Patient of >9 years (57 year old female) getting occasional transfusions (CLL patient). Always has been A POS with no atypical antibodies. Last week on pre admit XM typed A NEG. (Last received blood 89 days prior) Antibody screen was positive with what is most probably passive D. She had received winRho the day before the crossmatch was collected. Her auto and direct coombs are negative. Two different techs did the typing on different specimens by tube and gel. The next day she returned for transfusion and was restuck. Testing remained the same as the day before. She has not had a bone marrow transplant. I have talked to 3 pathologists, ARC reference lab, other area hospital blood banks and the patient's oncologist. No one can explain this. Any ideas? The little bit of info I can find on the blocked D phenomenon is limited to newborns and since this patient had a negative DAT I do not think this is the answer.

It may be worth doing an eluate even though the DAT is negative.

Many, many years ago we had an A Positive patient with myeloproliferative disorder. He was chronically transfused over many years. He had a history of a positive DAT and warm autoantibody that responded to prednisone. He showed up in the ED one Christmas Eve in blast crisis. His sample typed O Negative. A new sample was requested and also typed O Negative. Since he lived in an adjoining state, we figured he may have received multiple transfusions of O Neg red cells at a local hospital before being transferred to us. This turned out not to be the case. He came from home directly to our hospital and had not been transfused since the last time we had seen him about four months earlier. Further testing showed microscopic mixed field reactions with anti-A and anti-A,B but his D typing was consistently negative. This was long before flow cytometry and molecular testing. Our only explanation was antigen loss due to his hematologic malignancy. This is not uncommon for ABH antigens but much rarer with Rh. Having loss of both A and D antigens is extremely unusual. Unfortunately, since this happened during the Christmas holiday and the patient passed away within two days of admission we did not have the opportunity to send sample out to any reference lab.

Please keep us informed on any new findings. Interesting case!

This does sound very similar. I would like to find some literature.

Human Blood Groups, Geoff Daniels, second edition, page 250:

'Abnormal expression of some Rh antigens has occasionally been observed in patients with myeloid leukaemias, polycythaemia, and other myeloproliferative disorders. In most cases these patients appear to be mosaics with two populations of red cells of different Rh phenotype (), although a few have complete loss of certain Rh antigens (662-665). One patient with myeloid metaplasia, previously known to be D+, was found to be D-, and had made anti-D+C (663)........

663: Cooper et al: Loss of Rh antigen associated with aquired Rh antibodies and a chromosome translocation in a patient with myeloid metaplasia. Blood 1979; 54:642-7

664: Mohandas K et al: Loss and reappearance of Rh (D) antigen in an individual with acute myelogenous leukaemia. Immunohaematology 1994; 10: 134-5

665: Chérif-Zahar B et al: Shift from Rh-positive to Rh-negative phenotype caused by a somatic mutation within the RHD gene in a patient with chronic myeloid leukaemia. Br. J. haematol 1998; 102: 1263-70

Good reading!

Anna

cudos to Anna Galvania. Great references.

I just have a quick question. Have you done the D, C and E typings (along with an Rh control) with IS and extended incubation at RT or 37 (depending on your source of Rh reagents and the package insert) and looked at the typings microscopic for mixed field?

You might want to follow the person, because we had a patient years ago who was really an R2r and both the D and E typings were only micro and she appeared to be rr (D-E-) and when her anemia was corrected her and D and E typings were reactive macroscopic. She was the first report of this phenomenon in anemia.

MarilynM

I have not done C and E typings. The D was done at IS and 37 degree 15 minute incubation with LISS and looked at microscopically. I have not had time to do anything else with this patient, but we do have plenty blood, so hopefully I can 'play' with it Friday. Thanks.

Just an overly simplistic thought. It was mentioned the patient had received winRho the day before. Could this be a prozone effect with her antigen sites being blocked by the passive D. I would think the DAT would be positive but maybe not.

My immediate thoughts are along the line of John Staley. Would this be a blocking phenomenon due to the WinRho? However that does not explain the negative DAT. We do not carry WinRho at our facility. Is the WinRho product composed of IgG or IgM?

Do you have another source of anti-D at your facility? For example, if you routinely use an Ortho product, do you have access to an Immucor anti-D? Since Immucor is a different clone you might have different reactions. Or even a different clone source from your same supplier?

Just a few random thoughts that I hope might help. I'll check back later for other possibilities.

Randy

Patient of >9 years (57 year old female) getting occasional transfusions (CLL patient). Always has been A POS with no atypical antibodies. Last week on pre admit XM typed A NEG.

We have quite a few patients who receive WinRho (it seems like it slowed down for a year or so, but in the past few months we are seeing it again from our cancer care center physicians) and they have always had positive DATs and still type 4+ D pos. I can't find references for WinRho blocking all the D antigen sites, but who knows. I really appreciate all the ideas I am getting.