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Blood Bank Case Studies Case Studies from the reference laboratory Jackie Ensley, MLS(ASCP) CM SBB 1.

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Presentation on theme: "Blood Bank Case Studies Case Studies from the reference laboratory Jackie Ensley, MLS(ASCP) CM SBB 1."— Presentation transcript:

1 Blood Bank Case Studies Case Studies from the reference laboratory Jackie Ensley, MLS(ASCP) CM SBB 1

2 Present various case studies and describe the approach to serologic problem solving and antibody identification. Determine possible causes of pan-reactivity and steps to resolve complex antibody cases. Briefly review serologic and molecular characteristics of antibodies identified and their respective blood group system, including clinical significance. Explain the various techniques and methods used in the case studies for antibody identification. Objectives 2

3 Antibody detection and identification is a complex problem-solving process Many techs may have a gut-feeling about the antibody before testing completion and intuitively know what needs to be done for antibody identification o Be prepared to reevaluate your hypothesis if testing results do not fit with initial assessment Antibody Identification 3

4 Use the tools available to help you detect and then identify the antibody: o Gel/solid phase o Tube testing: saline/PeG/LISS/albumin/Room temperature/4˚C o Enzymes such as ficin, papain, trypsin o Chemicals such as 0.2M DTT o Adsorption/elution o Reticulocyte/sickle cell separation o Phenotypically similar cells o Antisera/rare antigen negative cells Antibody Identification 4

5 Know phases of reactivity o Some antibodies react best at room temperature/4˚C (M, N, P 1, Lewis, etc) o Some antigens destroyed by enzymes/chemicals (Ficin destroys Fy a, Fy b, M, N, etc) o Enzyme treatment of red cells enhances reactivity of some antibodies such as those in the Rh system, Jk a, Jk b, Le a, Le b, P 1 Know strength/pattern of reactivity o Some antigens show variable antigen expression and some antibodies show variable reactivity and may show dosage, such as -Jk a /-Jk b and -M/-N o Note: different strengths may also indicate more than one antibody is present Antibody Identification 5

6 Besides using the blood bank techniques available to detect the antibody, also keep in mind these tips to aid you in the identification process: o Review patients records, including medication, age, gender, race, diagnosis and transfusion history o Investigate/repeat any inconsistent or contradictory reactions in the patients workup o Phenotype the patient to confirm they are antigen negative for the suspected or identified antibodies Antibody Identification 6

7 Case Study 1 PATIENT HISTORY Female, 51 years old Caucasian Diagnosis: Anemia and GI bleed The patient was seen on 12/12/2013. She typed as A Positive and had a negative antibody screen. She was transfused at that time. Current H/H: 7.7/ 24.8 The hospital reports on 2/14/2014 a positive antibody screen in tubes with LISS (3+) with a positive autocontrol. The DAT/IgG is positive (2+). 4 out of 4 units are crossmatch incompatible. Hospital decides to send to the reference laboratory.

8 Case Study 1 Reference Lab testing: – ABO/Rh performed: – DAT Performed: Anti-AAnti-BAnti-DA1 CellB CellABO/Rh A Positive Anti-IgG/ GelAnti-C3/ Gel 3+0

9 Plasma

10 Rh SystemKellDuffyKiddLewisPMNSLutheran GEL Cell DCcEe Kk Kp a Kp b Js a Js b Fy a Fy b Jk a Jk b Le a Le b P1P1 MNSs Lu a Lu b w Auto 2+

11 Eluate Rh SystemKellDuffyKiddLewisPMNSLutheran GEL Cell DCcEe Kk Kp a Kp b Js a Js b Fy a Fy b Jk a Jk b Le a Le b P1P1 MNSs Lu a Lu b w The Eluate Last Wash is negative

12 Lets look at what we know: – Phase of reactivity: AHG – Strength/pattern of reactivity: pan-reactive, about the same strength. – Patient history: recently transfused – DAT/autocontrol: positive/reactive – Other info: eluate is also pan-reactive with same strength Serologic Problem Solving Question to ask yourself: So where do we go at this point?

13 Narrowed down possibilities: 1.Warm autoantibody 2.Multiple antibodies in plasma (and eluate) 3.Antibody to a high incidence antigen Serologic Problem Solving Question to ask yourself: So where do we go at this point?

14 Next Step: Reference tech decides to perform adsorption on plasma only. Why not an adsorption on the eluate? The patient has been transfused in the last 3 months… Technical Manual States that newly developed antibodies initially detectable only in the eluate are usually detectable in the serum after about 14 to 21 days

15 Blood Bank Technique: Adsorption What is an adsorption? Blood bank technique where red cells and plasma (or eluate) are mixed, causing antibody to be adsorbed onto the red cell surface. Types of Adsorption: Autologous: Patient plasma is mixed with patient cells PATIENT MUST NOT HAVE BEEN TRANSFUSED last 3 months Differential/Allogeneic: Patient plasma is mixed with R1R1, R2R2, and rr donor cells of known phenotypes. Antibodies to high incidence antigens may be adsorbed out

16 How is an alloadsorption performed? Alloadsorption: Patient has been transfused or transfusion is unknown. Patients Plasma + Donor RBCs Incubate together to adsorb the antibodies onto the donor red cells = R1R1 rr R2R2 Blood Bank Technique: Adsorption

17 How is an alloadsorption performed? Incubation allows any antibody to adsorb onto the red cells (alloantibody or autoantibody) = Adsorption Cells- discard Adsorption Plasma- Test R1R1 R2R2 rr Centrifuge the tubes and separate the adsorbed plasma from the red cells for testing

18 How is an alloadsorption performed? R1R1 (D+C+E-c-e+) R2R2 (D+C-E+c+e-) rr (D-C-E-c+e+) Run each adsorbed plasma with panel cells to identify any antibodies. Antibodies in adsorbed plasma will depend on the phenotype of the adsorbing cell. Example: anti-E

19 R1R1 Adsorption Rh SystemKellDuffyKiddLewisPMNSLutheran X2 PeG - Plasma Cell DCcEeKk Kp a Kp b Js a Js b Fy a Fy b Jk a Jk b Le a Le b P1P1 MNSs Lu a Lu b R1R1 Cell Phenotype w

20 R2R2 Adsorption Rh SystemKellDuffyKiddLewisPMNSLutheran X3 GEL-Plasma Cell DCcEeKk Kp a Kp b Js a Js b Fy a Fy b Jk a Jk b Le a Le b P1P1 MNSs Lu a Lu b R2R2 Cell Phenotype w

21 rr Adsorption Rh SystemKellDuffyKiddLewisPMNSLutheran X3 GEL-Plasma Cell DCcEeKk Kp a Kp b Js a Js b Fy a Fy b Jk a Jk b Le a Le b P1P1 MNSs Lu a Lu b r r Cell Phenotype w

22 R1R1 Adsorption Rh SystemKellDuffyKiddLewisPMNSLutheran X2 PeG - Plasma Cell DCcEeKk Kp a Kp b Js a Js b Fy a Fy b Jk a Jk b Le a Le b P1P1 MNSs Lu a Lu b R1R1 Cell Phenotype w

23 Autoantibody Confirmation Testing Patient had been transfused in the last 3 months so need to perform reticulocyte separation – Want to be testing patient cells and not donor cells

24 How is a Reticulocyte Cell Separation Performed? Patient has been transfused so need to separate patient cells from donor red cells Spin the sample down and fill microhematocrit tubes with the red cells. Stopper one end of the hematocrit tube with clay. Blood Bank Technique: Reticulocyte Cell Separation

25 How is a Reticulocyte Cell Separation Performed? Clay Plug Newer Red Cells Older Red Cells Air Excess saline/plasma Buffy Coat Spin the microhematocrit tubes and then cut the tubes to get the reticulocytes Blood Bank Technique: Reticulocyte Cell Separation

26 Autoantibody Confirmation Testing Now that we have the retics: DAT/IgG had been positive so perform DAT/IgG on retics: Retics Anti-IgG/ tube 1+ Can not proceed with testing to identify warm autoantibody until the DAT is negative

27 How do we get the DAT/IgG negative?

28 EGA Treatment What is EGA? – EDTA glycine acid dissociates IgG from red blood cells so the treated red cells can be used for further testing or antigen typing using the AHG phase. – Use when direct antiglobulin phase (DAT) is positive – Does not impair red cell surface antigens Blood Bank Technique: EGA Treatment

29 EGA Treatment The Process – Wash IgG coated red cells thoroughly – Suspend cells briefly in EGA solution to dissociate bound IgG antibody – Bring mixture to neutral pH – Centrifuge and wash cells with saline Test treated cells by performing a DAT Limitation: destroys Kell, Er a, Bg antigens Blood Bank Technique: EGA Treatment

30 Autoantibody investigation EGA testing performed and DAT negative retics obtained To confirm the antibody is warm autoantibody the DAT negative retics are tested against the plasma and eluate: Retics-PlasmaRetics-Eluate Gel 2+3+ This is what was expected if the antibody was autoantibody! Further testing is not required, the warm autoantibody has been confirmed.

31 Antibody Confirmation Lastly need to confirm anti-Jk a (JK1) by antigen typing Use retics so that typing patient cells and not donor cells Anti-Jk Tube 0 Patient types Jk a negative

32 Results Patient has warm autoantibody and anti-Jk a (JK1). Transfusion recommendations: Transfuse Jk a - (JK1), AHG crossmatch least incompatible, red blood cell products.

33 Kidd Blood Group System ·Daniels, G. (2013) Kidd Blood Group System, in Human Blood Groups, 3rd edition, Wiley- Blackwell, Oxford, UK. Located Chromosome 18 Glycoprotein with 10 membrane spanning domains Located Chromosome 18 Glycoprotein with 10 membrane spanning domains Kidd antibodies are often difficult to work with and are a common cause of delayed hemolytic reactions

34 Jk a (JK1) Antibody & Antigen Jk a Antibody Characteristics History1951 Clinical SignificanceYes! Clinically significant ·Transfusion Reactions possible, immediate or delayed hemolytic ·HDN possible, mild to moderate AntibodyIgG/IgM Other facts·Jk a has been demonstrated on fetal cells as early as 11 weeks ·Antibody fades in vitro and in vivo ·Can show dosage Jk a Antigen Characteristics OccurrenceCaucasians 77% Blacks 92% Reid, Marion and Christine Lomas-Francis (2012). The Blood Group Antigen FactsBook, 3 rd Edition, Elsevier.

35 Case Study 2 PATIENT HISTORY Female, 38 years old African American DIAGNOSIS: -Severe Sepsis--blood cultures showed Finegoldia magna (normal flora of the gastrointestinal and genitourinary tract, and can be isolated from skin and the oral; often regarded as a contaminant in cultures) with subsequent cultures after that date with no growth. -Probable pneumonia-Cardiac arrest-Hypertensive -Acute respiratory failure -Acute renal failure-Positive for influenza A

36 Case Study 2 PATIENT HISTORY The patient arrived as in-patient on 1/15/2014 and was typed as B Positive with negative antibody screen. Patient was transfused 2 B Positive RBCs at that time. Patient was monitored and was still very ill On 1/24/2014 patient required another transfusion and sample was sent to hospital blood bank.

37 Case Study 2 The 2 nd sample was collected on 1/24/2014, 9 days after transfusion. Sample was sent to the reference laboratory Hospital Results on 1/24/2014: B Positive All cells reactive 2+ in gel Autocontrol positive

38 Case Study 2 Reference Lab testing: – ABO/Rh performed: – DAT Performed: Anti-AAnti-BAnti-DA1 CellB CellABO/Rh 04+ 0B Positive Anti-IgG/ GelAnti-C3/ tube W+0

39 Plasma

40 Rh SystemKellDuffyKiddLewisPMNSLutheran GEL Cell DCcEe Kk Kp a Kp b Js a Js b Fy a Fy b Jk a Jk b Le a Le b P1P1 MNSs Lu a Lu b W Auto W+

41 Eluate Rh SystemKellDuffyKiddLewisPMNSLutheran GEL Cell DCcEeKk Kp a Kp b Js a Js b Fy a Fy b Jk a Jk b Le a Le b P1P1 MNSs Lu a Lu b W The Eluate Last Wash is negative

42 Lets look at what we know: – Phase of reactivity: AHG – Strength/pattern of reactivity: pan-reactive, same strength. – Patient history: recently transfused – DAT/autocontrol: positive/reactive – Other info: eluate is also pan-reactive with same strength Serologic Problem Solving Question to ask yourself: So where do we go at this point?

43 Narrowed down possibilities: 1.Warm autoantibody 2.Multiple antibodies in plasma and eluate 3.Antibody to a high incidence antigen Serologic Problem Solving

44 Next Step: Reference tech decides to perform adsorptions on plasma & eluate. Why perform an adsorption? To adsorb out suspected warm autoantibody and determine if there are any alloantibodies hiding under the pan-reactivity.

45 R1R1 Adsorption Rh SystemKellDuffyKiddLewisPMNSLutheran X3 GEL- Plasma X3 GEL- Eluate Cell DCcEeKk Kp a Kp b Js a Js b Fy a Fy b Jk a Jk b Le a Le b P1P1 MNSs Lu a Lu b R1R1 Cell Phenotype W

46 R2R2 Adsorption Rh SystemKellDuffyKiddLewisPMNSLutheran X3 GEL-Plasma X3 GEL-Eluate Cell DCcEeKk Kp a Kp b Js a Js b Fy a Fy b Jk a Jk b Le a Le b P1P1 MNSs Lu a Lu b R2R2 Cell Phenotype W

47 rr Adsorption Rh SystemKellDuffyKiddLewisPMNSLutheran X3 GEL-Plasma X3 GEL-Eluate Cell DCcEeKk Kp a Kp b Js a Js b Fy a Fy b Jk a Jk b Le a Le b P1P1 MNSs Lu a Lu b r r Cell Phenotype W

48 Results Appears to be warm autoantibody No alloantibodies were detected in the alloadsorbed plasma or eluate Need to confirm warm autoantibody

49 Autoantibody Confirmation Testing Patient had been transfused 9 days ago so perform reticulocyte separation. DAT/IgG had been positive so perform DAT/IgG on retics: Retics Anti-IgG/ Gel O Proceed with further testing to identify warm autoantibody

50 Autoantibody Confirmation Testing To confirm the antibody is warm autoantibody the retics are tested against the plasma and eluate: Retics-PlasmaRetics-Eluate Gel 00 This is NOT what was expected if the antibody was autoantibody! Further testing is required and now antibody to a high incidence antigen is suspected

51 Narrowed down possibilities: 1.Warm autoantibody 2.Multiple antibodies in plasma and eluate 3.Antibody to a high incidence antigen Serologic Problem Solving Question to ask yourself: So where do we go at this point?

52 Next Step: Use blood bank techniques, reagents and cells to try and determine the antibody

53 Ficin Panel Rh SystemKellDuffyKiddLewisPMNSLutheran GEL GEL-Ficin Cell DCcEeKk Kp a Kp b Js a Js b Fy a Fy b Jk a Jk b Le a Le b P1P1 MNSs Lu a Lu b W Auto W+1+

54 0.2 M DTT Panel Rh SystemKellDuffyKiddLewisPMNSLutheran GEL GEL-0.2M DTT Cell DCcEeKk Kp a Kp b Js a Js b Fy a Fy b Jk a Jk b Le a Le b P1P1 MNSs Lu a Lu b W Auto W+

55 Case Study 2 Ficin and DTT testing has helped narrow down the possibilities. Some high incidence antigens resistant to Ficin and 0.2M DTT Treatment: LanABTIPELUFy3 At a MAMDibGe3Fy5 EmmOk a Wr b En a FREr a Sd a (Ficin enhanced0 Co a CO3Vel (Ficin enhanced) Jr a (Ficin enhanced) Consider the race of patient and start with the easiest to test for The list is not all-inclusive. Refer to The Blood Group Antigen FactsBook by Marion E Reid and Christine Lomas-Francis for support regarding antigen/antibody reactivity.

56 Selected Cells Run Rh SystemKellDuffyKiddLewisPMNSLutheran GEL Donor DCcEeKk Kp a Kp b Js a Js b Fy a Fy b Jk a Jk b Le a Le b P1P1 MNSs Lu a Lu b U D N Rh SystemKellDuffyKiddLewisPMNSLutheran GEL Donor DCcEeKk Kp a Kp b Js a Js b Fy a Fy b Jk a Jk b Le a Le b P1P1 MNSs Lu a Lu b U D N Eluate Testing Plasma Testing Patient is antigen typed with the retics and is U-

57 BioArray Molecular Results Rhc+ DuffyFy a + DombrockDo a 0 C0 Fy b 0 Do b + e+MNSM+ Jo a + E0 N0 Hy+ KellK0 SLSLWLw a + k+ sLS Lw b 0 Kp a 0LutheranLu a 0SciannaSc1+ Kp b + Lu b + Sc20 Js a 0DiegoDi a 0Hemoglobin SHbS0 Js b + Di b +U (-) KiddJk a +ColtonCo a + Jk b + Co b 0

58 Results The antibody is anti-U (MNS5), not a warm autoantibody as was suspected at first.

59 Antigen Negative Units Requested: Two U- (MNS5) units were deglycerolized and sent to hospital Deglycerolization Red cells are frozen with glycerol, a cryoprotective agent that prevents cellular damage and hemolysis as well as allows them to be frozen at < -65°C for 10 years. To deglycerolize, the red cells are warmed and then washed with decreasing % NaCl to remove the glycerol and then suspended for transfusion. Once thawed they have a shelf life of 24 hours (if an open system was used).

60 U (MNS5) Antibody U Antibody Characteristics HistoryAnti-U was first described by Wiener et al in It was called U for the universal distribution of the antigen. Not naturally occuring Clinical Significance·Yes! Clinically significant ·Transfusion Reactions possible, mild to severe ·HDN possible, mild to severe Antibody·IgG, reacts best at 37°C/AHG ·Autoanti-U is possible Other factsSome examples of anti-U are not compatible with all U- red cells. This is because some U- red cells are actually U variant and so have small quantities of U antigen. Reid, Marion and Christine Lomas-Francis (2012). The Blood Group Antigen FactsBook, 3 rd Edition, Elsevier.

61 U (MNS5) Antigen U Antigen Characteristics OccurrenceCaucasians 99.9% Blacks 99% Well developed at birth Other Facts·All U- individuals are S-s- but not all S-s- individuals are U-. ·The S-s- phenotype not common in the Caucasian population ·U negative phenotype is associated with absence of Glycophorin B (GPB) VariantsU variant is possible Sources for further reading: ·Reid, Marion and Christine Lomas-Francis (2012). The Blood Group Antigen FactsBook, 3 rd Edition, Elsevier. ·Daniels, G. (2013) MNS Blood Group System, in Human Blood Groups, 3rd edition, Wiley-Blackwell, Oxford, UK.

62 Genetics and Biochemistry Genes encoding MNS system antigens reside on chromosome 4 – Responsible for the production of glycophorin A (GPA) and glycophorin B (GPB) on red cells

63 Genetics and Biochemistry GPA and GPB are the major sialic acid containing structures of the red cell membrane. Photo Source:

64 U variants S-s-U+ or S-s-U+ var Almost exclusively in those of African Origin About 50% of S-s- are U+ var Strength of expression is variable; adsorption/elution tests may be needed to detect the U antigen Strong correlation of U variant antigen cells being He+ (low frequency MNSs antigen).

65 Reactivity – The anti-U of S-s-U- will react with S-s-U+ var – The anti-U of U variants will not react with S-s-U- cells. GPB of the cell – U- cells are totally GPB-deficient – U variants have a variant GPB molecule that doesnt express S or s U vs U variants

66 Case Study 3 PATIENT HISTORY Female, 65 years old African American DIAGNOSIS: stroke Patient had 45 minute seizure at nursing home before being transported to hospital. Speech was slurred upon arrival to emergency department with facial drooping. Patient has history of seizures, hypothyroidism, GERD, severe anemia, hypertension, congestive heart failure, etc. H/H: 9.9/ 32.1Last transfusion was 10/27/2012 (>3 months)

67 Case Study 3 The sample was collected on 01/30/2013 Sample was sent to the reference laboratory Hospital Results on 1/30/2013: O Positive All cells reactive 2+ in gel Autocontrol not tested Additional history includes anti-Chido and antibody in Knops system from another facility.

68 Case Study Reference Lab testing: – ABO/Rh performed: – DAT Performed: Anti-AAnti-BAnti-DA1 CellB CellABO/Rh Positive Anti-IgG/ tubeAnti-C3/ tube 00

69 Plasma

70 Rh SystemKellDuffyKiddLewisPMNSLutheran GEL Cell DCcEe Kk Kp a Kp b Js a Js b Fy a Fy b Jk a Jk b Le a Le b P1P1 MNSs Lu a Lu b Auto 0

71 Lets look at what we know: – Phase of reactivity: AHG – Strength/pattern of reactivity: pan-reactive, different strengths. – Patient history: not recently transfused – DAT/autocontrol: negative Serologic Problem Solving Question to ask yourself: So where do we go at this point?

72 Narrowed down possibilities: 1.One antibody with different strengths 2.Multiple antibodies in plasma Keep in mind that patient has history of anti- Chido or antibody in Knops system Serologic Problem Solving Question to ask yourself: So where do we go at this point?

73 Next Step: Use blood bank techniques, reagents and cells to try and determine the antibody

74 Patient phenotype Rhc+DuffyFy a 0 C0 Fy b 0 e+MNSM+ E+ N0 KellK0 S0 KiddJk a + s+ Jk b 0LewisLe a 0 Le b +

75 Some of the Selected Cells Rh SystemKellDuffyKiddLewisPMNSLutheran GEL DCcEe Kk Kp a Kp b Js a Js b Fy a Fy b Jk a Jk b Le a Le b P1P1 MNSs Lu a Lu b Co(b+) w Co(b+) 1+

76 Ficin Panel Rh SystemKellDuffyKiddLewisPMNSLutheran GEL GEL- Ficin DCcEe Kk Kp a Kp b Js a Js b Fy a Fy b Jk a Jk b Le a Le b P1P1 MNSs Lu a Lu b w Auto 00

77 0.2M DTT Panel Rh SystemKellDuffyKiddLewisPMNSLutheran GEL GEL-Ficin GEL-DTT DCcEe Kk Kp a Kp b Js a Js b Fy a Fy b Jk a Jk b Le a Le b P1P1 MNSs Lu a Lu b w Auto 00

78 Patient History anti-Chido Knops Reactivity FicinDTT NegativeReactive Reactivity FicinDTT WeakenedNegative

79 Knops System AntigenOccurrence Caucasian Occurrence Blacks Kn a 98%99% Kn b 4.5%<.01% McC a 98%94% McC b 0%45% Sl a (Sl1) 98%50-60% (30% West Africans) Yk a 92%98% Vil (Sl2) 0%80% Sl3 100% Reid, Marion and Christine Lomas-Francis (2012). The Blood Group Antigen FactsBook, 3 rd Edition, Elsevier.

80 Available Selected Knops Cells Rh SystemKellDuffyKiddLewisPMNSLutheran GEL DCcEe Kk Kp a Kp b Js a Js b Fy a Fy b Jk a Jk b Le a Le b P1P1 MNSs Lu a Lu b Yk(a-) Sl(a-) Appears to be anti-Sl a but due to known weak reactivity of the antibody do molecular to confirm

81 Molecular Testing Rhc+ MNSM+ DombrockDo a 0 C0 N0 Do b + e+ S0 Jo a + E+ s+ Hy+ KellK0LutheranLu a 0LWLw a + k+ Lu b + Lw b 0 Kp a 0DiegoDi a 0SciannaSc1+ Kp b + Dib+ Sc20 Js a 0 CromerCr a + Js b +ColtonCo a +Knops Kn a + Kn b 0 KiddJk a + Co b 0 McC a + Jk b 0 CartwrightYt a + McC b 0 DuffyFy a 0Yt b 0 Sl10 Fy b 0Hemoglobin SHbS0 Sl2+

82 Knops System Knops antigens are located on complement receptor 1 (CR1) CR1 gene resides on chromosome 1

83 Complement Receptors

84 What is CR1 (CD35)? CR1 is a glycoprotein on cells that binds particles coated with C3b and C4b Neutophils and monocytes then phagocytize those particles and processes the immune complexes. These are transported to the liver/spleen for removal from circulation. Has inhibitory effect on complement activities by classical and alternative pathways so it protects the red cells from autohemolysis

85 What is CR1 (CD35)? https://www.inkling.com/read/the-immune-system-peter-parham-3rd/chapter-9/antibody-production-by-b

86 Knops system Structure of CR1 glycoprotein (CD35)

87 Knops system characteristics Variation in antigen strength, related to CR1 red cell levels Generally, a reduction in antigen strength with storage of red cells as the CR1 copy per RBC may be decreased in stored samples High titer low avidity (HTLA) has been used to describe the antibodies Difficult to adsorb out antibodies Can be hard to distinguish antigen negative from weakly positive cells Clinically benign but can mask other significant antibodies

88 Knops System Null phenotype: Kn(a-b-), McC(a-), Sl(a-), Yk(a-) aka Helgeson type Knops antigens can be depressed in cutaneous lupus erythematosus (CLE) Cold Hemagglutinin Disease (CHAD) Paroxysmal nocturnal hemoglobinuria (PNH) hemolytic anemiainsulin-dependent diabetes AIDS some malignant tumors any condition with increased clearance of immune complexes

89 Sl a antibody Sl a Antibody Characteristics HistoryReported in 1980 and named after Swain and Langely, the first two antibody producers. Clinical SignificanceNo! Clinically insignificant ·No Transfusion Reactions ·No HDN Antibody·IgG, reacts best at 37°C/AHG Other factsMay be confused with anti-Fy3 because most Fy(a-b-) red cells are likely to be Sl(a-). Common antibody made by blacks. Reid, Marion and Christine Lomas-Francis (2012). The Blood Group Antigen FactsBook, 3 rd Edition, Elsevier.

90 Sl a antigen Sl a Antigen Characteristics Occurrence98%50-60% (30% West Africans) Other FactsAlso known as Sl1 Disease processes causing red cell CR1 deficiency can lead to false negative antigen typing. Also, variability in antigen strength has been described. Sources for further reading: ·Reid, Marion and Christine Lomas-Francis (2012). The Blood Group Antigen FactsBook, 3 rd Edition, Elsevier. ·Daniels, G. (2013) MNS Blood Group System, in Human Blood Groups, 3rd edition, Wiley-Blackwell, Oxford, UK.


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