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Chapter 6: Other Blood Group System

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ISBT defines 23, most clinically significant. Some are more significant that others based on their reactivity ... Biochemistry of the Duffy antigen: ... – PowerPoint PPT presentation

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Title: Chapter 6: Other Blood Group System


1
Chapter 6 Other Blood Group System
2
  • gt 200 Unique antigens on the RBC
  • ISBT defines 23, most clinically significant
  • Some are more significant that others based on
    their reactivity
  • To identify antibodies one must know if
  • Clinically significant-can it cause a transfusion
    reaction.
  • Is it IgG or IgM form
  • Optimal reaction temperature 37º or 22º
  • Optimal phase of reaction
  • Enhancement enzyme activity

3
  • The different optimal phases
  • IS agglutination observed at immediate spin
  • 4ºC agglutination observed at 4ºC incubation
  • RT Room temperature agglutination
  • 37ºC Agglutination enhanced on incubation at
    37ºC.
  • AHG agglutination enhanced in IAT or addition of
    AHG

4
  • Enzyme (papain or ficin) can effect the
    antibodies activity by
  • No significant strength
  • Increase the strength
  • No agglutination agglutination dispersed
  • Variable reaction
  • The RBC has various functions with the body and
    in relation to blood banking and the possession
    of certain antigens are microbial receptors
    (Duffy)

5
  • Kell system
  • Discovered in 1946- Coombs
  • Associated with HDN- IgG, developed at birth
  • Antigens are termed Kell antigens (K and k)
  • Antibodies anti-K and anti-k
  • Various forms of the Kell antigens (22 RBC
    antigens).
  • k or k2- originally Cellano- high frequency
    antigen in 1949 (99.8)
  • Kpa or K3 (Penny)- low frequency antigen (2)
  • Kpb or K4 (Rautenberg)- High frequency antigen
    (99.9)

6
  • Jsa or K6 (Sutter) and Jsb or K7 (Matthews) low
    frequency antigen and added to the Kell system
    later.
  • Six significant antigens that are defined by 3
    pair of linked alleles
  • Kk
  • Kpa Kpb
  • Jsa Jsb
  • K, Kpa and Jsa are low frequency antigens, rare
    and usually not a problem to find antigen
    negative blood products for these antigens.

7
  • High Frequency antigens of the Kell system are
    k, Kpb and Jsb
  • Found almost on all RBC, antibodies rarely found.
  • Difficult to find antigen neg blood products if
    individual has antibody.
  • 4,000 18,000 Kell antigen sites per RBC
  • Sensitive to treatment with sulfhydryl reagents
    such as
  • 2-ME (2-mercaptoethanol)
  • DTT (dithiothreitol)
  • AET ( 2- aminoethylosothiouroniium bromide)

8
  • Kell system immunogenicity
  • Strongly immunogenic
  • 2nd to the D antigen in immune response
  • Kº or Kell null antigens
  • Phenotype lacking the expression of Kell
    glycoprotein's
  • Homozygous inheritance pattern
  • X-linked from the mother
  • Table 6-1, pg 128

9
  • Characteristics of Kell antibodies
  • IgG class
  • Antibodies produces from exposure
  • Agglutinate optimally at IAT
  • Associated with Transfusion reaction and HDN
  • No enhancement with enzyme treatment
  • LISS depress the reactivity.
  • Anti-K or K1 is the most commonly observed
    antibody.

10
  • Other antigens and antibodies associated with
    the Kell system
  • XK or 019
  • Kx is phenotypically related to Kell system
  • McLeod Phenotype
  • Abnormal cell, lacks Kx antigen on RBC
  • Decrease survival of RBC- Hemolytic anemia,
    acanthocytes formation
  • Associated with various disease.

11
  • Duffy system (Fya and Fyb)
  • Discovered in 1950
  • Well developed on fetal cells
  • Destroyed by enzyme treatment
  • Table 6-39 (population frequency) and
  • 6-4, pg 131
  • White population (Fya, Fyb)
  • Black population (Fya-, Fya-)

12
  • Biochemistry of the Duffy antigen
  • Their membrane make-up makes them sensitive to
    proteolytic degradation by the enzymes ficin and
    papain. (destroys the antigen).
  • Duffy and Malarial disease
  • Individuals that posses the antigen phenotype
    Fy(a-b-) are resistant to certain malarial
    diseases.
  • P. Knowlesi and P. Vivax

13
  • Kidd system
  • Characteristic alleles Jka, Jkb and Jk
    (silent gene JkJk or Jka-Jkb-)
  • Alloantibodies produced in response to antigens
    cause significant clinical reaction.
  • Antibody titers rise quickly after exposure and
    plummet to undetectable levels.
  • Cause delayed hemolytic reactions and
    extravascular hemolysis.
  • May be present in combination of other
    antibodies.
  • Require AHG technique to detect
  • Enhance activity with LISS and PEG

14
  • Lutheran blood group
  • Comprised of 18 antigens (numbered LU1-LU20,
    includes Auberger antigens-Aua, Aub)
  • Weakly expressed on Cord Blood
  • High frequency antigen
  • 2 primary antigens Lua and Lub, we do find
    antibodies occasionally to these antigens.
  • Lua and Lub are resistant to enzyme treatment
  • Lu(a-b) is found in highest frequency
  • Dosage effect
  • Linked to Se (secretor locus)

15
  • Lutheran antibodies (anti-Lua and anti-Lub)
  • Anti-Lua may be present without RBC stimulation
  • IgM and IgG forms
  • Room temperature reactivity
  • Mix field agglutination
  • Not clinical significant
  • Anti-Lub rare antibody because it is a high
    frequency antigen
  • IgG form, AHG phase, MF pattern

16
  • Lewis Blood Group
  • Found primarily in secretions and plasma-they are
    not integral parts of the RBC membrane-they are
    adsorbed.
  • Development begins after birth and up to 6 years
    old. Newborns RBC possess the Le(a-b-) phenotype
    then may transition to Le(ab) until final
    designation of Le(a-b)
  • Similar to the ABO system in it is dependent on 3
    sets of inherited genes. (H, Se and Le)
  • Not clinically significant (IgM antibody),
    usually show-up at RT agglutination, but can show
    up at 37 or AHG.

17
  • Ii Blood Group System
  • Present on both glycoprotein and glycolipid
    structures of the RBC membrane.
  • Found as soluble glycoprotein antigens in plasma
    and body secretions
  • I is not well developed until adult age
  • IgM antibody
  • Not clinically significant, cold reacting,
    pre-warm technique will disperse agglutination
  • Will react stronger in the present of more H
    antigens.
  • Diseases associated with Ii Mycoplasma
    Pneumonia, Cold hemaagglutinin, Mononucleosis,
    lymphoproliferative disorders pose a problem.

18
  • P Blood Group System
  • Antigens P, Pk and Luke
  • Structurally related to the A,B, and H antigens.
  • P1 is present in soluble form (secretions)
  • Most common phenotype of the P system is P1 and
    P2.
  • P1 individuals have P and P1 antigens present on
    the RBC
  • P2 express only P antigens and may produce anti-P1

19
  • P1 is poorly developed at birth
  • Antigen expression weakens or deteriorates upon
    storage.
  • Soluble forms detectable in plasma and hydatid
    cyst fluid.
  • P, Pk and LKE
  • High frequency antigens, antibodies not a problem

20
  • P system inheritance thru 2 independently
    inherited genes or alleles.
  • Locus 1 P1k, PK and p
  • Locus 2 P2 and P2.0
  • Autoanti-P associated with immune hemolytic
    anemia- Paroxysmal Cold Hemoglobinuria.
  • IgG antibody known as the Donath-Landsteiner ,
    binds to P() RBC at low temps.
  • Biphasic hemolysis
  • Seen in children with viral infection and adults
    with tertiary syphilis
  • May cause a () DAT because of the complement

21
  • Anti-P
  • Seen in serum of P2
  • IgM
  • Enzyme enhanced
  • Use P1 substance to neutralize the antibody
  • If x-match ok at 37 and IAT negative-give the
    blood.

22
  • MNS blood group system
  • Includes 40 antigens on the RBC
  • Inheritance 1 gene codes for M or N and the
    another for S and s.
  • The most frequent haplotype is Ns, followed by
    Ms, MS and NS.
  • GLycophorin A codes for M and N antigens and
    Glycophorin B codes for S and s

23
  • M and N antigens
  • Homozygous inheritance pattern influences
    agglutination such as MN- or M-N
  • S and s antigens
  • Based on differ amino acid
  • U inherited with S or s

24
  • M, N, S antibodies
  • Anti-M
  • IgG and IgM form
  • Occurs naturally
  • Not clinically significant (except at AHG)
  • Reacts better at 6.5 pH
  • Marked dosage effect

25
  • Anti-N
  • IgM
  • Cold reacting
  • N-like substance identified in dialysis patients
    from exposure to formaldehyde in cleaning the
    tubing or membrane.
  • Anti-S,s and U
  • IgG Clinically significant
  • HDN
  • U is high incident antigen- 99 population .

26
  • Chapter 7 Antibody detection and I.D.
  • Antibody screen are used to detect atypical and
    unexpected antibodies
  • Antibodies other than ABO
  • Produced from previous transfusion or exposure
  • Alloantibodies vs auto antibodies
  • To determine specificity or antibody I.D. you
    must know the typical characteristics

27
  • Antibody detection starts with the antibody
    screen.
  • Antibody screen 2 cell or 3 cell reagent based
    testing phase (reagent RBC)
  • Difference in 2 vs 3 cell 3 cell provide rr,
    homozygous duffy and kidd identification.
  • Perform IAT to detect IgG and Complement
    antibodies
  • DAT detects in vivo sensitization of RBC (HDN,
    Transfusion reaction, autoimmune hemolytic
    reaction, drug induced hemolytic reaction).

28
  • 3 phases of the IAT
  • Immediate spin (M, N, S, Lea, Leb, P1)
  • 37ºC incubation (Kell, Rh, Kidd, Duffy)
  • AHG (Lewis)
  • AABB require that a 37ºC and AHG phase are
    performed on all specimens.
  • Autocontrol Pts. Serum in addition to pts RBC
    and a poteniator- carried out through all 3
    phases.

29
  • Potentiators used include (based on pt.
    population and workload)
  • LISS (most common)
  • BSA (works well to enhance Rh system)
  • PEG (IgM and warm autoantibodies)
  • Papain and Ficin (good for complex antibody
    problems)
  • Medical history and demographics important when
    investigating.

30
  • Antibodies detected in IAT
  • IgM Primary response antibody, Macromolecule,
    highly effective agglutinin, activates
    complement, NO HDN, Reacts at RT or decreased
    temps., usually not clinically significant.
  • IgG Secondary response antibody, clinically
    significant, cross placenta, requires enhancement
    media, 37ºC, AHG phase of testing.

31
  • Population that need antibody screens
  • Prenatal
  • Transfusion candidates
  • Donor blood product
  • Purpose of antibody screen to identify any
    antibodies that might be present to interact
    with antigens present on RBC.

32
  • Antibody Identification
  • Once an antibody screen is positive, an antibody
    identification test is performed.
  • Consist of a panel of cells with known antigens
    present. (Series of reagents cells 1- 16)
  • Routinely tested in the same manner as the
    antibody screen. (RT, 37 and AHG) and results
    recorded for each cell reaction.
  • Auto control tube is used.
  • Results for each cell is recorded as or and
    strength of reactions, hemolysis must be noted
    also.

33
  • Once testing is complete we must interpret the
    results.
  • Perform antigen elimination by crossout method.
  • Start with a straight edge or ruler and find the
    first cell that is negative throughout all the
    reactions phases (IS, 37 and AHG).
  • Then go across the panel antigen profile and
    wherever a homozygous expression of an antigen
    appears (in the same line from above), cross that
    antigen out at the top of the sheet. This
    eliminates the crossed out antigen. Continue
    doing this until all cell that are completely
    negative at the reaction phases.

34
  • The antigens that has not been eliminated should
    match the pattern for the corresponding antibody
    reaction.
  • Reaction strengths suggest homozygous vs
    heterozygous presence and multiple antibodies.
  • Rule of three, there must be at least three
    antigens red blood cell that react and three
    antigen negative RBC that do not react to
    consider the identification.

35
  • Phenotype helps rule out complex and multiple
    antibody situations.
  • Select specific antigens to rule out or rule in
    the antibody.
  • Test patients RBC to make sure they are negative
    for antigen corresponding to Identified antibody.
  • Multiple antibodies
  • Use auto control
  • See variation of strength and reaction phase
  • Use protoelytic enzyme treatment to eliminate or
    enhance reactions

36
  • Additional testing
  • DTT (Dithiothreitol Treatment)
  • High Titer Low avidity
  • Typically weal
  • May be diluted out
  • May react in AHG
  • Not enhanced by potentiators
  • Can mask the clinically significant antibodies.

37
  • Antibodies of Low Frequency
  • Seen in a panel with one one reactive cell
  • Associated with Anti- Cw, Wra, V, Co, Bga, Kpa,
    Lua
  • Pg. 169, Table 7-4
  • When performing cross match, if no significant
    problem seen in AHG phase of crossmatch, may
    transfuse the patient

38
  • Enhancing Weak antibodies- IgG
  • Usually difficult to I.D. because of the weak
    reaction pattern.
  • Use enhancement to strengthen reactions.
  • Cold alloantibodies (IgM)
  • React at IS or RT
  • Clinically insignificant
  • If test is Okay at the AHG ant 37 ºC phase may
    transfuse.
  • Neutralization or inhibition technique
  • Prewarmed or enzyme to get rid of the antibody.

39
  • Autoantibodies
  • Need differentiate alloantibodies for
    autoantibodies
  • Serological technique
  • Adsorption
  • Absorption
  • Clues to Autoantibody
  • () DAT or autocontrol (table 7-6)
  • Patients Diagnosis
  • Medication history

40
  • Cold Autoantiibodies
  • Result of complement coated RBC and panel cells
    that react at R.T.
  • See discrepancy in forward and reverse grouping.
  • Specificity
  • Perform a cold panel-select panel of cold react
    antibodies to identify the specific antibody
    causing the problem. (Most common I, H, IH)

41
  • Warm antibody characteristics (table 7-9)
  • Cold antibody Characteristics (table 7-9)
  • Eluate Methods (table 7-10)
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