigen= H
N-acetyl D galactosaminyl
A
D- galactosyl
B
T or F. Almost 100% of the population will inherit two H genes
T!
as long as one H is inherited, then L-fucosyl transferase will be produced giving rise to an L-fucose being added to the PS
the __ antigen allows for other transferases to add sugars and form A and B antigens
H
antigen structure
glycosphingolipids or glycoproteins
lectins
- proteins (found in nature) that bind specific carbs
- act as artificial Abs that bind certain antigens
Ulex europaeus
- Anti-H
- seeds have lectin that binds H
Secretors
- 80% of population (SeSe, Sese)
- make soluble proteins found in plasma, sweat, tears, etc.
ABO group with most amount of H
O
who produces Anti-H
produced by people who did not inherit at least one H allele
- Bombay blood group
- IgM & naturally occurring
determination of ABO
- forward = testing for ABO involves determination of the antigen on the patient’s cells
- reverse = presence of ABO antibodies in their plasma
Anti-A,B
can be used to check on the forward grouping (newborn)
or help pick up weak subgroups of A or B causing ABO discrepancies
seldom used routinely
What do Bombay people type as?
O
- must be transfused ith Bombay blood due to anti-H
How do we test for Bombay?
- test patient’s red cells with anti-H lectin (Ulex europaeus) => will be 0 because Bombay don’t have H at all
- test for anti-H (which Bombaypeople should have) with O cells which is rich in H => positive!
Subgroups of A
- A1 = 80%
A1A1, A1A2, A1O - A2 = 20%
A2A2, A2O
** no difference in Ags; just clustering that is different **
- A3 = rare; weak in the forward group; 1+ MFA; reverse group is normal
this subgroup of A is a more efficient transferase and puts more terminal sugars on the H antigen
- A1 = one million antigens per RBC
- A2 = 250 000 antigens per RBC
- A3 = 30 000 A antigens per RBC
Anti-A1
- made in response to something else in the environment (naturally occurring)
- cross-reacts with A1
- cold, clinically insignificant IgM (not same properties as anti-A, -B)
- anti-A1 is unexpected; only made by 2-5% of people; <10% of A2B
Dolichus biflorus
anti-A1 lectin
- monoclonal anti-A1
Who makes anti-A1
A2 people and A2B people
T or F. A1 people can make anti-A2, anti-A2B
F!
Other subgroups of A
Ael, Aend, Ax
- small amounts of A or no A antigens on the cell; but have Ag in secretions
Subgroups of B
exist but rare
- B3, Bx, Bm
This may be useful in resolving a discrepancy
auto-control
- 2 drops of patient plasma with 1 drop of patient cells
OR
- anti-A,B may be useful in resolving a discrepancy
missing/weak antibodies
- newborns; <4 mos - <6 mos
- older person (70-90s)
hypo/agammaglobulinemia
- decreased Ab production
how to resolve missing/weak antibodies
either coax it to react stronger or inhibit Abs
- add more plasma (4 drops instead of 2) to cells to promote shift to right (4:1 ratio of plasma cells)
- incubate RT for 30 mins
- incubate at4C (react best in cold)
if not resolved = ABO questionable
extra antibodies
- irregular IgM alloantibodies (Lewis, P1, M, N)
- cold autoagglutinins (anti-I, -IH, -H, -IA, -IB)
- anti-A1
- Rouleaux
extra Abs = irregular IgM alloantibodies
- Lewis, P1, M, N
- naturally occurring IgM that some patients have; insignificant; read 4C (usually <15C)
- resolve by prewarming; aliquot of plasma, warm 10 mins, drop of B cells and warm for 10 mins; use pipette that has been warmed; mix
- if all else fails, then identify Ab (anti-M for ex), use own M negative B reverse grouping cell
extra Abs = cold agglutinins
- clinically insignificant for the most part
- autoAb
- naturally occurring
- behave like regular IgM => react in cold, not warm
- resolve by prewarming
** can vary in titre; ex: responding to infection = can increase that month, etc. **
extra Abs = anti-A1
- only made A2 or A2B ppl
- usually 1-2+ strength
- IgM; clinically insignificant; reacts in the cold
- investigate by using the lectin => if pos = A1; if neg = A2; ID the Ab => confirm
- resolve by driving rxn to the left
- use A2
- pre-warm (quicker + easier so start with this first)
extra Abs = Rouleaux
- increased protein in the plasma (multiple myeloma, acute phase reactants)
- rxn will only be 1+
- resolve by doing saline replace = remove plasma, replace with 2 drops of saline, mix, spin read, reaction should be 0
other causes of discrepancies not resolved serologically
- recent transfusion with non-identical ABO red cells
- hematopoietic stem cell transplants (BM)
- chimerism
- passive ABO antibody from blood products
