W. Dahr, in Recent Advance in Blood Group Biohchemistrv, V. Vengelen-Tyler and W.J. Judd, eds. American Association of Blood Banks, Arlington, VA (1986) pp. 23-65. 32. J-P. Cartron, in Monoclonal antibodies against human red blood cell and related antigens. P. Rouger and C. Salmon, eds. Arnette, Paris (1987) pp. 69-97. 33. D.J. Anstee, Vox Sang., 58, 1-20 (1990). 34. P. Tippett, in Blood Group Systems: Rh. V. Vengelen-Tyler and S. Pierce, eds. American Association of Blood Banks, Arlington, VA (1987) pp. 25-53 35. C. Lomas, J. Poole, N. Salaru, M. Redman, K. Kirkley, M. Moulds, J. McCreary, G.S. Nicholson, H. Hustinx and C. Green, Vox Sang., 59, 39-43 (1990). 36. J. Poole, H. Hustinx, H. Gerber, C. Lomas, Y.W. Liew, and P. Tippett, Vox Sang., 59, 44-47 (1990). 37. M. Bizot, C. Lomas, F. Rubio and P. Tippett, Transfusion, 28, 342-345 (1988). 38. N.A. Ellis, T-Z. Ye, S. Patton, J. German, P.N. Goodfellow and P. Weller, Nature Genet., 6, 394-400 (1994). 39. C. Gelin, F. Aubrit, A. Phalipon, B. Raynal, S. Cole, M. Kaczorek and A. Bernard, EMBO J., 8, 3253-3259 (1989). 40. M.N. Dworzak, G. Fritsch, P. Buchinger, C. Fleischer, D. Printz, A. Zellner, A. Schollhammer, G. Steiner, P.F. Ambros and H. Gadner, Blood, 83, 415-425 (1994). 41. R. Levy, J. Dilley, R.l. Fox and R. Warnke, Proc. Natl. Acad. Sci. USA, 76, 6552-6556 (1979). 42. G.S. Banting, B. Pym, S.M. Darling and P.N. Goodfellow, Mol Immunol., 26, 181-188 (1989). 43. P. Goodfellow, G. Banting, D. Sheer, H.H. Ropers, A. Caine, M.A. Ferguson-Smith, S. Povey and R. Voss, Nature, 302. 346-349 (1983). 44. S.M. Darling, G.S. Banting, B. Pym, J. Wolfe and P.N. Goodfellow, Proc. Natl. Acad. Sci. USA, 83, 135-139 (1986). 45. P.N. Goodfellow and P. Tippett, Nature, 289. 404-405 (1981). 46. P. Tippett, M-A. Shaw, C.A. Green and G.L. Daniels, Ann. Hum. Genet., 50, 339-347 (1986). 47. G.S. Banting, B. Pym and P.N. Goodfellow, EMBO J., 4, 1967-1972 (1985). 48. F. Latron, D. Blanchard and J-P. Cartron, Biochem. J., 247, 757-764 (1987). 49. R. Herron and G.A. Smith, Biochem. J., 262. 369-371 (1989). 50. A.C. Petty and P. Tippett Submitted.

1995 ◽  
pp. 200-205
Keyword(s):  
Monoclonal Antibodies ◽  
Blood Cell ◽  
Blood Group ◽  
Red Blood Cell ◽  
American Association ◽  
Blood Banks

scholarly journals Prevalence of Red Blood Cell Major Blood Group Antigens and Phenotypes among Omani Blood Donors

2019 ◽  
Vol 34 (6) ◽  
pp. 496-503
Author(s):  
Arwa Z. Al-Riyami ◽  
Ali Al-Marhoobi ◽  
Saif Al-Hosni ◽  
Sabah Al Mahrooqi ◽  
Michael Schmidt ◽  
...  
Keyword(s):  
Blood Cell ◽  
Blood Group ◽  
Red Blood Cell ◽  
Blood Donors ◽  
Blood Group Antigens

Transfusion Of Thawed Rare Red Blood Cell Units In Finland

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 4823-4823
Author(s):  
Eeva Juvonen ◽  
Inna Sareneva ◽  
Katri Haimila ◽  
Anu Elina Korhonen ◽  
Susanna Sainio
Keyword(s):  
Blood Cell ◽  
Blood Group ◽  
Red Blood Cell ◽  
Conflicts Of Interest ◽  
Blood Groups ◽  
Red Cross ◽  
Reference Laboratory ◽  
Red Cell ◽  
Chronic Anemia ◽  
Blood Hemoglobin

The Finnish Red Cross Blood Service performs blood grouping of all blood donations in Finland and serves as a national reference laboratory in pre-transfusion testing of patients. In addition to ABO and RhD blood groups, other Rh antigens and K antigen are also determined from all red cell units. The antigens of JK, FY, and MNS blood group systems are analyzed from selected donors. The extensive donor typing procedure includes antigens from KEL, LW, LU, CO, DO, DI, YT, GE and CROM blood group systems, performed either serologically or by genotyping. Patients negative for a high frequency blood group antigen present a challenge for transfusion laboratories. A blood group is considered rare if the prevalence is 1:1000 or less, with the most common rare phenotypes in Finland being LWa neg, Jk:-3 and Pk. To ensure the availability of matching blood for patients with a rare blood group, we started a freezing program of rare blood in Finland with Haemonetics ACP 215 process in April 2010. The system is closed, therefore after thawing the units are safe for use for 7 days. 18 blood groups which were included in the program were determined based on the known rare blood groups in the Finnish population. Blood groups which are globally rare but more common in Finland, such as Jk:-3 and LWa neg, are represented in our storage and also available internationally. The aim of the present study was to analyze the status of the freezing program of rare red blood cells in Finland. For the analysis we asked the transfusion data of rare red blood cell units delivered to 10 national and 2 international hospitals. Results: In 2010-2012, altogether 204 units of rare blood were stored, including units of all the predefined rare phenotypes except Vel neg. With the exception of Vel neg, Hrs neg and Oh blood groups, we have been able to meet the need for rare blood in Finland using Finnish donors. Altogether 55 units have been thawed and distributed to 27 adult patients. The indication was delivery in 3 cases, surgery in 6 cases, and chronic anemia in 4 cases. For the present analyses the transfusion data of 49 units was available. The data of 6 Coa neg units is missing. Altogether 22 / 49 (45%) of the units were transfused. In 14 cases the blood was transfused to the patient it was intended for, and in 8 cases to another patient, 27 units were discarded. There were no transfusion associated complications. The hemoglobin response was evaluable in 7 patients. In 4 patients with a chronic anemia the median blood hemoglobin response per a unit was +8 g/l, range +2 - +16 g/l. In 3 patients with blood loss during an operation the median increase in blood hemoglobin value was +7 g/l per unit, range +4 – +12 g/l. Conclusions: Compared to the common 24 hour eligibility of thawed red cell units, our units valid for 7 days are preferable in countries like Finland with long distances and in international rare blood deliveries. We have been able to offer rare blood to Finnish patients. The hemoglobin response was reasonable and there were no transfusion associated complications. Our next challenge will be to recruit Finnish blood donors with different ethnic backgrounds (eg. immigrants) and identify their rare blood groups. We have already expanded our program to include rare combinations of common blood groups. Disclosures: No relevant conflicts of interest to declare.

Effect of red blood cell preservation by droplet freezing with non-permeable cryoprotective agents in blood group antigen reactivity

2017 ◽  
Vol 27 (2) ◽  
pp. 142-146 ◽  
Author(s):  
M. A. B. Chagas ◽  
D. G. Chaves ◽  
S. K. Haddad ◽  
E. M. A. Ubiali ◽  
L. C. Schmidt ◽  
...  
Keyword(s):  
Blood Cell ◽  
Blood Group ◽  
Red Blood Cell ◽  
Blood Group Antigen ◽  
Cryoprotective Agents ◽  
Cell Preservation ◽  
Antigen Reactivity

RECOVERY OF HEMATOPOIESIS AFTER BLOOD-GROUP-INCOMPATIBLE BONE MARROW TRANSPLANTATION WITH RED-BLOOD-CELL-DEPLETED GRAFTS

1985 ◽  
Vol 39 (5) ◽  
pp. 514-519 ◽  
Author(s):  
J. H. F. FALKENBURG ◽  
M. R. SCHAAFSMA ◽  
J. JANSEN ◽  
A. BRAND ◽  
H. M. GOSELINK ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Transplantation ◽  
Blood Cell ◽  
Blood Group ◽  
Red Blood Cell ◽  
Marrow Transplantation

scholarly journals Blood Group Changed in a Patient with Acute Myelocytic Leukemia

2013 ◽  
Vol 14 (1) ◽  
pp. 77-79 ◽  
Author(s):  
Shah Md. Sarwer Jahan ◽  
A.K.M Kamruzzaman ◽  
Md. Ismail Hossain ◽  
Md. Abdul Matin ◽  
Md. Zakir Hossain
Keyword(s):  
Blood Cell ◽  
Blood Group ◽  
Red Blood Cell ◽  
Acute Myelocytic Leukemia ◽  
Blood Group A ◽  
Myelocytic Leukemia ◽  
Group A

Gain of red blood cell antigens has been described in patients with acute myelocytic leukemia (AML). This paper describes the gain of blood group A antigen in a patient with AML. At the time of diagnosis the patient’s red cellsshowed the 0 Rh (D) - phenotype. After induction of remission with one courses of Daunorubicin, Cytarabine, her blood group was changed to A Rh (D) - phenotype.DOI: http://dx.doi.org/10.3329/jom.v14i1.14559 J MEDICINE 2013; 14 : 77-79

scholarly journals Red Blood Cell Allo-Antibodies after Allogeneic Hematopoietic Stem Cell Transplantation

Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 2551-2551
Author(s):  
Astrid Beerlage ◽  
Joerg Halter ◽  
Sabine Gerull ◽  
Michael Medinger ◽  
Tanja Ruefli ◽  
...  
Keyword(s):  
Risk Factors ◽  
Stem Cell ◽  
Hematopoietic Stem Cell Transplantation ◽  
Stem Cell Transplantation ◽  
Blood Cell ◽  
Cell Transplantation ◽  
Blood Group ◽  
Red Blood Cell ◽  
Hematopoietic Stem ◽  
Rbc Transfusion

Abstract Introduction Patients undergoing allogeneic hematopoietic stem cell transplantation (HSCT) may require red blood cell (RBC) transfusions. AB0 blood group barrier is the clinically most important RBC group in transfusion medicine and HSCT and patients always receive AB0 compatible RBC transfusions. Some patients however develop allo-antibodies against minor RBC antigens. To date there is only limited information about the specificity, immuniser and risk factors for the development of RBC allo-antibodies. In this retrospective single centre study we aimed to identify specificities, risk factors and clinical significance of the development of RBC allo-antibodies in HSCT patients. Methods In this study, we examined the occurrence of RBC alloantibodies in all consecutive patients treated with allogeneic HSCT at the University Hospital Basel between 1996 and 2017 receiving RBC transfusions. RBC and PLT components were all leukocyte depleted. As of 2012, all PLT components were pathogen reduced using the Intercept Blood system. AB0 and extended RBC typing of donor/ recipient pairs, the total number of RBC transfusions and their blood group typing (AB0 and extended RBC antigen typing when available) and the detection of RBC allo-antibodies were analysed and related to clinical outcome parameters. Results 1314 donor/ recipient pairs were analysed. 110 (13%) of patients developed RBC allo-antibodies, 66 patients (5%) prior to HSCT, and 103 (8%) developed the first RBC allo-antibody after HSCT. 8 patients (0.6%) with an RBC allo-antibody before HSCT developed further RBC allo-antibodies after HSCT. Most patients developed only one RBC allo-antibody but in single patients up to 6 antibodies could be detected. The median time between HSCT and the detection of the antibody was 61 days, corresponding to the phase of the most intensive immunosuppressive treatment. In 60% of the patients developing RBC allo-antibodies after HSCT, the antibody was neither directed against the stem cell donor nor the recipient. In these cases, immunization occurred most likely by RBC transfusion. Anti-Rhesus-group antibodies are the most common antibodies (57%). >10 RBC transfusions and the development of GvHD were risk factors for the development of antibodies. There was no significant difference in the occurrence of RBC allo-antibodies between donor type (related vs. unrelated), age or sex of the recipient. Only few patients showed significant haemolysis in the period of the detection of the antibody. The direct antiglobulin test (DAT) was positive in 66% of the cases. Haemolysis defined as an increase of bilirubin, LDH or reticulocytes and a haemoglobin drop of more than 10 g/l could only be reported in 6% of the cases with antibodies detected. The development of RBC allo-antibodies per se has no effect on the survival of patients (1y-survival 70±3% (without antibody) versus 68 ± 9%). However, evidence of haemolysis (even without drop of haemoglobin) in the context of allo-antibodies, is associated with significantly worse survival (1y- survival 75 ± 10% versus 42 ± 20%). Conclusion Allo-Antibodies after HSCT significantly contribute to the difficulties in transfusion management of these patients. Formation of RBC allo-antibodies is not frequent, but patients showing haemolysis after the development of an RBC allo-antibody show decreased survival. Most RBC allo-antibodies appear to be induced by RBC transfusion rather than by minor blood group mismatching between donor/ recipient pairs. Disclosures Heim: Novartis: Research Funding.

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