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Posts posted by cbaldwin
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We had a OB patient with anti-Goa years ago when I was new blood banker. CORD DAT was positive for a baby whose blood type was same as mother. The DAT was weak positive. Performed it 3X, showed microscopic reaction to my supervisor, then my supervisor also repeated DAT which was positive. Mother and baby's specimen sent out and Anti-Goa was id'd. Please do not ask me for nationality becasue I do not remember patient's name. I was very excited!!!!!!!
It sounds as if it was a very weakly positive DAT--did the cells roll off the button roughly and that made you suspicious so that you examined it under the microscope? I would have missed it! I applaud you!
I promise not to ask you for the nationality of the patient, but according to The Blood Group Antigen Facts Book, Goa is only found in Blacks (2%) and anti-Goa can cause mild to severe HDFN. Anti-Goa was first discovered in a Mrs. Gonzales and named after her.
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How exciting!
Were the anti-Inb and anti-Yta in the same individual, and if so, did you use trypsin to differentiate between the two? We just had an exam and one of the questions was what enzyme to use to differentiate between anti-Yta and Inb. The answer was “trypsin” because Yta is resistant to trypsin and Inb is sensitive.
Also, did the anti-Yta react with almost all cells in the panel since the incidence of Yta is about 99%?
Lastly, if the anti-Yta and anti-Inb were not in the same individual, was the Yta negative patient Jewish or from Israel and was the Inb negative individual from Asian, Iran or an Arabic country?
It’s fun being a student.....
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Thanks L106--I think the information I was looking for is that the vast majority of Rh negative units are r,r (dce/dce)--C
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I am posting this in the Education forum because I am a student. In the thread, "Topics for Education", numerous suggestions were offered, and I have a question about one of the suggestions. I am starting a new thread because it is a new subject.
“plus understanding the risks of making anti-c and why you don't screen the O negs for c when you have gone through all the O pos units”
I would like to make sure I understand this one. Anti-c is clinically the most important Rh antibody after D.
First, I'm assuming this is an emergency and the O positive units were given without screening, so the patient has been exposed to c. Secondly, the incidence of the c antigen in Caucasians is 80%, in Blacks 96% and in Asians 47%, so there is a good chance that if the patient is Caucasian or Black they won't develop anti-c.
I hope someone will correct me or comment on my musings. I am adsorbing a lot of information (such as the difference between adsorbtion and absorbtion) but information is not knowledge and I need all the help I can get!
Thank you!
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We are a 25 bed hospital, 4 hours from our blood supplier (although the Highway Patrol can make the trip to deliver emergency blood products to us in 2 hours). We are an overstock hospital for two smaller hospitals near us. We stock 14 OP, 12 AP, 4 AN, 2 ABP, 4BP, and 8 ON. We need to order before 7am if we want delivery and delivery is only Monday through Friday. Otherwise, it's the highway patrol.
We seldom waste units, not because we use them—our usage is low—but because our blood supplier has asked us to return units between 14 and 21 days outdate. It seems odd at times, but it works. When we order blood we always request “long dated” units.
But it is worrisome. Last week, Thursday afternoon, an A, Rh negative GI bleeder came in. She went from 7.2 to 5.1 hemoglobin in an hour, took 2 units AN, then was whisked off to surgery. The physician ordered 4 more units. Friday morning, her H/H was stable, but I was in a quandary as to how many ON units to stock up for the weekend. Would our patient need a lot more blood? Would there be a big trauma? It turned out that our blood supplier had no ON to send us, the patient didn't need anymore blood, and there were no traumas.
Except for a 10 year stint in Oregon, I have been at this hospital since 1983. The one thing that has really helped us maintain an adequate blood supply and reduce usage was when the narrow 2 lane highway that winds up our valley from metropolitan Southern California to the ski resort north of us was enlarged to 4 lanes. 2 lanes to 4 lanes—much fewer Friday evening head-on crashes.
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Unfortunately nor Pony. If only it were that simple!
Until fairly recently, if the mutation resulted in a change to an amino acid residue either in the cytoplasm of the cell or was in the transmembraneous part of the Rh molecule, but not any change to the extra cellular amino acid residues, we (in the Reference Service) tended to call it a Weak D. If the amino acid residue alteration was in the extracellular part of the Rh polypeptide, we would call it a Partial D. This, however, did not take into account the fact that amino acid residue alterations in the cytoplasmic or transmembraneous part of the Rh polypeptide can drastically alter the tertiary structure of the molecule, including that part of the molecule that is extracellular.
It is partly because of this that I agree that any RHD gene that is different from the wild-type should be called a variant.
All that having been said though, very many individuals within the hospital community (and some in the Reference community, to be fair), seem to use the terms Weak D, Partial D, D variant and Du interchangably (if that is how it is spelt!), and this becomes immensely confusing as one person talking to another, about exactly the same mutation, may be totally at odds with one another, and not undertsand for a long time that they are talking about exactly the same thing!
The first ever thread I started on this site was about the use of correct nomenclature. It bombed!!!!!!!!!!!!!!!!!!!
I have yet to be in a conversation regarding mutations to RHD or RHCE, but I am preparing myself to be understood.
Malcolm, here is someone who agrees with your opinion!
From page 210, "Human Blood Groups", 2nd edition, 2007,Geoff Daniels:
"Weak D red cells are considered to have all epitopes of D, expressed weakly. Partial D red cells have some epitopes missing, the remainder being expressed normally. Partial weak D cells have some epitopes missing, the remainder being expressed weakly. These divisions, however, are often not distinct and are difficult to differentiate, although the ability to make alloanti-D in partial D phenotypes, but not in weak D phenotypes, is probably the most suitable definition if one is required. However, some individuals with red cell phenotypes initially regarded to be weak D have produced alloanti-D. Weak D is often associated with RHD mutations encoding amino acid substitutions in the cytoplasmic or membrane-spanning domains of the D protein, whereas partial D is usually caused by changes in the extracellular loops. However, this is not absolute and is dependent, to some extent, on the model for the conformation of the Rh proteins in the membrane used. The terms "weak D" and "partial D" are retained here to assist in providing some degree of order to the large number of aberrant D antigens, but there is a compelling argument in favour of scrapping the terms and replacing them with "D variant".
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UBS does not defer donors who have received B12 injections
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Hi everyone,
I need your help in figuring this one out:cries:. patient is Hispanic; Autocontrol: negative
DAT= negative
All screen cells(3 cell panel) and antibody panel positive: all tests ran in PeG at 37C
immediate spin= 2+
coomb's phase= 3-4+ all cells;
DTT treated cells= same reactions(resistant)
Enzyme(Papain)= enhanced reactions(resistant)
I tested with Lub-, I-, Vel-, Jk(a-b-), P- cells but all same reactions= 2+ immediate spin (RT), and 3+ AHG phase;
Also tried testing patients cells with anti-Ge2, -Ge3, -Dib, -Wrb antisera =all tested positive for the antigen.
I hope you let us know what this antibody turns out to be!
In the meantime, please, would somebody educate me as to why the Lub-, I-, Vel-, Jk(a-b-), P- cells were chosen for testing, and why the anti-Ge2, -Ge3, -Dib, -Wrb antisera was chosen? I am a BB newbie and am learning. And please, get technical!
Thank you!
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I just came across a letter to the editor in Transfusion about “naturally occurring” anti-Jka. It is in Transfusion, Volume 45, Issue 6, pages 1043–1044, June 2005
It involves a case of “naturally occurring” anti-Jka in a 7-month-old boy with orchitis, epididymitis, and an Escherichia coli urinary tract infection.
An antibody detection test was positive and anti-Jka was identified by gel test using a low-ionic-strength saline. Repeat antibody detection tests were the same during the patient’s 8-day hospitalization. 6 months later the antibody detection test was negative.
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cbaldwinHi Mabel! What test would we request if we wanted DNA testing on the baby from the mom's sample? And how are the baby's RBCs separated from the mom's RBCs for testing? Catherine
Oops--RBCs don't have DNA! What company does this test?
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Hi Mabel! What test would we request if we wanted DNA testing on the baby from the mom's sample? And how are the baby's RBCs separated from the mom's RBCs for testing? Catherine
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My source for the information regarding the "growing trend" ("becoming common practice" is the exact wording) is Geoff Daniel's "Human Blood Groups". I wonder if it is a growing trend in Europe, but not in the United States. It is just something I wonder about...
Okay, so here is my next question...It seems that anti-K in OB patients is treated as a more serious issue in the Netherlands and in the UK than in the US. Am I correct about that and is there an explanation?
Sorry, I can't help but wonder about this, and I have no practical knowledge or experience in this matter....my information comes from books.
I am looking forward to whatever instruction is available! Thank you!
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Aakupaku! Thank you for your feedback!
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Thank you for this very thorough explanation. The association with HLA-DRB1 polymorphism is interesting--wonder what's behind that and what your staff member will find in her research!
And, I still wonder if there is a growing trend in the US to transfuse K negative units to K negative women of child-bearing age!
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I recently read that because anti-K can cause severe HDN it is becoming common practice for girls and women of child-bearing age to be transfused only with K- red cells and, if I understand this correctly, in the Netherlands K negative units are always given to women under 45.
What is the policy at your facility? How frequently is HDN caused by anti-K seen? I would like to hear opinions on this!
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Thank you Peter and Malcolm for your input!
It is interesting that in the Netherlands K-negative blood is given routinely to women below 45 and I am wondering if many facilities in the US have this policy and how frequently anti-K HDN is seen in the US. I just got Geoff Daniel's "Human Blood Groups" and what is said about anti-K HDN is slightly different than what is in the AABB but confirms what Peter relates.
I think I will start a new thread on anti-K and HDN since this thread is really about anti-S. May I refer to your statements in this thread?
Thank you!
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Okay--I just found where I read that a titer of 8 is significant for anti-K. Page 633 17th edition of AABB manual.
"The critical titer for anti-D......should be selected at each facility and is usually 16 or 32 in the AHG phase......These titer criteria apply to anti-D, to other Rh antibodies, and generally to other clinically significant antibodies, with Kell system antibodies being an exception. Kell system antigens are present on early red cell precursors, so even a maternal anti-K of relatively low titer can cause erythropoietic failure and severe anemia. A critical titer of 8 is generally accepted for anti-K."
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Yes! Thank you! And is anti-K significant at a titer of 8 in OB patients? Just am wondering. Thank you!
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Forgot to mention that this OB patient with the anti-S is 6 weeks pregnant.
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We have a 34 year old OB patient with a weak anti-S--the titer is "1". She has never been transfused and has never been officially diagnosed as pregnant, although she and her physician suspect that she has been pregnant and has miscarried very early in the pregnancy before she suspected she was pregnant. She has been trying to get pregnant for several years.
How often do you see an anti-S in a patient like this? How could she have developed anti-S? (She is negative for the S antigen).
How early is the S antigen expressed on fetal RBCs? Is it a strong expression? Could this anti-S be part of the reason she is having trouble conceiving?
She will be coming in monthly for antibody titers. I vaguely remember that a significant titer for anti-D is 16, but a significant titer for anti-K is lower (8?) because K is expressed earlier on fetal cells and is a strong immunogen. Where does anti-S fit here? What is a significant titer for anti-S?
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What type of AHG reagent are you using? I have recently learned that sometimes anti-Jka will not be detected unless the AHG reagent includes complement. Using monospecific anti-IgG can miss some anti-Jkas.
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Thank you Malcolm for putting the lectin power point presentation together and making it available. It is beautiful. I didn't realize there were so many but there must be many more considering we all develop anti-A and anti-B in our first months of life! And the culinary side note is great!
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Perfect! Thank you very much! It's a beautiful slide show!
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We have tried several computers and tried the internet connection at work and at home--no luck with opening this file. We can open other power point presentations! Is it difficult to split it into smaller parts?
anti-e or not?
in Case Studies
Posted
Hi Malcolm! Hope you are doing well!
I have a question about Ch/Rg reactivity in LISS, PEG and gel. Joann Moulds, in a presentation called "Don't Call them HTLA's!" mentions that a characteristic of Ch/Rg is reactivity in gel and non-reactivity in LISS and PEG. I can't find a scientific explanation--is it because the Ch/Rg antigens are adsorbed onto RBCs and in LISS and PEG they disassociate?
Thanks!
Catherine