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Unit 9 Other Blood Group Systems Part 1

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  1. Unit 9 Other Blood Group SystemsPart 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 • 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 • Row 1 of reactions confirms anti-I • Row 2 of reactions indicates some “other” alloantibody.

  15. Prewarmed Technique • 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.

  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

  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

  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 NOTimplicated 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 • 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.

  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) • 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

  30. P1 • Strength of the P1antigenvaries 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-P1has rarely been reported to cause hemolysis in vivo.

  32. Neutralization of P1 Antibodies • Hydatid cyst fluid or P1 substance derived from pigeon eggsinhibits 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

  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. • Wikipedia, http://tinyurl.com/4jysjyc