Presentation on theme: "Blood Bank Case Studies"— Presentation transcript:
1 Blood Bank Case Studies Case Studies from the reference laboratoryJackie Ensley, MLS(ASCP)CMSBB
2 ObjectivesPresent 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.
3 Antibody Identification Antibody detection and identification is a complex problem-solving processMany techs may have a “gut-feeling” about the antibody before testing completion and intuitively know what needs to be done for antibody identificationBe prepared to reevaluate your hypothesis if testing results do not fit with initial assessment
4 Antibody Identification Use the tools available to help you detect and then identify the antibody:Gel/solid phaseTube testing: saline/PeG/LISS/albumin/Room temperature/4˚CEnzymes such as ficin, papain, trypsinChemicals such as 0.2M DTTAdsorption/elutionReticulocyte/sickle cell separationPhenotypically similar cellsAntisera/rare antigen negative cells
5 Antibody Identification Know phases of reactivitySome antibodies react best at room temperature/4˚C (M, N, P1, Lewis, etc)Some antigens destroyed by enzymes/chemicals (Ficin destroys Fya, Fyb, M, N, etc)Enzyme treatment of red cells enhances reactivity of some antibodies such as those in the Rh system, Jka, Jkb, Lea, Leb, P1Know strength/pattern of reactivitySome antigens show variable antigen expression and some antibodies show variable reactivity and may show dosage, such as -Jka/-Jkb and -M/-NNote: different strengths may also indicate more than one antibody is present
6 Antibody Identification Besides using the blood bank techniques available to detect the antibody, also keep in mind these tips to aid you in the identification process:Review patient’s records, including medication, age, gender, race, diagnosis and transfusion historyInvestigate/repeat any inconsistent or contradictory reactions in the patient’s workupPhenotype the patient to confirm they are antigen negative for the suspected or identified antibodies
7 Case Study 1 Female, 51 years old Caucasian PATIENT HISTORYFemale, 51 years oldCaucasianDiagnosis: Anemia and GI bleedThe patient was seen on 12/12/ She typed as A Positive and had a negative antibody screen. She was transfused at that time.Current H/H: 7.7/ 24.8The 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/Rh4+A PositiveAnti-IgG/ GelAnti-C3/ Gel3+
9 Plasma + 2+ 1+ D C c E e K k AHG-PeG Cell I II III Auto Room Temp Kpa Rh SystemKellDuffyKiddLewisPMNSLutheranRoom TempAHG-PeGCellDCcEeKkKpaKpbJsaJsbFyaFybJkaJkbLeaLebP1MNSsLuaLubI+2+II1+IIIAuto
10 Plasma + 2+ w D C c E e K k M N S s Rh System Kell Duffy Kidd Lewis P Rh SystemKellDuffyKiddLewisPMNSLutheranGELCellDCcEeKkKpaKpbJsaJsbFyaFybJkaJkbLeaLebP1MNSsLuaLub1+2+234567891011wAuto
11 Eluate + 3+ w The Eluate Last Wash is negative D C c E e K k M N S s Rh SystemKellDuffyKiddLewisPMNSLutheranGELCellDCcEeKkKpaKpbJsaJsbFyaFybJkaJkbLeaLebP1MNSsLuaLub1+3+234567891011wThe Eluate Last Wash is negative
12 Let’s look at what we know: Serologic Problem SolvingQuestion to ask yourself: So where do we go at this point?Let’s look at what we know:Phase of reactivity: AHGStrength/pattern of reactivity: pan-reactive, about the same strength.Patient history: recently transfusedDAT/autocontrol: positive/reactiveOther info: eluate is also pan-reactive with same strength
13 Narrowed down possibilities: Warm autoantibody Serologic Problem SolvingQuestion to ask yourself: So where do we go at this point?Narrowed down possibilities:Warm autoantibodyMultiple antibodies in plasma (and eluate)Antibody to a high incidence antigen
14 Why not an adsorption on the eluate? 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 cellsPATIENT MUST NOT HAVE BEEN TRANSFUSED last 3 monthsDifferential/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? Blood Bank Technique: AdsorptionAlloadsorption: Patient has been transfused or transfusion is unknown.R1R1=R2R2rrIncubate together to adsorb the antibodies onto the donor red cellsPatient’s Plasma +Donor RBC’s
17 How is an alloadsorption performed? R1R1Adsorption Cells- discardAdsorption Plasma- TestR2R2=rrIncubation allows any antibody to adsorb onto the red cells (alloantibody or autoantibody)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+)Example: anti-EExample: anti-ERun each adsorbed plasma with panel cells to identify any antibodies. Antibodies in adsorbed plasma will depend on the phenotype of the adsorbing cell.
19 R1R1 Adsorption w + 0√ 1+ 2+ D C c E e K k M N S s Rh System Kell Rh SystemKellDuffyKiddLewisPMNSLutheranX2 PeG- PlasmaCellDCcEeKkKpaKpbJsaJsbFyaFybJkaJkbLeaLebP1MNSsLuaLubR1R1 Cell Phenotype+10√21+342+567891011w
20 R2R2 Adsorption w + 0√ D C c E e K k M N S s Rh System Kell Duffy Kidd Rh SystemKellDuffyKiddLewisPMNSLutheranX3 GEL-PlasmaCellDCcEeKkKpaKpbJsaJsbFyaFybJkaJkbLeaLebP1MNSsLuaLubR2R2 Cell Phenotype+10√234567891011w
21 rr Adsorption w + 0√ D C c E e K k M N S s Rh System Kell Duffy Kidd Rh SystemKellDuffyKiddLewisPMNSLutheranX3 GEL-PlasmaCellDCcEeKkKpaKpbJsaJsbFyaFybJkaJkbLeaLebP1MNSsLuaLubr r Cell Phenotype+10√234567891011w
22 R1R1 Adsorption w + 0√ 1+ 2+ D C c E e K k M N S s Rh System Kell Rh SystemKellDuffyKiddLewisPMNSLutheranX2 PeG- PlasmaCellDCcEeKkKpaKpbJsaJsbFyaFybJkaJkbLeaLebP1MNSsLuaLubR1R1 Cell Phenotype+10√21+342+567891011w
23 Autoantibody Confirmation Testing Patient had been transfused in the last 3 months so need to perform reticulocyte separationWant to be testing patient cells and not donor cells
24 How is a Reticulocyte Cell Separation Performed? Blood Bank Technique: Reticulocyte Cell SeparationHow is a Reticulocyte Cell Separation Performed?Patient has been transfused so need to separate patient cells from donor red cellsStopper one end of the hematocrit tube with clay.Spin the sample down and fill microhematocrit tubes with the red cells.
25 How is a Reticulocyte Cell Separation Performed? Blood Bank Technique: Reticulocyte Cell SeparationHow is a Reticulocyte Cell Separation Performed?AirExcess saline/plasmaBuffy CoatNewer Red CellsOlder Red CellsSpin the microhematocrit tubes and then cut the tubes to get the reticulocytesClay Plug
26 Autoantibody Confirmation Testing Now that we have the retics:DAT/IgG had been positive so perform DAT/IgG on retics:ReticsAnti-IgG/ tube1+Can not proceed with testing to identify warm autoantibody until the DAT is negative
28 Blood Bank Technique: 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 positiveDoes not impair red cell surface antigens
29 Blood Bank Technique: EGA Treatment The ProcessWash IgG coated red cells thoroughlySuspend cells briefly in EGA solution to dissociate bound IgG antibodyBring mixture to neutral pHCentrifuge and wash cells with salineTest treated cells by performing a DATLimitation: destroys Kell, Era, Bg antigens
30 Autoantibody investigation EGA testing performed and DAT negative retics obtainedTo confirm the antibody is warm autoantibody the DAT negative retics are tested against the plasma and eluate:Retics-PlasmaRetics-EluateGel2+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-Jka (JK1) by antigen typingUse retics so that typing patient cells and not donor cellsAnti-JkTubePatient types Jka negative
32 Results Patient has warm autoantibody and anti-Jka (JK1). Transfusion recommendations:Transfuse Jka- (JK1), AHG crossmatch least incompatible, red blood cell products.
33 Kidd Blood Group System Located Chromosome 18Glycoprotein with 10 membrane spanning domains·Daniels, G. (2013) Kidd Blood Group System, in Human Blood Groups, 3rd edition, Wiley-Blackwell, Oxford, UK.Kidd antibodies are often difficult to work with and are a common cause of delayed hemolytic reactions
34 Jka (JK1) Antibody & Antigen Jka Antibody CharacteristicsHistory1951Clinical SignificanceYes! Clinically significant·Transfusion Reactions possible, immediate or delayed hemolytic·HDN possible, mild to moderateAntibodyIgG/IgMOther facts·Jka has been demonstrated on fetal cells as early as 11 weeks·Antibody fades in vitro and in vivo·Can show dosageJka Antigen CharacteristicsOccurrenceCaucasians 77%Blacks 92%Reid, Marion and Christine Lomas-Francis (2012). The Blood Group Antigen FactsBook, 3rd Edition, Elsevier.
35 Case Study 2 Female, 38 years old African American DIAGNOSIS: PATIENT HISTORYFemale, 38 years oldAfrican AmericanDIAGNOSIS:-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 2PATIENT HISTORYThe 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 illOn 1/24/2014 patient required another transfusion and sample was sent to hospital blood bank.
37 Case Study 2The 2nd sample was collected on 1/24/2014, 9 days after transfusion.Sample was sent to the reference laboratoryHospital Results on 1/24/2014:B PositiveAll cells reactive 2+ in gelAutocontrol positive
38 Case Study 2 Reference Lab testing: ABO/Rh performed: DAT Performed: Anti-AAnti-BAnti-DA1 CellB CellABO/Rh4+B PositiveAnti-IgG/ GelAnti-C3/ tubeW+0√
39 Plasma + 1+ 2+ 0√ D C c E e K k AHG-PeG Cell I II III Auto Room Temp Rh SystemKellDuffyKiddLewisPMNSLutheranRoom TempAHG-PeGCellDCcEeKkKpaKpbJsaJsbFyaFybJkaJkbLeaLebP1MNSsLuaLubI+1+II2+IIIAuto0√
40 Plasma + W 2+ W+ D C c E e K k M N S s Rh System Kell Duffy Kidd Lewis Rh SystemKellDuffyKiddLewisPMNSLutheranGELCellDCcEeKkKpaKpbJsaJsbFyaFybJkaJkbLeaLebP1MNSsLuaLub1+W2+234567891011AutoW+
41 Eluate + W 4+ The Eluate Last Wash is negative D C c E e K k M N S s Rh SystemKellDuffyKiddLewisPMNSLutheranGELCellDCcEeKkKpaKpbJsaJsbFyaFybJkaJkbLeaLebP1MNSsLuaLub1+W4+234567891011The Eluate Last Wash is negative
42 Question to ask yourself: So where do we go at this point? Serologic Problem SolvingQuestion to ask yourself: So where do we go at this point?Let’s look at what we know:Phase of reactivity: AHGStrength/pattern of reactivity: pan-reactive, same strength.Patient history: recently transfusedDAT/autocontrol: positive/reactiveOther info: eluate is also pan-reactive with same strength
43 Question to ask yourself: So where do we go at this point? Serologic Problem SolvingQuestion to ask yourself: So where do we go at this point?Narrowed down possibilities:Warm autoantibodyMultiple antibodies in plasma and eluateAntibody to a high incidence antigen
44 Why perform an adsorption? 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 + W D C c E e K k M N S s Rh System Kell Duffy Kidd Rh SystemKellDuffyKiddLewisPMNSLutheranX3 GEL- PlasmaX3 GEL- EluateCellDCcEeKkKpaKpbJsaJsbFyaFybJkaJkbLeaLebP1MNSsLuaLubR1R1 Cell Phenotype+1W234567891011
46 R2R2 Adsorption + W D C c E e K k M N S s Rh System Kell Duffy Kidd Rh SystemKellDuffyKiddLewisPMNSLutheranX3 GEL-PlasmaX3 GEL-EluateCellDCcEeKkKpaKpbJsaJsbFyaFybJkaJkbLeaLebP1MNSsLuaLubR2R2 Cell Phenotype+1W234567891011
47 rr Adsorption + W D C c E e K k M N S s Rh System Kell Duffy Kidd Rh SystemKellDuffyKiddLewisPMNSLutheranX3 GEL-PlasmaX3 GEL-EluateCellDCcEeKkKpaKpbJsaJsbFyaFybJkaJkbLeaLebP1MNSsLuaLubr r Cell Phenotype+1W234567891011
48 Results Appears to be warm autoantibody No alloantibodies were detected in the alloadsorbed plasma or eluateNeed 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:ReticsAnti-IgG/ GelOProceed 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-EluateGelThis 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: Warm autoantibody Serologic Problem SolvingQuestion to ask yourself: So where do we go at this point?Narrowed down possibilities:Warm autoantibodyMultiple antibodies in plasma and eluateAntibody to a high incidence antigen
52 Some Techniques/Options Available: Next Step:Use blood bank techniques, reagents and cells to try and determine the antibodySome Techniques/Options Available:Enzymes (ficin, papain, trypsin, etc)Chemicals such as DTTPhenotype PatientRare antiseraRare cells
53 Ficin Panel + W 2+ 3+ W+ 1+ GEL-Ficin GEL D C c E e K k M N S s Rh SystemKellDuffyKiddLewisPMNSLutheranGELGEL-FicinCellDCcEeKkKpaKpbJsaJsbFyaFybJkaJkbLeaLebP1MNSsLuaLub1+W2+3+234567891011AutoW+1+
54 0.2 M DTT Panel + W 2+ W+ D C c E e K k M N S s Rh System Kell Duffy Rh SystemKellDuffyKiddLewisPMNSLutheranGELGEL-0.2M DTTCellDCcEeKkKpaKpbJsaJsbFyaFybJkaJkbLeaLebP1MNSsLuaLub1+W2+234567891011AutoW+
55 Consider the race of patient and start with the easiest to test for Case Study 2Ficin and DTT testing has helped narrow down the possibilities.Some high incidence antigens resistant to Ficin and 0.2M DTT Treatment:LanABTIPELUFy3AtaMAMDibGe3Fy5EmmOkaWrbEnaFREraSda (Ficin enhanced0CoaCO3Vel (Ficin enhanced)Jra (Ficin enhanced)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.Consider the race of patient and start with the easiest to test for
56 Patient is antigen typed with the retics and is U- Selected Cells RunPlasma TestingRh SystemKellDuffyKiddLewisPMNSLutheranGELDonorDCcEeKkKpaKpbJsaJsbFyaFybJkaJkbLeaLebP1MNSsLuaLubUD1083+N1727Eluate TestingRh SystemKellDuffyKiddLewisPMNSLutheranGELDonorDCcEeKkKpaKpbJsaJsbFyaFybJkaJkbLeaLebP1MNSsLuaLubUD1083+N1727Patient is antigen typed with the retics and is U-
58 ResultsThe 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 hospitalDeglycerolizationRed 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 Antibody Characteristics U (MNS5) AntibodyU Antibody CharacteristicsHistoryAnti-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 severeAntibody·IgG, reacts best at 37°C/AHG·Autoanti-U is possibleOther 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, 3rd Edition, Elsevier.
61 U Antigen Characteristics U (MNS5) AntigenU Antigen CharacteristicsOccurrenceCaucasians 99.9%Blacks 99%Well developed at birthOther 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 possibleSources for further reading:·Reid, Marion and Christine Lomas-Francis (2012). The Blood Group Antigen FactsBook, 3rd 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 4Responsible for the production of glycophorin A (GPA) and glycophorin B (GPB) on red cellsPhoto:http://ghr.nlm.nih.gov/gene/GYPA
63 Genetics and Biochemistry Glycophorin A (GPA)M and N antigensGPA and GPB are the major sialic acid containing structures of the red cell membrane.Glycophorin B (GPB)S, s and U antigensPhoto Source:
64 U variants S-s-U+ or S-s-U+var Almost exclusively in those of African OriginAbout 50% of S-s- are U+varStrength of expression is variable; adsorption/elution tests may be needed to detect the U antigenStrong correlation of U variant antigen cells being He+ (low frequency MNSs antigen).
65 U vs U variants Reactivity GPB of the cell The anti-U of S-s-U- will react with S-s-U+varThe anti-U of U variants will not react with S-s-U- cells.GPB of the cellU- cells are totally GPB-deficientU variants have a variant GPB molecule that doesn’t express S or s
66 Case Study 3 Female, 65 years old African American DIAGNOSIS: stroke PATIENT HISTORYFemale, 65 years oldAfrican AmericanDIAGNOSIS: strokePatient 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 laboratoryHospital Results on 1/30/2013:O PositiveAll cells reactive 2+ in gelAutocontrol not testedAdditional 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/Rh4+0 PositiveAnti-IgG/ tubeAnti-C3/ tube0√
69 Plasma + 1+ w+ 0√ D C c E e K k AHG-PeG Room Temp Kpa Kpb Jsa Jsb Fya Rh SystemKellDuffyKiddLewisPMNSLutheranRoom TempAHG-PeGDCcEeKkKpaKpbJsaJsbFyaFybJkaJkbLeaLebP1MNSsLuaLub+1+w+0√
70 Plasma + 1+ 2+ D C c E e K k M N S s Rh System Kell Duffy Kidd Lewis P LutheranGELCellDCcEeKkKpaKpbJsaJsbFyaFybJkaJkbLeaLebP1MNSsLuaLub1+1+2342+567891011Auto
71 Question to ask yourself: So where do we go at this point? Serologic Problem SolvingQuestion to ask yourself: So where do we go at this point?Let’s look at what we know:Phase of reactivity: AHGStrength/pattern of reactivity: pan-reactive, different strengths.Patient history: not recently transfusedDAT/autocontrol: negative
72 Narrowed down possibilities: One antibody with different strengths Serologic Problem SolvingQuestion to ask yourself: So where do we go at this point?Narrowed down possibilities:One antibody with different strengthsMultiple antibodies in plasmaKeep in mind that patient has history of anti-Chido or antibody in Knops system
73 Some Techniques/Options Available: Next Step:Use blood bank techniques, reagents and cells to try and determine the antibodySome Techniques/Options Available:Enzymes (ficin, papain, trypsin, etc)Chemicals such as DTTPhenotype PatientRare antiseraRare cells
74 Patient phenotype Rh c + Duffy Fya C Fyb e MNS M E N Kell K S Kidd Jka CFybeMNSMENKellKSKiddJkasJkbLewisLeaLeb
75 Some of the Selected Cells Rh SystemKellDuffyKiddLewisPMNSLutheranGELDCcEeKkKpaKpbJsaJsbFyaFybJkaJkbLeaLebP1MNSsLuaLub+1+Co(b+)2+w+
76 Ficin Panel + 1+ 2+ w+ D C c E e K k M N S s Rh System Kell Duffy Kidd LewisPMNSLutheranGELGEL-FicinDCcEeKkKpaKpbJsaJsbFyaFybJkaJkbLeaLebP1MNSsLuaLub+1+2+w+Auto
77 0.2M DTT Panel + 1+ 2+ w+ D C c E e K k M N S s Rh System Kell Duffy KiddLewisPMNSLutheranGELGEL-FicinGEL-DTTDCcEeKkKpaKpbJsaJsbFyaFybJkaJkbLeaLebP1MNSsLuaLub+1+2+w+Auto
78 Patient History anti-Chido Knops Reactivity Ficin DTT Negative ReactiveReactivityFicinDTTWeakenedNegative
79 Knops System Kna Knb McCa McCb Sla (Sl1) Yka Vil (Sl2) Sl3 Antigen OccurrenceCaucasianBlacksKna98%99%Knb4.5%<.01%McCa94%McCb0%45%Sla (Sl1)50-60% (30% West Africans)Yka92%Vil (Sl2)80%Sl3100%Reid, Marion and Christine Lomas-Francis (2012). The Blood Group Antigen FactsBook, 3rd Edition, Elsevier.
80 Available Selected Knops Cells Rh SystemKellDuffyKiddLewisPMNSLutheranGELDCcEeKkKpaKpbJsaJsbFyaFybJkaJkbLeaLebP1MNSsLuaLub+Yk(a-)1+Sl(a-)Appears to be anti-Sla but due to known weak reactivity of the antibody do molecular to confirm
81 Molecular Testing Rh c + MNS M Dombrock Doa C N Dob e S Joa E s Hy MNSMDombrockDoaCNDobeSJoaEsHyKellKLutheranLuaLWLwakLubLwbKpaDiegoDiaSciannaSc1KpbDibSc2JsaCromerCraJsbColtonCoaKnopsKnaKnbKiddJkaCobMcCaJkbCartwrightYtaMcCbDuffyFyaYtbSl1FybHemoglobin SHbSSl2
82 Knops System Knops antigens are located on complement receptor 1 (CR1) CR1 gene resides on chromosome 1
84 What is CR1 (CD35)?CR1 is a glycoprotein on cells that binds particles coated with C3b and C4bNeutophils 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-bhttps://www.inkling.com/read/the-immune-system-peter-parham-3rd/chapter-9/antibody-production-by-b
86 Structure of CR1 glycoprotein (CD35) Knops systemStructure of CR1 glycoprotein (CD35)
87 Knops system characteristics Variation in antigen strength, related to CR1 red cell levelsGenerally, a reduction in antigen strength with storage of red cells as the CR1 copy per RBC may be decreased in stored samplesHigh titer low avidity (HTLA) has been used to describe the antibodiesDifficult to adsorb out antibodiesCan be hard to distinguish antigen negative from weakly positive cellsClinically benign but can mask other significant antibodies
88 Knops antigens can be depressed in Knops SystemKnops antigens can be depressed incutaneous lupus erythematosus (CLE)Cold Hemagglutinin Disease (CHAD)Paroxysmal nocturnal hemoglobinuria (PNH)hemolytic anemiainsulin-dependent diabetesAIDSsome malignant tumorsany condition with increased clearance of immune complexesNull phenotype: Kn(a-b-), McC(a-), Sl(a-), Yk(a-) aka Helgeson type
89 Sla Antibody Characteristics HistoryReported in 1980 and named after Swain and Langely, the first two antibody producers.Clinical SignificanceNo! Clinically insignificant·No Transfusion Reactions·No HDNAntibody·IgG, reacts best at 37°C/AHGOther factsMay be confused with anti-Fy3 because mostFy(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, 3rd Edition, Elsevier.
90 Sla Antigen Characteristics Occurrence98%50-60% (30% West Africans)Other FactsAlso known as Sl1Disease 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, 3rd Edition, Elsevier.·Daniels, G. (2013) MNS Blood Group System, in Human Blood Groups, 3rd edition, Wiley-Blackwell, Oxford, UK.