Rh discrepancies caused by variable reactivity of partial and weak D types with different serologic techniques
dc.contributor.author | Denomme, Gregory A. | en_US |
dc.contributor.author | Dake, Louann R. | en_US |
dc.contributor.author | Vilensky, Daniel | en_US |
dc.contributor.author | Ramyar, Lily | en_US |
dc.contributor.author | Judd, W. John | en_US |
dc.date.accessioned | 2010-06-01T22:36:53Z | |
dc.date.available | 2010-06-01T22:36:53Z | |
dc.date.issued | 2008-03 | en_US |
dc.identifier.citation | Denomme, Gregory A.; Dake, Louann R.; Vilensky, Daniel; Ramyar, Lily; Judd, W. John (2008). "Rh discrepancies caused by variable reactivity of partial and weak D types with different serologic techniques." Transfusion 48(3): 473-478. <http://hdl.handle.net/2027.42/75591> | en_US |
dc.identifier.issn | 0041-1132 | en_US |
dc.identifier.issn | 1537-2995 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/75591 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=18067505&dopt=citation | en_US |
dc.description.abstract | RhD discrepancies between current and historical results are problematic to resolve. The investigation of 10 discrepancies is reported here. STUDY DESIGN: Samples identified were those that reacted by automated gel technology and were negative with an FDA-approved reagent. Reactivity with a commercially available panel of monoclonal anti-D was performed. Genomic DNA was evaluated for RHD alleles with multiplex RHD exon polymerase chain reaction (PCR), weak D PCR-restriction fragment length polymorphism, and RHD exon 5 and 7 sequence analyses. RESULTS: The monoclonal anti-D panel identified two samples as DVa, yet possessed the DAR allele. Two weak D Type 1 samples had a similar monoclonal anti-D profile, but only one reacted directly with one of two FDA-approved anti-D. Only two of four weak D Type 2 samples reacted directly with one FDA-approved anti-D, and their D epitope profile differed. CONCLUSIONS: The monoclonal anti-D reagents did not distinguish between partial and weak D Types 1 and 2. Weak D Types 1 and 2 do not show consistent reactivity with FDA-approved reagents and technology. To limit anti-D alloimmunization, it is recommended that samples yielding an immediate-spin tube test cutoff score of not more than 5 (i.e., ≤1+ agglutination) or a score of not more than 8 (i.e., ≤2+ hemagglutination) by gel technology be considered D– for transfusion and Rh immune globulin prophylaxis. That tube test anti-D reagents react poorly with some Weak D Types 1 and 2 red cells is problematic, inasmuch as they should be considered D+ for transfusion and prenatal care. Molecular tests that distinguish common partial and Weak D types provide the solution to resolving D antigen discrepancies. | en_US |
dc.format.extent | 76730 bytes | |
dc.format.extent | 3109 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.publisher | Blackwell Publishing Inc | en_US |
dc.rights | 2007 American Association of Blood Banks | en_US |
dc.title | Rh discrepancies caused by variable reactivity of partial and weak D types with different serologic techniques | en_US |
dc.type | Article | en_US |
dc.subject.hlbsecondlevel | Oncology and Hematology | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.identifier.pmid | 18067505 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/75591/1/j.1537-2995.2007.01551.x.pdf | |
dc.identifier.doi | 10.1111/j.1537-2995.2007.01551.x | en_US |
dc.identifier.source | Transfusion | en_US |
dc.identifier.citedreference | Flegel WA, Wagner FF. Molecular biology of partial D and weak D: implications for blood bank practice. Clin Lab 2002; 48: 53 - 9. | en_US |
dc.identifier.citedreference | Flegel WA, Wagner FF. RHD epitope density profiles of RHD variant red cells analyzed by flow cytometry. Transfus Clin Biol 1996; 3: 429 - 31. | en_US |
dc.identifier.citedreference | Wagner FF, Frohmajer A, Ladewig B, Eicher NI, Lonicer CB, MÜller TH, Siegel MH, Flegel WA. Weak D alleles express distinct phenotypes. Blood 2000; 95: 2699 - 708. | en_US |
dc.identifier.citedreference | Noizat-Pirenne F, Ansart-Pirenne H, Menanteau C, Braddock D, Rouzaud AM, Klein MT, Patereau C, Rouger P, Le Pennec PY. Serological studies of monoclonal RH antibodies with RH1 (D), RH2 (C), RH3 (E) and RH5 (e) variant RBCs. Transfus Clin Biol 2003; 10: 319 - 23. | en_US |
dc.identifier.citedreference | Tippett P, Lomas-Francis C, Wallace M. The Rh antigen D: partial D antigens and associated low incidence antigens. Vox Sang 1996; 70: 123 - 31. | en_US |
dc.identifier.citedreference | Flegel WA. Molecular genetics of RH and its clinical application. Transfus Clin Biol 2006; 13: 4 - 12. | en_US |
dc.identifier.citedreference | Williams M. Monoclonal reagents for rhesus-D typing of Irish patients and donors: a review. Br J Biomed Sci 2000; 57: 142 - 9. | en_US |
dc.identifier.citedreference | Denomme GA, Wagner FF, Fernandes BJ, Li W, Flegel WA. Partial D, weak D types, and novel RHD alleles among 33,864 multiethnic patients: implications for anti-D alloimmunization and prevention. Transfusion 2005; 45: 1554 - 60. | en_US |
dc.identifier.citedreference | Fung Kee FK, Eason E, Crane J, Armson A, De La Ronde S, Farine D, Keenan-Lindsay L, Leduc L, Reid GJ, Aerde JV, Wilson RD, Davies G, Desilets VA, Summers A, Wyatt P, Young DC; Maternal-Fetal Medicine Committee, Genetics Committee. Prevention of Rh alloimmunization. J Obstet Gynaecol Can 2003; 25: 765 - 73. | en_US |
dc.identifier.citedreference | Jones J, Scott ML, Voak D. Monoclonal anti-D specificity and Rh D structure: criteria for selection of monoclonal anti-D reagents for routine typing of patients and donors. Transfus Med 1995; 5: 171 - 84. | en_US |
dc.identifier.citedreference | Scott M. Rh serology–coordinator's report. Transfus Clin Biol 1996; 3: 333 - 7. | en_US |
dc.identifier.citedreference | Wagner FF. The RhesusBase [database on the Internet]. Ulm: DRK-Blutspendedienst Baden-Wurttemberg-Hessen; 2006. Available from: http://www.uni-ulm.de/%7Efwagner/RH/RB/ | en_US |
dc.identifier.citedreference | Wagner FF, Ernst M, Sonneborn HH, Flegel WA. A D(V)-like phenotype is obliterated by A226P in the partial D DBS. Transfusion 2001; 41: 1052 - 8. | en_US |
dc.identifier.citedreference | Hemker MB, Ligthart PC, Berger L, van Rhenen DJ, van der Schoot CE, Wijk PA. DAR, a new RhD variant involving exons 4, 5, and 7, often in linkage with ceAR, a new Rhce variant frequently found in African blacks. Blood 1999; 94: 4337 - 42. | en_US |
dc.identifier.citedreference | Gassner C, Schmarda A, Kilga-Nogler S, Jenny-Feldkircher B, Rainer E, MÜller TH, Wagner FF, Flegel WA, SchÖnitzer D. RHD/CE typing by polymerase chain reaction using sequence-specific primers. Transfusion 1997; 37: 1020 - 6. | en_US |
dc.identifier.citedreference | Flegel WA, Wagner FF, Muller TH, Gassner C. Rh phenotype prediction by DNA typing and its application to practice. Transfus Med 1998; 8: 281 - 302. | en_US |
dc.identifier.citedreference | Legler TJ, Eber SW, Lakomek M, Lynen R, Maas JH, Pekrun A, Repas-Humpe M, Schroter W, Kohler M. Application of RHD and RHCE genotyping for correct blood group determination in chronically transfused patients. Transfusion 1999; 39: 852 - 5. | en_US |
dc.identifier.citedreference | Legler TJ, Maas JH, Kohler M, Wagner T, Daniels GL, Perco P, Panzer S. RHD sequencing: a new tool for decision making on transfusion therapy and provision of Rh prophylaxis. Transfus Med 2001; 11: 383 - 8. | en_US |
dc.identifier.citedreference | Marsh WL. Scoring of hemagglutination reactions. Transfusion 1972; 12: 352. | en_US |
dc.identifier.citedreference | Mourant A. The distribution of human blood groups and other polymorphisms. 2nd ed. London: Oxford University Press; 1976. | en_US |
dc.identifier.citedreference | Bennett PR, Le Van KC, Colin Y, Warwick RM, ChÉrif-Zahar B, Fisk NM, Cartron JP. Prenatal determination of fetal RhD type by DNA amplification. N Engl J Med 1993; 329: 607 - 10. | en_US |
dc.identifier.citedreference | Maaskant-Van Wijk PA, Faas BH, de Ruijter JA, Overbeeke MA, von dem Borne AE, van Rhenen DJ, van der Schoot CE. Genotyping of RHD by multiplex polymerase chain reaction analysis of six RHD-specific exons. Transfusion 1998; 38: 1015 - 21. | en_US |
dc.identifier.citedreference | Wagner FF, Gassner C, Muller TH, SchÖnitzer D, Schunter F, Flegel WA. Molecular basis of weak D phenotypes. Blood 1999; 93: 385 - 93. | en_US |
dc.identifier.citedreference | Wagner FF, Ladewig B, Angert KS, Heymann GA, Eicher NI, Flegel WA. The DAU allele cluster of the RHD gene. Blood 2002; 100: 306 - 11. | en_US |
dc.identifier.citedreference | Altschul SF, Gish W, Miller W, Myers EW, Lipman DJ. Basic local alignment search tool. J Mol Biol 1990; 215: 403 - 10. | en_US |
dc.identifier.citedreference | Nicholson G, Lawrence A, Ala FA, Bird GW. Semi-quantitative assay of D antigen site density by flow cytometric analysis. Transfus Med 1991; 1: 87 - 90. | en_US |
dc.identifier.citedreference | Gorick B, McDougall DC, Ouwehand WH, Overbeeke MA, Tippett P, Hughes-Jones NC, van Rhenen DJ. Quantitation of D sites on selected “weak D” and “partial D” red cells. Vox Sang 1993; 65: 136 - 40. | en_US |
dc.identifier.citedreference | Jones JW, Lloyd-Evans P, Kumpel BM. Quantitation of Rh D antigen sites on weak D and D variant red cells by flow cytometry. Vox Sang 1996; 71: 176 - 83. | en_US |
dc.identifier.citedreference | Flegel WA, Wagner FF. RHD antigen density and agglutination in RHD variant red cells. Transfus Clin Biol 1996; 3: 385 - 6. | en_US |
dc.identifier.citedreference | Beckers EA, Faas BH, Ligthart P, Overbeeke MA, von dem Borne AE, van der Schoot CE, van Rhenen DJ. Lower antigen site density and weak D immunogenicity cannot be explained by structural genomic abnormalities or regulatory defects of the RHD gene. Transfusion 1997; 37: 616 - 23. | en_US |
dc.identifier.citedreference | Wagner FF. Influence of Rh phenotype on the antigen density of C, c, and D: flow cytometric study using a frozen standard red cell. Transfusion 1994; 34: 671 - 6. | en_US |
dc.identifier.citedreference | Araszkiewicz P, Szymanski IO. Quantitative studies on the Rh-antigen D. Effect of the C gene. Transfusion 1987; 27: 257 - 61. | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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