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Phenotype Matched RBC Procedure?


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We match Rh/K/Fya for all peds SS patients and all adult SS patients who have made at least a single RBC alloantibody.  We make every effort to send warm autos for RBC genotyping and match everything we reasonably can.  Our blood supplier maintains an online antibody registry for their customers, so it helps with continuity of care if people hospital hop (assuming all customers utilize it).

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25 minutes ago, Ensis01 said:

Rh/K for WAA and SS patients, plus neg antigens for any antibodies made.

There are several papers (based on SS populations) that show matching Rh and K will effectively prevents the patient developing antibodies (with exceptions). I can not remember the papers though.  

Some of these papers are referenced in an essay I submitted some years ago now in the library bit of this site on the use of phenotyped blood, bu they are a bit old now.  There may be some more recent ones.

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On 5/18/2018 at 3:01 AM, Malcolm Needs said:

Some of these papers are referenced in an essay I submitted some years ago now in the library bit of this site on the use of phenotyped blood, bu they are a bit old now.  There may be some more recent ones.

I'll apologize in advance for the lengthy answer.  

I had always been taught that matching Rh and Kell were helpful in preventing alloimmunization for SS patients, but I attended a lecture by Dr. Gehrie last week on this topic and he had a very different opinion. I'm looking forward to discussing this with my medical director-it's so different from everything I've previously read.

Dr. Gehrie said the 2014 NHLBI Expert Panel made a moderate recommendation based on low-quality evidence that RBC units that SS patients should include matching for C, E, and Kell antigens and that serologic antibody matching programs results were varied. He also advocated that only 30% of SS patients form alloantibodies which makes studies difficult-patients may not have made antibodies, but maybe they are part of the 70% that wouldn't make antibodies.

He shared the Chou et al 15 year retrospective analysis from Children's Hospital of Philadelphia. The patients were provided D, C, E, and K matched RBCs from mainly african american donors.

N=123 chronically transfused, N=59 episodically transfused.

58% of the chronically transfused and 15% of the episodically transfused were alloimmunized.

91/146 antibodies were to Rh antigens. 

The biggest takeaway for me was 87.6% of the patients had Rh variant alleles which help explains the  alloimmunization rate.

Dr. Gehrie's protocol at Johns Hopkins is to do nothing for SS patients until they form an antibody, then genotype the patient and provide matched products based on the genotyping.

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29 minutes ago, MOBB said:

I'll apologize in advance for the lengthy answer.  

I had always been taught that matching Rh and Kell were helpful in preventing alloimmunization for SS patients, but I attended a lecture by Dr. Gehrie last week on this topic and he had a very different opinion. I'm looking forward to discussing this with my medical director-it's so different from everything I've previously read.

Dr. Gehrie said the 2014 NHLBI Expert Panel made a moderate recommendation based on low-quality evidence that RBC units that SS patients should include matching for C, E, and Kell antigens and that serologic antibody matching programs results were varied. He also advocated that only 30% of SS patients form alloantibodies which makes studies difficult-patients may not have made antibodies, but maybe they are part of the 70% that wouldn't make antibodies.

He shared the Chou et al 15 year retrospective analysis from Children's Hospital of Philadelphia. The patients were provided D, C, E, and K matched RBCs from mainly african american donors.

N=123 chronically transfused, N=59 episodically transfused.

58% of the chronically transfused and 15% of the episodically transfused were alloimmunized.

91/146 antibodies were to Rh antigens. 

The biggest takeaway for me was 87.6% of the patients had Rh variant alleles which help explains the  alloimmunization rate.

Dr. Gehrie's protocol at Johns Hopkins is to do nothing for SS patients until they form an antibody, then genotype the patient and provide matched products based on the genotyping.

I was there as well! He was an excellent speaker.  We should find a way to post when there is an upcoming B.B. event so that some of us may meet in real life.

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I would tend to agree with some of what Dr Gehrie was saying (although, of course, I wasn't there to hear the lecture), and I would reference a paper that I referenced in a different thread (Chou ST, Jackson T, Vege S, Smith-Whitley K, Friedman DF, Westhoff CM.  High prevalence of red blood cell alloimmunization in sickle cell disease despite transfusion from Rh-matched minority donors.  Blood 2013; 122: 1062-1071; doi: https://doi.org/10.1182/blood-2013-03-490623), however, the experience in the UK is certainly that, if you can match the Rh type of the donor and the recipient (by that, I mean giving Ro donor blood to an Ro recipient; not rr blood to an Ro recipient, unless this cannot be avoided), then the formation of other antibody specificities is somewhat reduced.  This is partly due, of course, to the Ro type being far more common in both donors and recipients of Black ethnicity, which, in a way, takes care of both the Rh and K antigens (excluding mutations), but, almost by accident, also takes care of some other antigens and antibodies.  For example, the Fya antigen is only expressed on the red cells of approximately 10% of these donors, while the Jkb antigen, not the most immunogenic antigen one can quote, is only expressed on the red cells of approximately 49% of these donors, compared with the mid to high 70%s in most other donors.

I am not saying, therefore, that matching Rh and K types is a panacea for preventing antibody production, but we have found (both empirically and by more rigorous research) that antibody production is lower by adopting this fairly simple measure.  We have also recently genotyped many of our haemoglobinopathy patients, revealing those with, amongst other things, RH gene mutations.  What we have to do now is genotype our donors from the Black ethnic backgrounds, and then match the two, so that bespoke units are provided.  This is ambitious, but should be attainable, at least at a decent level, within the next few years.

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10 hours ago, Carrie Easley said:

I was there as well! He was an excellent speaker.  We should find a way to post when there is an upcoming B.B. event so that some of us may meet in real life.

That would be awesome :)

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6 hours ago, Malcolm Needs said:

I would tend to agree with some of what Dr Gehrie was saying (although, of course, I wasn't there to hear the lecture), and I would reference a paper that I referenced in a different thread (Chou ST, Jackson T, Vege S, Smith-Whitley K, Friedman DF, Westhoff CM.  High prevalence of red blood cell alloimmunization in sickle cell disease despite transfusion from Rh-matched minority donors.  Blood 2013; 122: 1062-1071; doi: https://doi.org/10.1182/blood-2013-03-490623), however, the experience in the UK is certainly that, if you can match the Rh type of the donor and the recipient (by that, I mean giving Ro donor blood to an Ro recipient; not rr blood to an Ro recipient, unless this cannot be avoided), then the formation of other antibody specificities is somewhat reduced.  This is partly due, of course, to the Ro type being far more common in both donors and recipients of Black ethnicity, which, in a way, takes care of both the Rh and K antigens (excluding mutations), but, almost by accident, also takes care of some other antigens and antibodies.  For example, the Fya antigen is only expressed on the red cells of approximately 10% of these donors, while the Jkb antigen, not the most immunogenic antigen one can quote, is only expressed on the red cells of approximately 49% of these donors, compared with the mid to high 70%s in most other donors.

I am not saying, therefore, that matching Rh and K types is a panacea for preventing antibody production, but we have found (both empirically and by more rigorous research) that antibody production is lower by adopting this fairly simple measure.  We have also recently genotyped many of our haemoglobinopathy patients, revealing those with, amongst other things, RH gene mutations.  What we have to do now is genotype our donors from the Black ethnic backgrounds, and then match the two, so that bespoke units are provided.  This is ambitious, but should be attainable, at least at a decent level, within the next few years.

Our current protocol is to genotype our WAA, SS, patient's with multiple antibodies, and anyone else with difficult workups.

I read that the Swiss genotyped their blood supply rather inexpensively using the Maldi-Tof. I could be wrong, but I think it only cost them $80,000-$30/donor. This was mind blowing to me since we pay significantly more than $30/genotyping and it's the HEA one that does not include all the rares and variants.

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  • 1 month later...

Still old school........why..........because I'm old..............

Is RBC genotyping our future? But first..............

Has research revealed if the extent of RBC antigen polymorphism higher than previously known by the number of antigen specificities?  Are there serologically indistinguishable variants or subtypes identified, and if these variants are different from the wild type only by a very few amino acid substitutions, can these be functionally distinct and relevant in genotype matching for transfusion and hematopoietic stem cell transplantation?   Which are clinically significant for transfusion purposes or hematopoietic stem cell transplantation or GVHD?

These are similar issues that the HLA transplantation field has been discussing.   Are blood bankers (Immunohematology field) today also discussing similar issues at regional and national meetings?

I may be off track and need to get back involved with meeting to get "re-educated" and how far we have progressed over the last 20 years.

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  • 2 weeks later...

Sorry for leaving this so long mrmic; I completely forgot.

We know of many mutations within the genes of the MNS, Rh, Diego and Kell Blood Group Systems, but others are beginning to "show up", as it were.  We know more about the MNS, Rh, Diego and Kell Blood Group Systems simply because these systems contain the highest number of antigens, and so have been studied extensively.  Indeed, more is known about the Rh Blood Group System than any other, because there are 55 different antigens within this system, and because the antigens are protein-based, and so can easily be isolated from the red cell membrane.  The RHD and RHCE genes were isolated in the late 1980s/early 1990s by, amongst others, Neil Avent (a friend and colleague of mine, I am honoured to say), and from then onwards, the world of blood group serology began to change.

To give you some idea as to where we are now, there are 24 genetic backgrounds to the categorised D antigens, 88 genetic backgrounds to D Negative, 21 genetic backgrounds to apparently normal D Positive, 45 genetic backgrounds to the DEL type, 116 genetic backgrounds to known Partial D antigens that are not part of those categorised, and at least 171 genetic backgrounds to various Weak D antigens.  These are just the mutations known within the RHD gene!  Not all of these are clinically significant, but many will look, phenotypically, like a normal D, but can produce an allo-anti-D if immunologically challenged with blood that is either from a "normal" D Positive donor, or from blood from a donor with a different mutation.

Of more clinical importance are the mutations within the RHCE gene, many of which have been identified within the Black populations, where, of course, most sickle cell patients are found, and some of whom are transfusion-dependent.  Amongst these individuals (both donors and recipients) we find many who are either hrB Negative or hrS Negative (or both), but who, phenotypically, look "normal" (for want of a better way of putting it).  The antibodies directed against these two antigens are usually not considered to be particularly clinically significant (only rarely causing anything more than a delayed haemolytic transfusion reaction.  They tend to result in an almost sub-clinical delayed haemolytic transfusion reaction, resulting in a need for more frequent transfusions, but no renal failure and other clinical sequelae.  That notwithstanding, frequent transfusions can lead to iron overload, difficulty in finding compatible blood and increased costs in bed occupancy.  If, therefore, we could match hrB Negative donors to hrB Negative recipients, even before they have made an anti-hrB, there would be benefits for the patient, in that they would undergo less frequent transfusions, leading to less in the way of iron overload, and benefits to the Health System in that the donor blood could be directed and there would be shorter bed occupancy.

I hope that helps, but, if not, get back to me.

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