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SYSTEM
CRISTEL SABBAN
CARLA CARANGUIAN
Historical Background
Cold reactive IgM or IgG saline agglutinin that does not bind complement or
react with enzyme-treated RBCs.
Can demonstrate dosage reacting better with M+N- (NN) RBCs than witn
M+N+ (MN) RBCs.
Rare examples are pH- or glucose- dependent.
Not clinically significant unless it reacts at 37C.
Implicated only with rare cases of HDFN.
Less common than anti-M.
Seen in renal patients, who are dialyzed on equipment sterilized with
formaldehyde
Anti-S and Anti-s
Most examples are IgG reactive at 37C and the antiglobulin test phase.
Implicated with severe HTRs with hemoglobinuria and HDFN.
More likely to be clinically significant and may bind complement.
It can be difficult to provide blood for a patient with anti-s because only
11% of whites and 3% of blacks are s. Compared with S that is much
easier to find, whites has 45% and blacks has 69% of S.
GPA- and GPB- Deficient phenotypes
A. U-phenotype
-U for universal
-Antigen is located on GPB very close to the RBC membrane between
amino acids 33 and 39
-High prevalence antigen is found on RBCs of individuals except about
1% of African Americans ( and 1 to 35% of Africans) who lack GPB.
- In S-s-U- individuals , complete loss or recombination of GPB occurs,
leading to altered expression of S/s and U antigens.
-Anti-U is rare but can be formed in S-s- individuals; typically IgG and can
also cause HDFN and HTRs. It is enhanced with enzyme treatment.
GPA- and GPB- Deficient phenotypes
B. En(a) Phenotype
Darnborough and Furuhjelm(1969)described an antibody to the same
high prevalence antigen called Ena(for envelope)
Most En(a) individuals produce anti-Ena
Anti-EnaTS recognizes a trypsin-sensitive(TS) area on GPA between
amino acids 20 and 39
Anti-EnaFS reacts with a ficin sensitive (FS) area betweemn amino acids
46 and 56.
Anti-EnaFR reacts with a ficin resistant (FR) area around amino acids 62
and 72.
GPA- and GPB- Deficient phenotypes
C. Mk phenotype
Named by Metaxas and Metaxas-Buhler (1964) when they found an allele that
did not produce M or N.
Lacks all MNS antiges including En(a) as a result of recombination and deletion
of glycophorins A and B .
In 1979 two related MkMk blood donors were found, the RBCs of these
individuals typed M-N-S-s-U-En(a-)Wr(a-b-) but they had normal hematologic
picture.
Mk genes represents a single , near complete deletion of both GYPA and GYPB
MkMk genotype is associated with decreased RBC sialic acid content but
increased glycosylation of RBC membrane bands 3 and 4.1.
Other antibodies