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Chapter 8 Blood Group Terminology and Common Blood Groups 207

Panel Results
D C E c e f M N S s Lua Lub P1 Lea Leb K k Fya Fyb Jka Jkb IS 37C PEG IAT
1 + + 0 0 + 0 + 0 + 0 0 + + + 0 + + + 0 0 + 0 NH 3+
2 + + 0 0 + 0 0 + 0 + 0 + + 0 + 0 + 0 + + 0 0 NH 3+
3 + 0 + + 0 0 + + + + 0 + 0 + 0 0 + + 0 0 + 0 NH 3+
4 + 0 0 + + + + 0 + 0 0 + + 0 0 0 + 0 0 + 0 0 NH 3+
5 0 + 0 + + + + + 0 + 0 + + 0 + 0 + + 0 + + 0 NH 3+
6 0 0 + + + + + + 0 + 0 + 0 0 + 0 + + + + + 0 NH 3+
7 0 0 0 + + + 0 + 0 + 0 + + + 0 0 + 0 + 0 + 0 NH 3+
8 0 0 0 + + + + 0 + + 0 + 0 0 + + 0 + + + + 0 NH 3+
9 0 0 0 + + + 0 + + 0 0 + 0 0 + 0 + + + + + 0 NH 3+
10 0 0 0 + + + + 0 + + + + + + 0 0 + + 0 + 0 0 NH 3+
11 + 0 + + 0 0 + + + + 0 + + 0 + + + 0 + + + 0 NH 3+
AC 0 NH 0
Reactivity could be due to a high incidence antibody or multiple antibodies.
• Patient’s phenotype: C-c+E-e+; K-k+; Fy(a-b-); Jk(a+b+); Le(a-b-); M+N-S-s-.
• Genotype testing shows the presence of the GATA gene.

1. What is the patient’s ABO, Rh type, and antibody screen?

2. Does the antibody appear to be auto or allo and why?
3. What is the suspected ethnicity of the patient based on the phenotype results?
4. Based on the phenotype results, what high-prevalence antigen should be considered?
5. What specialized testing could be used to determine the significance of the Fy(a-b-) phenotype?
6. If rare high incidence cells are not available to rule out additional allow antibodies, what technique could be
performed?
7. If an underlying anti-N was detected, should it be considered to be potent?

SUMMARY CHART
Blood Group Terminology Lewis Blood Group
 The ISBT terminology for RBC surface antigens pro-  Lewis blood group antigens are not synthesized by the
vides a standardized numeric system for naming RBCs. These antigens are adsorbed from plasma onto
authenticated antigens that is suitable for electronic the RBC membrane.
data-processing equipment. This terminology was not  The Le gene codes for L-fucosyltransferase, which adds
intended to replace conventional terminology. L-fucose to type 1 chains.
 In the ISBT classification, RBC antigens are assigned a  The Le gene is needed for the expression of Lea sub-
six-digit identification number: the first three digits stance, and Le and Se genes are needed to form Leb
represent the system, collection, or series, and the sec- substance.
ond three digits identify the antigen. All antigens are  The lele genotype is more common among blacks than
catalogued into one of the following four groups: among whites and results in the Le(a–b–) phenotype.
• A blood group system if controlled by a single gene  Lewis antigens are poorly expressed at birth.
locus or by two or more closely linked genes
• A collection if shown to share a biochemical, sero-  Lewis antibodies are generally IgM (naturally occur-
logic, or genetic relationship ring) made by Le(a–b–) individuals.
• The high-prevalence series (901) if found in more  Lewis antibodies are frequently encountered in preg-
than 90% of most populations nant women.
• The low-prevalence series (700) if found in less than  Lewis antibodies are not considered significant for
1% of most populations transfusion medicine.
Continued
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208 PART II Blood Groups and Serologic Testing

SUMMARY CHART—cont’d
The P Blood Group  Anti-S and anti-s are IgG antibodies, reactive at 37°C
and the antiglobulin phase. They may bind comple-
 The P blood group consists of the biochemically re-
ment and have been associated with HDFN and HTRs.
lated antigens P, P1, Pk, PX2, NOR, and LKE.
 P1 antigen expression is variable; P1 antigen is poorly
 The S–s–U– phenotype is found in blacks.
developed at birth.  Anti-U is usually an IgG antibody and has been asso-
ciated with HTRs and HDFN.
 Anti-P1 is a common naturally occurring IgM antibody
in the sera of P1– individuals; it is usually a weak, cold- The Kell Blood Group System
reactive saline agglutinin and can be neutralized with
soluble P1 substance found in hydatid cyst fluid.  The Kell blood group antigens are well developed at
birth and are not destroyed by enzymes.
 Anti-PP1Pk is produced by the rare p individuals early
in life without RBC sensitization and reacts with all  The Kell blood group antigens are destroyed by DTT,
RBCs except those of other p individuals. Antibodies ZZAP, and glycine-acid EDTA.
may be a mixture of IgM and IgG, efficiently bind com-  Excluding ABO, the K antigen is rated second only to
plement, may demonstrate in vitro hemolysis, and can D antigen in immunogenicity.
cause severe HTRs. Anti-PP1Pk is associated with  The k antigen is high prevalence.
spontaneous abortions.  Anti-K is usually an IgG antibody reactive in the
 Alloanti-P is found as a naturally occurring alloanti- antiglobulin phase and is made in response to preg-
body in the sera of Pk individuals and is clinically sig- nancy or transfusion of RBCs; it has been implicated
nificant. Anti-P has also been associated with in severe HTRs and HDFN.
spontaneous abortion.  The McLeod phenotype, affecting only males, is de-
 Autoanti-P is most often the specificity associated with scribed as a rare phenotype with decreased Kell system
the cold-reactive IgG autoantibody in patients with antigen expression. The McLeod syndrome includes
paroxysmal cold hemoglobinuria (PCH). the clinical manifestations of abnormal RBC morphol-
 The autoanti-P of PCH usually does not react by rou- ogy, compensated hemolytic anemia, and neurological
tine tests but is demonstrable as a biphasic hemolysin and muscular abnormalities. Some males with the
only in the Donath-Landsteiner test. McLeod phenotype also have the X-linked chronic
granulomatous disease.
The I and i Antigens
The Duffy Blood Group System
 I and i antigens are not antithetical; they have a recip-
rocal relationship.  Fya and Fyb antigens are destroyed by enzymes and
 Most adult RBCs are rich in I and have only trace ZZAP; they are well developed at birth. The Fy(a–b–)
amounts of i antigen. phenotype is prevalent in blacks but virtually nonex-
istent in whites.
 At birth, infant RBCs are rich in i; I is almost unde-
tectable; over the next 18 months of development, the  Fy(a–b–) RBCs resist infection by the malaria organism
infant’s RBCs will convert from i to I antigen. P. vivax.
 Anti-I is typically a benign, weak, naturally occurring,  Anti-Fya and anti-Fyb are usually IgG antibodies and
saline-reactive IgM autoagglutinin, usually detectable react optimally at the antiglobulin phase of testing;
only at 4°C. both antibodies have been implicated in delayed HTRs
and HDFN.
 Pathogenic anti-I is typically a strong cold autoagglu-
tinin that demonstrates high-titer reactivity at 4°C and The Kidd Blood Group System
reacts over a wide thermal range (up to 30° to 32°C).
 Patients with M. pneumoniae infections may develop  Anti-Jka and anti-Jkb may demonstrate dosage, are
strong cold agglutinins with autoanti-I specificity. often weak, and are found in combination with other
antibodies; both are typically IgG and reactive in the
 Anti-i is a rare IgM agglutinin that reacts optimally at
antiglobulin phase of testing.
4°C; potent examples may be associated with infec-
tious mononucleosis.  Kidd system antibodies may bind complement and are
made in response to foreign RBC exposure during
The MNS Blood Group System pregnancy or transfusion.
 Anti-M and anti-N are cold-reactive saline agglutinins
 Kidd system antibodies are a common cause of delayed
HTRs.
that do not bind complement or react with enzyme-
treated cells; both anti-M and anti-N may demonstrate  Kidd system antibody reactivity is enhanced with en-
dosage. zymes, LISS, and PEG.
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Chapter 8 Blood Group Terminology and Common Blood Groups 209

SUMMARY CHART—cont’d
The Lutheran Blood Group System response to foreign RBC exposure during pregnancy
or transfusion.
 Lua and Lub are antigens produced by codominant
alleles; they are poorly developed at birth.  The Lu(a–b–) phenotype is rare and may result from
three different genetic backgrounds; only individuals
 Anti-Lua may be a naturally occurring saline agglutinin
with the recessive type Lu(a–b–) can make anti-Lu3.
that reacts optimally at room temperature.
 Anti-Lub is usually an IgG antibody reactive at
the antiglobulin phase; it is usually produced in

7. A type 1 chain has:

Review Questions
a. The terminal galactose in a 1-3 linkage to subterminal
1. The following phenotypes are written incorrectly except N-acetylglucosamine
for: b. The terminal galactose in a 1-4 linkage to subterminal
N-acetylglucosamine
a. Jka+
c. The terminal galactose in a 1-3 linkage to subterminal
b. Jka+
N-acetylgalactosamine
c. Jka(+)
d. The terminal galactose in a 1-4 linkage to subterminal
d. Jk(a+)
N-acetylgalactosamine
2. Which of the following characteristics best describes
8. Which of the following best describes Lewis antigens?
Lewis antibodies?
a. The antigens are integral membrane glycolipids
a. IgM, naturally occurring, cause HDFN
b. Lea and Leb are antithetical antigens
b. IgM, naturally occurring, do not cause HDFN
c. The Le(a+b–) phenotype is found in secretors
c. IgG, in vitro hemolysis, cause hemolytic transfusion
d. None of the above
reactions
d. IgG, in vitro hemolysis, do not cause hemolytic trans- 9. Which of the following genotypes would explain RBCs
fusion reactions typed as group A Le(a+b–)?
3. The Le gene codes for a specific glycosyltransferase that a. A/O Lele HH Sese
transfers a fucose to the N-acetylglucosamine on: b. A/A Lele HH sese
c. A/O LeLe hh SeSe
a. Type 1 precursor chain
d. A/A LeLe hh sese
b. Type 2 precursor chain
c. Types 1 and 2 precursor chains 10. Anti-LebH will not react or will react more weakly with
d. Either type 1 or type 2 in any one individual but not which of the following RBCs?
both a. Group O Le(b+)
4. What substances would be found in the saliva of a group b. Group A2 Le(b+)
B secretor who also has Lele genes? c. Group A1 Le(b+)
d. None of the above
a. H, Lea
b. H, B, Lea 11. Which of the following best describes MN antigens and
c. H, B, Lea, Leb antibodies?
d. H, B, Leb a. Well developed at birth, susceptible to enzymes, gen-
5. Transformation to Leb phenotype after birth may be as erally saline reactive
follows: b. Not well developed at birth, susceptible to enzymes,
generally saline reactive
a. Le(a–b–) to Le(a+b–) to Le(a+b+) to Le(a–b+)
c. Well developed at birth, not susceptible to enzymes,
b. Le(a+b–) to Le(a–b–) to Le(a–b+) to Le(a+b+)
generally saline reactive
c. Le(a–b+) to Le(a+b–) to Le(a+b+) to Le(a–b–)
d. Well developed at birth, susceptible to enzymes, gen-
d. Le(a+b+) to Le(a+b–) to Le(a–b–) to Le(a–b+)
erally antiglobulin reactive
6. In what way do the Lewis antigens change during
12. Which autoantibody specificity is found in patients with
pregnancy?
paroxysmal cold hemoglobinuria?
a. Lea antigen increases only
a. Anti-I
b. Leb antigen increases only
b. Anti-i
c. Lea and Leb both increase
c. Anti-P
d. Lea and Leb both decrease
d. Anti-P1
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210 PART II Blood Groups and Serologic Testing

13. Which of the following is the most common antibody 22. A patient with an M. pneumoniae infection will most
seen in the blood bank after ABO and Rh antibodies? likely develop a cold autoantibody with specificity to
a. Anti-Fya which antigen?
b. Anti-k a. I
c. Anti-Jsa b. i
d. Anti-K c. P
d. P1
14. Which blood group system is associated with resistance
to P. vivax malaria? 23. Which antigen is destroyed by enzymes?
a. P a. P1
b. Kell b. Jsa
c. Duffy c. Fya
d. Kidd d. Jka
15. The null Ko RBC can be artificially prepared by which
References
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