Blood groups Flashcards
What drives hyperacute solid organ rejection?
Major ABO incompatibility resulting in thrombosis due to recipient anti-A/anti-B.
When is ABO detectable in development? When do the antibodies form?
Detectable at 5wks in diminished quantity (due to non-branching i chains). Antibodies develop at 3-6mo and increase until 5-10yrs.
What factors can drive higher anti-ABO titers in donors?
Multiparity, probiotic use
What is the difference between the A and B glycosyltransferases?
Only 3 amino acids differ. Hybrids between the two may have specificity for both sugars (cis-AB)
What is the O glycosyltransferase?
Actually loss of the A/B sugar transferase, usually due to frameshift or nonsense mutations.
How does A1 subgroup differ from A2 subgroup?
A1 has about 5x as much A antigen, also qualitative differences probably reflecting contributions to T3 and T4 chains.
What is B(A) phenotype?
An autosomal dominant trait that results in weak expression of A antigen in predominantly group B patients (ie, a B transferase that can transfer NAcGlc)
What causes acquired B? How can it be avoided from the lab’s perspective?
Bacterial deacetylation of GlcNAc to Glc. Can be affected by reagent pH and specific anti-B clones (ES-4), so avoid those and use acidified reagent.
What is the order of blood groups by decreasing H antigen expression?
O > A2 > B > A2B > A1 > A1B
How do Bombay phenotype patients present on lab workup? What causes it? Associations?
“O” patients that show panagglutination to reagent O cells and no Ulex agglutination. Caused by loss of both FUT1 (missense) and FUT2 (deletion). Associated with leukocyte adhesion deficiency.
What is para-bombay phenotype?
Expression of FUT2 but not FUT1 (only secreted H antigen). Some soluble H antigen can adsorb onto red cells, resulting in “Ah/Bh/ABh/Oh” phenotype, but they still don’t really react with Ulex and can express anti-H.
Where is anti-H seen?
In Bombay, para-bombay, but also randomly in healthy A1 and A1B people (not significant in these cases)
On what chains are Lewis antigens expressed?
Type 1 chains
Who may express both Lewis A and B antigens?
Infants (during development, secretor enzyme is weak) and asians (FUT2 variant “SeW”).
When does lewis antigen expression mature?
5-6 years of age.
What condition is associated with Le(a-b-) phenotype in African American patients?
Leukocyte adhesion deficiency. (E and P selectins bind CD15, or sialyl-lewis X)
What is the difference between I and i?
The degree of branching in the type 2 chain backbone sugar; I is branched, i isn’t. I is adult, i is pediatric (mostly).
i(adult)
Results from autosomal recessive GCNT2 mutations, mostly in asians. Associated with HEMPAS, congenital dyserythropoietic anemia, and cataracts (not in all forms).
Anti-I
Auto: Strong cold-reacting IgM
Allo: Only seen in i(adult), insignificant
Cold agglutinin syndrome
Autoanti-I/i seen in cancer or mycoplasma infection. Can cause hemolysis if thermal amplitude is broad.
How are P, Pk, and P1 made?
Pk is synthesized from lactosylceramide.
P (globoside) is synthesized from Pk
P1 is synthesized from Paragloboside.
How many P phenotypes are there? What are they?
P1 (common) - P+/Pk+u/P1+ P2 (uncommon) - P+/Pk+u/P1- p (rare) - No antigens P1k (rare) - P-/Pk+/P1+ P2k (rare) - P-/Pk+/P1-
What anti-P group antibodies are significant?
Anti-PP1Pk (seen in p phenotype).
Anti-P (allo in Pk, auto in PCH)
What is FORS?
A single low-prevalence antigen attached to P antigen which resembles A (may react with anti-A). Encoded by GBGT1 (Forssman synthase).