ElinF

For decades we hired only MTs, but have had to hire a few MLTs over the last couple of years due to MT shortages. I find the quality of work varies not from the number of college courses they took but the innate ability, initiative and interest of the worker. We train equally and job responsibilities are equal (although the MTLs cannot do some things, like review results etc).
 
I had a MLT generalist on last weekend. He had a patient who got 4 units of blood the week before who now presented with anti-c and a positive DAT, weak mixed field. Pretty classic delayed reaction, except that the eluate reacted with all the panel cells. DAT was negative the week before. He dug into it and tested some more c-negative cells and found that there was also anti-Fya and -Jkb in the eluate (but not in the plasma yet). En route he tested the eluate with ficin-treated cells and PeG and ficin-treated some additional ones himself to help untangle the specificities. I did give him some phone coaching along the way, but it was an excellent job of blood banking. "Just" a MLT, but he really digs BB.

I use the recipes below for students/new techs. We use mostly gel for testing, and these work pretty well most of the time. The Rh, K, and M are very consistent and we get 2+ reactions or better. I don't know what kind of reactions you would get with tube testing with the Rh and K. I've had problems with the Fy, so I only use it in combination with other antibodies. Sometimes I mix it up based on what our expired panels look like. If I'm feeling particularly evil (or want to stump a student who thinks they can solve anything), I will choose several antibodies that are very difficult to identify with a particular panel. We use mostly monoclonal antisera, and I try to use expired, but since I'm only using a drop or two, I don't feel bad about using in-date reagents. I either match the antibodies to an expired panel cell to use as "patient" cells, or use some segments from a phenotyped unit if one is available. I've tried making positive DATs with reagents other than D, but haven't had much success.


Elution: Anti- D, mixed field DAT
2 O Pos Segments and 2 O Neg segments
Put O pos segments in 12x 75 tube.
Add 1 drop of Anti-D, 2-3 drops of albumin and a little bit of saline
Incubate at 37 for 30 minutes
Add O neg segments

[*]Gel ab screen- Anti- C

Fill 12x75 tube 1/3 full of saline
Add 1 drop Anti-C, 2 drops albumin

[*]Gel ab screen- anti-Jka

Fill 12x75 tube 1/3 full of saline
Add 1 drop Anti-Jka, 2 drops albumin

[*]Gel ab screen- anti-K and Anti- c

Fill 12x75 tube 1/3 full of saline
Add 1 drop Anti-K, 1 drop Anti-c, 2 drops albumin

[*]Tube Ab screen – Anti-M

Fill 12x75 tube 2/3 full of saline
Add 2 drops Anti-M, 2 drops albumin

[*]Gel Ab screen - Anti-Fya, Anti-E, Anti-K

Fill 12x75 tube 1/3 full of saline
Add 2 drops Anti-Fya, 1 drop Anti-E, 1 drop Anti-K, 3 drops albumin

For those of who works in transfusion service laboratory and would like to learn more reference cases, I can post some mock-up cases here. If you would like me to do it, please hit the "heart" button on this post. If enough folks want to practice case studies on reference lab cases, I can post mock-up cases here weekly or so.. 

I worked in Red Cell Immunohaematology for most of my 43 years before retirement, including two times at the International Blood Group Reference Laboratory (IBGRL), and for over a decade at one of the NHS Blood and Transplant Centres in London.  During that time, I saw some pretty weird Kidd antibodies, but never came across an example of one that reacted with red cells with Jk(a) heterozygous expression, but not with Jk(a) homozygous expression.
One such "weird" type (although I never saw one) was the extremely rare, dominant inhibitor type In(Jk), similar, but, of course, not identical to In(Lu).  These red cells usually type as Jk(a-b-), but their true Kidd type can be ascertained by Adsorption and elution tests..  These red cells are also more resistant to haemolysis by 2M Urea than red cells with "normal" expression of the Kidd antigens, but less resistant to haemolysis by 2M Urea than true "amorphic" Jk(a-b-) red cells.
There are approximately 14, 000 copies of the Kidd carrier molecule per red cell (quite a small number, when compared with some other carrier molecules, such as the D antigen).
The amino acid residue that defines either the Jka or Jkb antigens is very close to the red cell membrane in the 4th extracellular loop but is largely “hidden” by the 3rd extracellular loop (steric hindrance).
 Both facts may contribute to the weak reactions between Kidd antibodies and Kidd antigens.

Schematic of the Kidd carrier molecule (after Wester ES, Storry JR, Olsson ML.  Characterization of Jk(a+weak): a new blood group phenotype associated with an altered JK*01 allele.  Transfusion 2011; 15: 380-392.  DOI: 10.1111/j.1537-2995.2010.02795.x.
In this paper, Wester et al also describe weakened forms of both the Jka and the Jkb antigens, but in each case, the amino acid substitution is remote from position 280 of the mature protein. 
 In addition, an individual with the Trp171Arg mutation with weak Jk(a) expression has produced an anti-Jk3 or anti-Jk3-like antibody, and so they may be “dangerous patients” (Whorley T, Vage S, Kosanka J, Lose SR, Sandquist AR, Copeland TR, Westhoff CM.  JK alleles associated with altered Kidd antigen expression.  Transfusion 2009; 41 (Suppl.): 48A-49A (abstract).
Lastly (for now anyway!), most foetal red cells sensitised by maternal antibodies react only with anti-IgG, but I (and a colleague Grant Webb) have both noticed, but not published, occasions when such red cells also react with anti-C3d and, in one case, only anti-C3d (see genuine photographs below)..

We are a small hospital.  We were cited for this a few years ago by the Joint Commission and were kind of shocked.   Several years before that they asked us for our daily Qc on our panels. We never did QC on panels we only QC'ed the method (gel or tube) with screen cells.  (our reference lab was confused with QCing panel cells as well, I mean what antibody to you QC? all? 2? 3?)  So we had to start doing on receipt QC and every day of use and we can no longer use outdated panels.  I just  use the Ortho antibody in the QC kit and test Cells 1 and 5 (pos and neg for D and little c) We currently stock a panel for tube and gel. If we can't rule out based on those 2 we need to special order blood or send the specimen out.  I am not really sure what the pathologist can or can't sign off on as far as validating anything as far as using outdated cells.  Since you are a larger facility maybe see what your reference lab does. 
 
 

MTP and Emergency release is a verbal phone call to the blood bank with a signed form during the event.  Routines need an order faxed from the provider or orders placed into Epic.  Happy New Year! 

MTP and Emergency release is a verbal phone call to the blood bank with a signed form during the event.  Routines need an order faxed from the provider or orders placed into Epic.  Happy New Year! 

I could "listen" to Malcolm explain stuff all day!!  

So our sister lab was cited last week (September 2022) by TJC for not QCing panel cells. That lab had at one time been a branch of a reference lab so of course they never QC'ed panel cells for reasons given above.  We are arguing back that it is a procedural QC process that we would never do a panel if the screen was negative.  So if they don't react when they expect them to then we do other processes.  (ie repeat, check for gel junk/misc reactivity in the screen, run it on tube, etc).  Our lab does QC our panels on receipt (because a TJC surveyor told us to years back) to make sure they are reactive, but we currently do not Qc them every day of use.  And the IFU now states that we need to look at our "regional and national guidance, standards, regulations and professional preferences. and Each lab must develop specific procedures..."  All AABB states is to have a QC policy that works basically.  
I told our manager to ask them exactly what they want.  (I am sure every surveyor will be different, and  we may just have to satisfy them with the smoke and mirrors QC unfortunately.)

A few of our newer employees state that their previous employers had required this, but I had never heard of this.  We were trained by our ortho rep back in 2005 or so to pipette straight up and down for both reagent cells and plasma.  My question is since many labs are automated for blood bank now, how do the analyzers pipette the samples.  Is there an air gap in the testing with the Provue or the Vision? 

This sound like what we are doing...You are now my best friend  so we can trade tips and secrets!  haha

Blood products that were taken into isolation are never returned to us.    If they are not used, they are discarded in the room.

I could "listen" to Malcolm explain stuff all day!!  

I could "listen" to Malcolm explain stuff all day!!  

This is amazing and most definitely deserved!!  I love reading your responses to EVERYONE'S questions and your knowledge is unbelievable.  Thank you for all your help! 

We have also used the small Helmer incubator. It was very dependable over a lot of years. We have since upgraded to the next larger size.

We have the i Series Helmer incubator and have had no problems 

Interestingly enough, I was at a conference recently where forum threads from Bloodbanktalk were used as source material and included as part of the lecture.

Interesting patient #2 this month.  A multiple myeloma patient who had no history had all testing positive in Gel, including the  Auto control.  Expecting a Warm auto we sent the specimen to the reference lab.  Again, they sent it further to the American red Cross.  They discovered a new medication on the med list was a medication that pretty much interfered with all blood bank testing except Immediate spin crossmatches.    Darzalex is the name of the drug.  The bulletin is below from the AABB.   So, while the patients are on this drug, our reference lab will have to perform the antibody screens for us. 
 
 
 
Association Bulletin #16-02
Date: January 15, 2016
To: AABB Members
From: Donna M. Regan, MT(ASCP)SBB—President
Miriam A. Markowitz—Chief Executive Officer
Re: Mitigating the Anti-CD38 Interference with Serologic Testing
Summary
A new class of therapeutic agents for multiple myeloma, CD38 monoclonal antibodies, can result in interference with blood bank serologic tests and thereby cause delays in issuing Red Blood Cell (RBC) units to patients receiving these agents. To minimize these delays, hospitals should set up procedures to inform the transfusion service when patients start receiving these agents. Considerations for the transfusion service, both before and after initiation of anti-CD38 therapy, are detailed below.
The AABB Clinical Transfusion Medicine Committee has developed this bulletin to provide background information and guidance to members regarding anti-CD38 interference with serologic testing. The bulletin includes recommendations for its prevention and treatment.
Association Bulletins, which are approved for distribution by the AABB Board of Directors, may include announcements of standards or requirements for accreditation, recommendations on emerging trends or best practices, and/or pertinent information. This bulletin contains information and recommendations. No new standards are proposed.
Background
CD38 monoclonal antibodies are a new treatment for multiple myeloma
CD38, an integral membrane protein that is highly expressed on myeloma cells, has been identified as an effective target antigen for monoclonal antibody therapies. In November 2015, the first therapeutic CD38 monoclonal antibody [daratumumab (Darzalex, Janssen Biotech, Horsham, PA)] was approved by the Food and Drug Administration.1 Other CD38 monoclonal antibodies are under development.
CD38 monoclonal antibodies interfere with blood bank serologic tests
CD38 is weakly expressed on red cells. Anti-CD38 binds to CD38 on reagent RBCs, causing panreactivity in vitro.2,3 Plasma samples from anti-CD38-treated patients consistently cause positive reactions in indirect antiglobulin tests (IATs), antibody detection (screening) tests, antibody identification panels, and antihuman globulin (AHG) crossmatches. Agglutination due to anti-CD38 may occur in all media (eg, saline, low ionic strength saline, polyethylene glycol),
1
and with all IAT methods (eg, gel, tube, solid phase). Agglutination reactions caused by anti-CD38 are usually weak (1+), but stronger reactions (up to 4+) may be seen in solid-phase testing. However, anti-CD38 does NOT interfere with ABO/RhD typing or with immediate-spin crossmatches.
Other notes on anti-CD38 serologic interference:
 Adsorptions using either untreated or ZZAP-treated cells fail to eliminate the interference.
 Anti-CD38 variably interferes with direct antiglobulin tests (DATs) and antibody identification panel autocontrols.
 Some rare Lu(a–b–) cells are not reactive in the presence of anti-CD38, potentially giving the false impression that the patient has a Lutheran-related antibody.4,5
 Positive IATs can be observed for up to six months after anti-CD38 is discontinued.1,3
 Anti-CD38 may cause a small decrease in hemoglobin in vivo (~1 g/dL), but severe hemolysis has not been observed among treated patients.3,6
Anti-CD38 interference can cause delays in issuing RBCs
If the transfusion service is unaware that a patient has received anti-CD38, the following scenario may occur when the patient’s sample is tested:
1. ABO/RhD typing: no issues.
2. Antibody detection (screening) test: all cells positive.
3. Antibody identification panel: all cells positive (autocontrol may be negative).
4. DAT: positive or negative.
5. AHG crossmatches: positive with all RBC units tested.
6. Adsorptions: panreactivity cannot be eliminated.
This leads to delays in issuing RBCs to the patient. In some cases, the anti-CD38 interference could mask the presence of a clinically significant alloantibody.
Recommendations
To avoid problems with transfusion, hospitals should set up procedures to inform the transfusion service whenever any patient is scheduled to begin taking anti-CD38.
BEFORE a patient begins taking anti-CD38:
 A baseline type and screen should be performed.
 In addition, a baseline phenotype or genotype is recommended.
AFTER a patient begins taking anti-CD38:
 ABO/RhD typing can be performed normally.
 For antibody detection (screening) and identification, dithiothreitol (DTT)-treated cells can be used to eliminate the interference.2,7
o Because DTT treatment destroys Kell antigens, K-negative units should be provided unless the patient is known to be K-positive.
o Antibodies against other DTT-sensitive blood group antigens (anti-k, anti-Yta, anti-Doa/Dob, etc) will not be detectable when the antibody screen with DTT-
2
treated cells is performed; such antibodies are encountered infrequently, however.
Crossmatch
 For patients with a negative antibody screen using DTT-treated cells, an electronic or immediate-spin crossmatch with ABO/RhD-compatible, K-matched units may be performed.
 For patients with known alloantibodies, phenotypically or genotypically matched RBC units may be provided.6,8
o As some typing antisera require the use of AHG, phenotyping should be performed before the patient receives anti-CD38.
o Genotyping can be performed either before or after the patient receives anti-CD38.
o AHG crossmatches with phenotypically or genotypically matched units will still be incompatible.
o Some clinically significant antibodies may be missed with the use of uncrossmatched phenotypically or genotypically matched units, although this will occur infrequently.
 Alternatively, an AHG crossmatch may be performed using DTT-treated donor cells.
 If an emergency transfusion is required, uncrossmatched ABO/RhD-compatible RBCs may be given per local blood bank practices.
Future/alternative approaches to mitigating the anti-CD38 interference
It is possible to neutralize anti-CD38 in plasma and eliminate the interference using either recombinant soluble human CD38 or daratumumab idiotype antibody.2,3 Neither reagent is widely available at this time, and additional validation would be needed. In principle, soluble CD38 could be used to neutralize any anti-CD38, while different idiotype antibodies would be needed to neutralize different CD38 therapeutic antibodies. Finally, antigen-typed cord cells have been used for the antibody screen as an alternative to DTT-treated cells.9
3
References
1. Darzalex package insert. Horsham, PA: Janssen Biotech, 2015. [Available at: http://www.darzalex.com/shared/product/darzalex/darzalex-prescribing-information.pdf (accessed January 7, 2016).]
2. Chapuy CI, Nicholson RT, Aguad MD, et al. Resolving the daratumumab interference with blood compatibility testing. Transfusion 2015;55(6pt2):1545-54.
3. Oostendorp M, Lammerts van Bueren JJ, Doshi P, et al. When blood transfusion medicine becomes complicated due to interference by monoclonal antibody therapy. Transfusion 2015;55(6pt2):1555-62.
4. Velliquette RW, Shakarian G, Jhang J, et al. Daratumumab-derived anti-CD38 can be easily Mistaken for clinically significant antibodies to Lutheran antigens or to Knops antigens (abstract). Transfusion 2015;55(3S):26A.
5. Aye T, Arndt PA, Leger RM, et al. Myeloma patients receiving daratumumab (anti-CD38) can appear to have an antibody with Lutheran-related specificity (abstract). Transfusion 2015;55(3S):28A.
6. Chari A, Satta T, Tayal A, et al. (2015, December) Outcomes and management of red blood cell transfusions in multiple myeloma patients treated with daratumumab (oral and poster abstract presented Monday, December 7, 2015, 6:00 PM-8:00 PM at 57th Annual American Society of Hematology meeting). Blood 2015;26(Suppl):Abstract 3571.
7. Chapuy CI, Aguad MD, Nicholson RT, et al. International validation of a dithiothreitol (DTT)-based method to resolve the daratumumab interference with blood compatibility testing (oral and poster abstract presented Monday, December 7, 2015, 6:00 PM-8:00 PM at 57th Annual American Society of Hematology meeting). Blood 2015;126(Suppl):Abstract 3567.
8. Hannon JL, Caruk B, Clarke G. Serological findings related to treatment with a human monoclonal antibody (daratumumab) in patients with advanced plasma cell myeloma (abstract). Transfusion 2014;54(2S):162A.
9. Schmidt AE, Kirkley S, Patel N, et al. An alternative method to dithiothreitol treatment for antibody screening in patients receiving daratumumab (abstract). Transfusion 2015;55(3S):2292-3.
4

Interesting patient #2 this month.  A multiple myeloma patient who had no history had all testing positive in Gel, including the  Auto control.  Expecting a Warm auto we sent the specimen to the reference lab.  Again, they sent it further to the American red Cross.  They discovered a new medication on the med list was a medication that pretty much interfered with all blood bank testing except Immediate spin crossmatches.    Darzalex is the name of the drug.  The bulletin is below from the AABB.   So, while the patients are on this drug, our reference lab will have to perform the antibody screens for us. 
 
 
 
Association Bulletin #16-02
Date: January 15, 2016
To: AABB Members
From: Donna M. Regan, MT(ASCP)SBB—President
Miriam A. Markowitz—Chief Executive Officer
Re: Mitigating the Anti-CD38 Interference with Serologic Testing
Summary
A new class of therapeutic agents for multiple myeloma, CD38 monoclonal antibodies, can result in interference with blood bank serologic tests and thereby cause delays in issuing Red Blood Cell (RBC) units to patients receiving these agents. To minimize these delays, hospitals should set up procedures to inform the transfusion service when patients start receiving these agents. Considerations for the transfusion service, both before and after initiation of anti-CD38 therapy, are detailed below.
The AABB Clinical Transfusion Medicine Committee has developed this bulletin to provide background information and guidance to members regarding anti-CD38 interference with serologic testing. The bulletin includes recommendations for its prevention and treatment.
Association Bulletins, which are approved for distribution by the AABB Board of Directors, may include announcements of standards or requirements for accreditation, recommendations on emerging trends or best practices, and/or pertinent information. This bulletin contains information and recommendations. No new standards are proposed.
Background
CD38 monoclonal antibodies are a new treatment for multiple myeloma
CD38, an integral membrane protein that is highly expressed on myeloma cells, has been identified as an effective target antigen for monoclonal antibody therapies. In November 2015, the first therapeutic CD38 monoclonal antibody [daratumumab (Darzalex, Janssen Biotech, Horsham, PA)] was approved by the Food and Drug Administration.1 Other CD38 monoclonal antibodies are under development.
CD38 monoclonal antibodies interfere with blood bank serologic tests
CD38 is weakly expressed on red cells. Anti-CD38 binds to CD38 on reagent RBCs, causing panreactivity in vitro.2,3 Plasma samples from anti-CD38-treated patients consistently cause positive reactions in indirect antiglobulin tests (IATs), antibody detection (screening) tests, antibody identification panels, and antihuman globulin (AHG) crossmatches. Agglutination due to anti-CD38 may occur in all media (eg, saline, low ionic strength saline, polyethylene glycol),
1
and with all IAT methods (eg, gel, tube, solid phase). Agglutination reactions caused by anti-CD38 are usually weak (1+), but stronger reactions (up to 4+) may be seen in solid-phase testing. However, anti-CD38 does NOT interfere with ABO/RhD typing or with immediate-spin crossmatches.
Other notes on anti-CD38 serologic interference:
 Adsorptions using either untreated or ZZAP-treated cells fail to eliminate the interference.
 Anti-CD38 variably interferes with direct antiglobulin tests (DATs) and antibody identification panel autocontrols.
 Some rare Lu(a–b–) cells are not reactive in the presence of anti-CD38, potentially giving the false impression that the patient has a Lutheran-related antibody.4,5
 Positive IATs can be observed for up to six months after anti-CD38 is discontinued.1,3
 Anti-CD38 may cause a small decrease in hemoglobin in vivo (~1 g/dL), but severe hemolysis has not been observed among treated patients.3,6
Anti-CD38 interference can cause delays in issuing RBCs
If the transfusion service is unaware that a patient has received anti-CD38, the following scenario may occur when the patient’s sample is tested:
1. ABO/RhD typing: no issues.
2. Antibody detection (screening) test: all cells positive.
3. Antibody identification panel: all cells positive (autocontrol may be negative).
4. DAT: positive or negative.
5. AHG crossmatches: positive with all RBC units tested.
6. Adsorptions: panreactivity cannot be eliminated.
This leads to delays in issuing RBCs to the patient. In some cases, the anti-CD38 interference could mask the presence of a clinically significant alloantibody.
Recommendations
To avoid problems with transfusion, hospitals should set up procedures to inform the transfusion service whenever any patient is scheduled to begin taking anti-CD38.
BEFORE a patient begins taking anti-CD38:
 A baseline type and screen should be performed.
 In addition, a baseline phenotype or genotype is recommended.
AFTER a patient begins taking anti-CD38:
 ABO/RhD typing can be performed normally.
 For antibody detection (screening) and identification, dithiothreitol (DTT)-treated cells can be used to eliminate the interference.2,7
o Because DTT treatment destroys Kell antigens, K-negative units should be provided unless the patient is known to be K-positive.
o Antibodies against other DTT-sensitive blood group antigens (anti-k, anti-Yta, anti-Doa/Dob, etc) will not be detectable when the antibody screen with DTT-
2
treated cells is performed; such antibodies are encountered infrequently, however.
Crossmatch
 For patients with a negative antibody screen using DTT-treated cells, an electronic or immediate-spin crossmatch with ABO/RhD-compatible, K-matched units may be performed.
 For patients with known alloantibodies, phenotypically or genotypically matched RBC units may be provided.6,8
o As some typing antisera require the use of AHG, phenotyping should be performed before the patient receives anti-CD38.
o Genotyping can be performed either before or after the patient receives anti-CD38.
o AHG crossmatches with phenotypically or genotypically matched units will still be incompatible.
o Some clinically significant antibodies may be missed with the use of uncrossmatched phenotypically or genotypically matched units, although this will occur infrequently.
 Alternatively, an AHG crossmatch may be performed using DTT-treated donor cells.
 If an emergency transfusion is required, uncrossmatched ABO/RhD-compatible RBCs may be given per local blood bank practices.
Future/alternative approaches to mitigating the anti-CD38 interference
It is possible to neutralize anti-CD38 in plasma and eliminate the interference using either recombinant soluble human CD38 or daratumumab idiotype antibody.2,3 Neither reagent is widely available at this time, and additional validation would be needed. In principle, soluble CD38 could be used to neutralize any anti-CD38, while different idiotype antibodies would be needed to neutralize different CD38 therapeutic antibodies. Finally, antigen-typed cord cells have been used for the antibody screen as an alternative to DTT-treated cells.9
3
References
1. Darzalex package insert. Horsham, PA: Janssen Biotech, 2015. [Available at: http://www.darzalex.com/shared/product/darzalex/darzalex-prescribing-information.pdf (accessed January 7, 2016).]
2. Chapuy CI, Nicholson RT, Aguad MD, et al. Resolving the daratumumab interference with blood compatibility testing. Transfusion 2015;55(6pt2):1545-54.
3. Oostendorp M, Lammerts van Bueren JJ, Doshi P, et al. When blood transfusion medicine becomes complicated due to interference by monoclonal antibody therapy. Transfusion 2015;55(6pt2):1555-62.
4. Velliquette RW, Shakarian G, Jhang J, et al. Daratumumab-derived anti-CD38 can be easily Mistaken for clinically significant antibodies to Lutheran antigens or to Knops antigens (abstract). Transfusion 2015;55(3S):26A.
5. Aye T, Arndt PA, Leger RM, et al. Myeloma patients receiving daratumumab (anti-CD38) can appear to have an antibody with Lutheran-related specificity (abstract). Transfusion 2015;55(3S):28A.
6. Chari A, Satta T, Tayal A, et al. (2015, December) Outcomes and management of red blood cell transfusions in multiple myeloma patients treated with daratumumab (oral and poster abstract presented Monday, December 7, 2015, 6:00 PM-8:00 PM at 57th Annual American Society of Hematology meeting). Blood 2015;26(Suppl):Abstract 3571.
7. Chapuy CI, Aguad MD, Nicholson RT, et al. International validation of a dithiothreitol (DTT)-based method to resolve the daratumumab interference with blood compatibility testing (oral and poster abstract presented Monday, December 7, 2015, 6:00 PM-8:00 PM at 57th Annual American Society of Hematology meeting). Blood 2015;126(Suppl):Abstract 3567.
8. Hannon JL, Caruk B, Clarke G. Serological findings related to treatment with a human monoclonal antibody (daratumumab) in patients with advanced plasma cell myeloma (abstract). Transfusion 2014;54(2S):162A.
9. Schmidt AE, Kirkley S, Patel N, et al. An alternative method to dithiothreitol treatment for antibody screening in patients receiving daratumumab (abstract). Transfusion 2015;55(3S):2292-3.
4

Thank you for your reply.  This makes sense to me.  Better to be safe since he has had prior transfusions even if it was 3 years ago.  When he comes back in we will re-screen him and then once he is transfused he will be treated normally, we will just have to send his sample to the ARC for the special tesing.  

So, interesting patient last month.  We had a patient with a history of anti-e. (not good)  Worked her up and every cell on the panel was positive (even the e neg antigen cell).  Her auto control  and DAT were negative.  Come to find out after sending her to our reference lab for a full work up, which then sent her to the American Red cross that she has developed anti-Kpb.  She was Kpb antigen negative.  She would need blood negative for K, Kpb, e and C (could not rule out big C).   After a long search she is not compatible with any of the blood (rare donor databases I am assuming) in the US.   If we wanted to start a global search the physician would have to get in contact with the director the ARC directly.  It was crazy!  We are a small hospital who never sees this kind of crazy stuff, but I guess it was our turn.  (The patient is responding to iron treatments and has been doing ok with out blood transfusions thus far.) 
 
 

Yes, that is what I tell them. 

Thank you everyone for your feedback! 
 

In the USA, all AABB accredited IRLs (Immunohematology Reference Laboraotories) and American Red Cross IRLs are members of the American Rare Donor Program (ARDP). This program has over 45,000 Rare Donors registered from over 88 member centers. If your blood supplier is not a member of the ARDP,  your facility can access the program by sending a sample for evaluation to a member. If there are no member centers in your area, the Penn-Jersey American Red Cross can be a "portal" to the ARDP. After a sample is submitted and tested, Penn-Jersey will access the ARDP for the non-member hospital or blood center. Ninety four percent of the time, units are found.  In very complex cases, there may be no blood available. If the blood is not avaiable in the USA, then the ARDP, as a member of the World Health Organization (WHO) International Rare Donor Panel(IRDP), can request blood internationally after several qualifying steps are taken (prove no blood in USA, eligible sibling donors have been tested, MMA performed, patient and physician give permission). The WHO IRDP is managed by the International Blood Group Reference Laboratory headquartered in Bristol, UK under the direction of Nicole Thornton. No patient should be without the blood they need to survive, although some are very very rare with very few identified donors in the world [e.g. Rhnull, En(a-), Ko, Co(a-b-)] and that makes it difficult to supply lifesaving blood.
Sandra Nance, Senior Director, American Rare Donor Program, 1- 215 451 4362