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Unit 9 Other Blood Group Systems Part 1

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1 Unit 9 Other Blood Group Systems Part 1
Terry Kotrla, MS, MT(ASCP)BB

2 Introduction ISBT recognizes 30 blood group systems with over 600 antigens. Some VERY rare only found in certain ethnic groups. Some associated with diseases or resistance to infection. Most important are ABO and D “High incidence”, “public” or “high frequency” antigens are those present on almost every person’s red blood cells “Low incidence”, “private” or “low frequency” antigens are present on very, very few individuals red blood cells

3 Introduction Each known antigen initially identified through the detection of its specific antibody in the serum. Knowledge of serologic behavior and characteristics of blood group antibodies is CRITICAL for identification

4 Introduction Essential when evaluating antibody screen and panel studies. Considerations given to: Phase of reactivity Antibody class involved Ability to cause HDFN and HTR

5 Introduction Clinically insignificant Clinically significant
Reactive in-vitro at IS IgM class In-vivo- NO hemolysis/decreased RBC survival Clinically significant Reactive in-vitro at 37C and/or AHG IgG In-vivo implicated in HDFN and/or HTR.

6 Introduction For each blood group system you MUST know:
Antigen development, if important. Antibody class usually involved. Phase of reactivity in in-vitro tests. Clinical significance. Whether donor units must be antigen negative. Any unique characteristics of the blood group antigens and/or antibodies.

7 Introduction Most textbooks will divide discussion of the blood groups into two distinct groups: Cold reacting, considered nuisance, IgM Warm reacting, considered significant, IgG If you know the phase of reactivity you will know the antibody class involved AND the clinical significance.

8 I/i Blood Group (ISBT 027) Related to ABO and Lewis by its biochemical structure Two antigens: I and i Fetal RBCs rich in i antigen and lack I antigen. First 2 years I develops, lose i Anti-I reacts most strongly with adult cells, negative or weakly with cord RBCs Strength of I antigen varies on adult cells Rare instances I never develops.

9 I/i Blood Group Anti-I is associated with cold agglutinin hemagglutinin disease Decreased expression of I and increased expression of i antigens is observed in: oncogenesis, thalassemias, sickle cell anemias, associated with congenital cataracts in Asian populations.

10 I Antibodies Cause of non-specific agglutination in tests performed at RT Positive reactions with all cells tested: reverse, antibody screen and crossmatches regardless of ABO blood group May cause ABO discrepancy Can be detected in serum of most normal adults if serum is tested at 4C Associated with atypical pneumonia caused by M. pneumoniae , cold agglutinin titers used to monitor the disease. May cause hemolytic anemia when present in high titers

11 Anti-i Anti-i associated with certain diseases
Infectious mononucleosis Epstein-Barr virus Cytomegalovirus This antibody is rarely encountered

12 Clinical Significance of Anti-I
Usually benign Clinically significant examples seen in Cold Agglutinin Syndrome (CAS) Antibodies are of high titer (1000>) High thermal amplitude Cause hemolytic anemia Transfuse blood through blood warmer Cannot cause HDFN – TWO REASONS Antibody class is IgM Antigen not well developed on fetal RBCs Does not cause HTR

13 Serological Confirmation of Anti-I
Test serum agains 3 adult group O RBCs and 3 group O cord RBCs and an auto-control Adult cells and auto-control = positive Cord RBCs = negative/very weak positive Reactivity enhanced using enzyme treated cells

14 Serological Confirmation of Anti-I
O Cord O Adult AC 0/+w 4+ Row 1 of reactions confirms anti-I Row 2 of reactions indicates some “other” alloantibody.

15 Prewarmed Technique AHG Screen 1 Screen 2 Screen 3 Original 3+
Prewarmed technique will eliminate reactivity of most examples Original reactions at AHG Prewarmed 1 – no other alloantibody present. Prewarmed 2 – alloantibody present which must be identified. AHG Screen 1 Screen 2 Screen 3 Original 3+ Prewarmed 1 Prewarmed 2 2+

16 Cold Autoabsorption of Anti-I
Very strong examples of anti-I may react at AHG and require cold autoabsorption or rabbit erythrocyte stroma test (REST) to rule out presence of other antibodies. Collect EDTA blood samples, place at 37C Harvest EDTA cells, wash with 37C saline Place clotted blood sample at 4C, separate serum Add 1 mL serum to 1mL rbcs, incubate at 4C for 1 hour Harvest serum and test against screen cells, if negative, continue screen, if positive repeat absorption with new aliquot of RBCs.

17 Lewis System (ISBT 007) Identified in 1946 and named after antibody maker, Mrs. Lewis. Major antigens Lea and Leb , other antigens include Lec, Led and Lex

18 Lewis Antigenic Development
Antigens ARE NOT intrinsic to RBCs but are absorbed from the plasma and inserted into RBC membrane. Genetic control reside in single gene “Le” Amorph le, if homozygous will not have Lewis antigens Lea formed first, then modified to form Leb which is adsorbed preferentially over Lea Lewis phenotype of RBC can be changed by incubating with plasma containing Lea or Leb glycoplipid.

19 Lewis System Lewis Phenotypes and Their Frequencies White Black
Le (a+b-) 22% 23% Le (a-b+) 72% 55% Le (a-b-) 6% Le (a+b+) Rare rare

20 Lewis System Lewis antigens in infants
Antigens absent or extremely weak at birth Expression of Leb is gradual Birth Le (a-b-) 2 months Le(a+b-) 12 to 18 months Le(a+b+) 2 to 3 years Le (a-b+) Lewis antigens cannot be used for paternity testing on infants.

21 Lewis Antigens and Pregnancy
Antigen strength may decline dramatically during pregnancy. Transiently Le (a-b-) may produce Lewis antibodies during pregnancy. Antigens return after delivery and antibodies disappear.

22 Interaction of Le, Se and H Genes
The le, h and se genes are amorphs and produce no detectable products. lele will not have Lewis antigens, but if Se present will have A, B and H in secretions Genotype se/se and have one Lewis gene will have Lea in their secretions but no A, B or H.

23 Lewis System Le (a+b-) Le (a-b+) Le (a-b-) Lewis Phenotype
ABH Secretor Lewis Secretor Le (a+b-) All ABH NON-Secretors All Lea Secretors Le (a-b+) All ABH secretors All secretors of Lea and Leb Le (a-b-) 80% ABH secretors 20% ABH NON secretors NONE

24 Lewis Antibodies Naturally occurring, NOT clinically significant
Almost always IgM React most often at RT Agglutination relatively fragile, easily dispersed May cause ABO discrepancy if reverse cells have Lewis antigen. Occur almost exclusively in Le (a-b-) and production of anti-Lea AND –Leb not unusual Anti-Lea frequently encountered, anti-Leb rarely encountered.

25 Lewis Antibodies Although most react at RT reactivity may be seen at 37C, but is weaker and may be weakly reactive at AHG Can bind complement and cause IN-VITRO hemolysis, most often with enzyme treated cells Antibodies NOT implicated in HDFN – TWO REASONS Antibodies are IgM and Antigens are poorly developed at birth

26 Lewis Antibodies Can be neutralized in-vitro by addition of Lewis Substance Le antigens are present in secretions Add to serum with Lewis antibodies and the antibodies will be bound to the soluble Lewis antigens Useful when multiple antibodies are present and one is a Lewis, eliminates the reactivity of the antibody

27 Lewis Neutralization S1 S2 S3 Original 2+ Le Substance – only Le Ab
Row 2 antibody reacting with S1 and S3 which are Lewis positive. Row 2 indicates antibody was neutralized by Lewis substance, no other antibodies present. Row 3 indicates additional antibody present. S1 S2 S3 Original 2+ Le Substance – only Le Ab Le Substance-Le and additional Ab 1+

28 Lewis Antibodies - Transfusion Practice
Transfused RBCs will acquire the Lewis phenotype of the recipient within a few days Lewis antibodies in patient will be neutralized by Lewis substance in donor plasma Lewis antibodies rarely cause in-vivo hemolysis It is not necessary to phenotype donors for Lewis antigens prior to transfusion, give crossmatch compatible

29 P Blood Group (ISBT 003) Whites Blacks P1 79% 94% P2 21% 6%
Discovered 1927 when Landsteiner immunized rabbits with human RBCs Initially named “P” but as complexity of P blood group was discovered renamed “P1” RBCs lacking P1 are P2 Other P phenotypes exist but are rare(<1%): P, P1k and P2k Whites Blacks P1 79% 94% P2 21% 6%

30 P1 Strength of the P1 antigen varies among different RBC samples and antigen strength reported to diminish when RBCs are stored. Characteristics creates difficulties, both in testing RBCs for the antigen and in the identification of the antibody. Anti-P1 blood typing reagents usually sufficiently potent to detect weak forms of the antigen. An antibody that is weakly reactive at RT testing can often be shown to have anti-P1 specificity by lowering the incubation temperature or using enzyme treated RBCs.

31 Anti-P1 The sera of P2 persons commonly contain anti-P1.
The antibody reacts optimally at 4 C but may occasionally be detected at 37 C. Rarely may cause in-vitro hemolysis. As it is nearly always IgM, it does not cross the placenta and has not bee reported to cause HDFN (antigen poorly expressed on fetal cells). Anti-P1 little clinical significance unless reactive at 37 C. Anti-P1 has rarely been reported to cause hemolysis in vivo.

32 Neutralization of P1 Antibodies
Hydatid cyst fluid or P1 substance derived from pigeon eggs inhibits the activity of anti-P1. Neutralization or inhibition is a useful aid to the identification of anti-P1, especially if the antibody is present in a serum with multiple antibodies. The anti-P1 is neutralized (becomes non-reactive) revealing other specificities (if present).

33 Neutralization of P1 Antibodies
Row 1 – original testing Row 2 – antibody successfully neutralized, no underlying antibody. Row 3 – presence of additional antibody S1 (P1 pos) S2 (P1 neg) S3 (P1 pos) Original 2+ 1+ Neutralized

34 Transfusion Practice P
Clinically insignificant RT agglutinin. Not necessary to provide antigen negative blood. Must be crossmatch compatible. If reactive at 37C or AHG select crossmatch compatible blood.

35 References AABB Technical Manual, 2008.

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