Glucose‐6‐phosphate dehydrogenase deficiency is more prevalent in Duffy‐null red blood cell transfusion in sickle cell disease
Background Resistance to malaria infection may be conferred by erythrocyte genetic variations including glucose‐6‐phosphate dehydrogenase (G6PD) deficiency and lack of Duffy antigens. In red blood cell (RBC) transfusion, G6PD deficiency may shorten transfusion survival. Because Duffy‐null units are...
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| Veröffentlicht in: | Transfusion (Philadelphia, Pa.) Pa.), 2022-03, Vol.62 (3), p.551-555 |
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| creator | Yee, Marianne E. Francis, Richard O. Luban, Naomi L. C. Easley, Kirk A. Lough, Christopher M. Roback, John D. Josephson, Cassandra D. Fasano, Ross M. |
| description | Background
Resistance to malaria infection may be conferred by erythrocyte genetic variations including glucose‐6‐phosphate dehydrogenase (G6PD) deficiency and lack of Duffy antigens. In red blood cell (RBC) transfusion, G6PD deficiency may shorten transfusion survival. Because Duffy‐null units are commonly transfused in sickle cell disease (SCD) due to antigen matching protocols, we examined whether Duffy‐null donor RBC units have a higher prevalence of G6PD deficiency.
Materials and methods
Pediatric patients with SCD on chronic transfusion therapy were followed prospectively for multiple transfusions. RBC unit segments were collected to measure G6PD activity and RBC genotyping. The decline in donor hemoglobin (ΔHbA) following transfusion was assessed from immediate posttransfusion estimates and HbA measurements approximately 1 month later.
Results
Of 564 evaluable RBC units, 59 (10.5%) were G6PD deficient (23 severe, 36 moderate deficiency); 202 (37.6%) units were Duffy‐null. G6PD deficiency occurred in 40 (19.8%) Duffy‐null units versus 15 (4.5%) Duffy‐positive units (p |
| doi_str_mv | 10.1111/trf.16806 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_8940658</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2641214521</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4436-57759218364197f7a8c7b7fa88020daed1d123beed4f3ea0a67519bdeeeee49b3</originalsourceid><addsrcrecordid>eNp1kc9qFTEUxoMo9lpd-AIy4EYX0yaZzGSyEUq1f6AgSF2HzOSkNzU3GZOZyuxc-AA-o0_STKcWFTxwCIfzy8d3-BB6SfAByXU4RnNAmhY3j9CG1BUvqRD1Y7TBmJGSkIruoWcpXWOMqcDkKdqrasxYI_gG_Th1Ux8S_Pr-s8k9bEMatmqEQsN21jFcgVdpmYztLfh-LmwqdiFCMUS4UQ78WFhfvJ-MmfN_PzlXRNBF50LQRQ95HKPyyUzJBr-gyfZfHKwrbRNk-efoiVEuwYv7dx99PvlweXxWXnw8PT8-uih7xqqmrDmvBSVt1TAiuOGq7XnHjWpbTLFWoIkmtOoANDMVKKwaXhPRaViKia7aR-9W3WHqdqD7bD4qJ4dodyrOMigr_954u5VX4Ua2guGmbrPAm3uBGL5OkEa5s2m5RHkIU5K0oYTWohUio6__Qa_DFH0-L1OMUMJqSjL1dqX6GFKKYB7MECyXbGXOVt5lm9lXf7p_IH-HmYHDFfhmHcz_V5KXn05WyVsifbRX</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2641214521</pqid></control><display><type>article</type><title>Glucose‐6‐phosphate dehydrogenase deficiency is more prevalent in Duffy‐null red blood cell transfusion in sickle cell disease</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Yee, Marianne E. ; Francis, Richard O. ; Luban, Naomi L. C. ; Easley, Kirk A. ; Lough, Christopher M. ; Roback, John D. ; Josephson, Cassandra D. ; Fasano, Ross M.</creator><creatorcontrib>Yee, Marianne E. ; Francis, Richard O. ; Luban, Naomi L. C. ; Easley, Kirk A. ; Lough, Christopher M. ; Roback, John D. ; Josephson, Cassandra D. ; Fasano, Ross M.</creatorcontrib><description>Background
Resistance to malaria infection may be conferred by erythrocyte genetic variations including glucose‐6‐phosphate dehydrogenase (G6PD) deficiency and lack of Duffy antigens. In red blood cell (RBC) transfusion, G6PD deficiency may shorten transfusion survival. Because Duffy‐null units are commonly transfused in sickle cell disease (SCD) due to antigen matching protocols, we examined whether Duffy‐null donor RBC units have a higher prevalence of G6PD deficiency.
Materials and methods
Pediatric patients with SCD on chronic transfusion therapy were followed prospectively for multiple transfusions. RBC unit segments were collected to measure G6PD activity and RBC genotyping. The decline in donor hemoglobin (ΔHbA) following transfusion was assessed from immediate posttransfusion estimates and HbA measurements approximately 1 month later.
Results
Of 564 evaluable RBC units, 59 (10.5%) were G6PD deficient (23 severe, 36 moderate deficiency); 202 (37.6%) units were Duffy‐null. G6PD deficiency occurred in 40 (19.8%) Duffy‐null units versus 15 (4.5%) Duffy‐positive units (p < .0001). In univariate analysis, the fraction of Duffy‐null RBC units per transfusion was associated with greater decline in HbA (p = .038); however, in multivariate analysis, severe G6PD deficiency (p = .0238) but not Duffy‐null RBC (p = .0139) were associated with ΔHbA.
Conclusion
Selection of Duffy‐null RBC units may result in shorter in vivo survival of transfused RBCs due to a higher likelihood of transfusing units from G6PD deficient donors.</description><identifier>ISSN: 0041-1132</identifier><identifier>EISSN: 1537-2995</identifier><identifier>DOI: 10.1111/trf.16806</identifier><identifier>PMID: 35044697</identifier><language>eng</language><publisher>Hoboken, USA: John Wiley & Sons, Inc</publisher><subject>Anemia, Sickle Cell - genetics ; Anemia, Sickle Cell - therapy ; Antigens ; Blood Transfusion ; Child ; Dehydrogenase ; Dehydrogenases ; Disease resistance ; Duffy antigen ; Erythrocyte Transfusion - adverse effects ; Erythrocytes ; Genetic diversity ; Genotyping ; Glucose ; Glucose 6 phosphate dehydrogenase ; Glucosephosphate Dehydrogenase ; Glucosephosphate Dehydrogenase Deficiency - epidemiology ; Glucosephosphate Dehydrogenase Deficiency - genetics ; glucose‐6‐phosphate dehydrogenase deficiency ; Hemoglobin ; Humans ; Malaria ; Multivariate analysis ; Pediatrics ; Sickle cell disease ; Survival ; Transfusion ; Vector-borne diseases</subject><ispartof>Transfusion (Philadelphia, Pa.), 2022-03, Vol.62 (3), p.551-555</ispartof><rights>2022 AABB.</rights><rights>2022 AABB</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4436-57759218364197f7a8c7b7fa88020daed1d123beed4f3ea0a67519bdeeeee49b3</citedby><cites>FETCH-LOGICAL-c4436-57759218364197f7a8c7b7fa88020daed1d123beed4f3ea0a67519bdeeeee49b3</cites><orcidid>0000-0001-6082-8385 ; 0000-0001-8692-4041 ; 0000-0003-2543-991X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Ftrf.16806$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Ftrf.16806$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,776,780,881,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35044697$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yee, Marianne E.</creatorcontrib><creatorcontrib>Francis, Richard O.</creatorcontrib><creatorcontrib>Luban, Naomi L. C.</creatorcontrib><creatorcontrib>Easley, Kirk A.</creatorcontrib><creatorcontrib>Lough, Christopher M.</creatorcontrib><creatorcontrib>Roback, John D.</creatorcontrib><creatorcontrib>Josephson, Cassandra D.</creatorcontrib><creatorcontrib>Fasano, Ross M.</creatorcontrib><title>Glucose‐6‐phosphate dehydrogenase deficiency is more prevalent in Duffy‐null red blood cell transfusion in sickle cell disease</title><title>Transfusion (Philadelphia, Pa.)</title><addtitle>Transfusion</addtitle><description>Background
Resistance to malaria infection may be conferred by erythrocyte genetic variations including glucose‐6‐phosphate dehydrogenase (G6PD) deficiency and lack of Duffy antigens. In red blood cell (RBC) transfusion, G6PD deficiency may shorten transfusion survival. Because Duffy‐null units are commonly transfused in sickle cell disease (SCD) due to antigen matching protocols, we examined whether Duffy‐null donor RBC units have a higher prevalence of G6PD deficiency.
Materials and methods
Pediatric patients with SCD on chronic transfusion therapy were followed prospectively for multiple transfusions. RBC unit segments were collected to measure G6PD activity and RBC genotyping. The decline in donor hemoglobin (ΔHbA) following transfusion was assessed from immediate posttransfusion estimates and HbA measurements approximately 1 month later.
Results
Of 564 evaluable RBC units, 59 (10.5%) were G6PD deficient (23 severe, 36 moderate deficiency); 202 (37.6%) units were Duffy‐null. G6PD deficiency occurred in 40 (19.8%) Duffy‐null units versus 15 (4.5%) Duffy‐positive units (p < .0001). In univariate analysis, the fraction of Duffy‐null RBC units per transfusion was associated with greater decline in HbA (p = .038); however, in multivariate analysis, severe G6PD deficiency (p = .0238) but not Duffy‐null RBC (p = .0139) were associated with ΔHbA.
Conclusion
Selection of Duffy‐null RBC units may result in shorter in vivo survival of transfused RBCs due to a higher likelihood of transfusing units from G6PD deficient donors.</description><subject>Anemia, Sickle Cell - genetics</subject><subject>Anemia, Sickle Cell - therapy</subject><subject>Antigens</subject><subject>Blood Transfusion</subject><subject>Child</subject><subject>Dehydrogenase</subject><subject>Dehydrogenases</subject><subject>Disease resistance</subject><subject>Duffy antigen</subject><subject>Erythrocyte Transfusion - adverse effects</subject><subject>Erythrocytes</subject><subject>Genetic diversity</subject><subject>Genotyping</subject><subject>Glucose</subject><subject>Glucose 6 phosphate dehydrogenase</subject><subject>Glucosephosphate Dehydrogenase</subject><subject>Glucosephosphate Dehydrogenase Deficiency - epidemiology</subject><subject>Glucosephosphate Dehydrogenase Deficiency - genetics</subject><subject>glucose‐6‐phosphate dehydrogenase deficiency</subject><subject>Hemoglobin</subject><subject>Humans</subject><subject>Malaria</subject><subject>Multivariate analysis</subject><subject>Pediatrics</subject><subject>Sickle cell disease</subject><subject>Survival</subject><subject>Transfusion</subject><subject>Vector-borne diseases</subject><issn>0041-1132</issn><issn>1537-2995</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kc9qFTEUxoMo9lpd-AIy4EYX0yaZzGSyEUq1f6AgSF2HzOSkNzU3GZOZyuxc-AA-o0_STKcWFTxwCIfzy8d3-BB6SfAByXU4RnNAmhY3j9CG1BUvqRD1Y7TBmJGSkIruoWcpXWOMqcDkKdqrasxYI_gG_Th1Ux8S_Pr-s8k9bEMatmqEQsN21jFcgVdpmYztLfh-LmwqdiFCMUS4UQ78WFhfvJ-MmfN_PzlXRNBF50LQRQ95HKPyyUzJBr-gyfZfHKwrbRNk-efoiVEuwYv7dx99PvlweXxWXnw8PT8-uih7xqqmrDmvBSVt1TAiuOGq7XnHjWpbTLFWoIkmtOoANDMVKKwaXhPRaViKia7aR-9W3WHqdqD7bD4qJ4dodyrOMigr_954u5VX4Ua2guGmbrPAm3uBGL5OkEa5s2m5RHkIU5K0oYTWohUio6__Qa_DFH0-L1OMUMJqSjL1dqX6GFKKYB7MECyXbGXOVt5lm9lXf7p_IH-HmYHDFfhmHcz_V5KXn05WyVsifbRX</recordid><startdate>202203</startdate><enddate>202203</enddate><creator>Yee, Marianne E.</creator><creator>Francis, Richard O.</creator><creator>Luban, Naomi L. C.</creator><creator>Easley, Kirk A.</creator><creator>Lough, Christopher M.</creator><creator>Roback, John D.</creator><creator>Josephson, Cassandra D.</creator><creator>Fasano, Ross M.</creator><general>John Wiley & Sons, Inc</general><general>Wiley Subscription Services, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>7U9</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-6082-8385</orcidid><orcidid>https://orcid.org/0000-0001-8692-4041</orcidid><orcidid>https://orcid.org/0000-0003-2543-991X</orcidid></search><sort><creationdate>202203</creationdate><title>Glucose‐6‐phosphate dehydrogenase deficiency is more prevalent in Duffy‐null red blood cell transfusion in sickle cell disease</title><author>Yee, Marianne E. ; Francis, Richard O. ; Luban, Naomi L. C. ; Easley, Kirk A. ; Lough, Christopher M. ; Roback, John D. ; Josephson, Cassandra D. ; Fasano, Ross M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4436-57759218364197f7a8c7b7fa88020daed1d123beed4f3ea0a67519bdeeeee49b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Anemia, Sickle Cell - genetics</topic><topic>Anemia, Sickle Cell - therapy</topic><topic>Antigens</topic><topic>Blood Transfusion</topic><topic>Child</topic><topic>Dehydrogenase</topic><topic>Dehydrogenases</topic><topic>Disease resistance</topic><topic>Duffy antigen</topic><topic>Erythrocyte Transfusion - adverse effects</topic><topic>Erythrocytes</topic><topic>Genetic diversity</topic><topic>Genotyping</topic><topic>Glucose</topic><topic>Glucose 6 phosphate dehydrogenase</topic><topic>Glucosephosphate Dehydrogenase</topic><topic>Glucosephosphate Dehydrogenase Deficiency - epidemiology</topic><topic>Glucosephosphate Dehydrogenase Deficiency - genetics</topic><topic>glucose‐6‐phosphate dehydrogenase deficiency</topic><topic>Hemoglobin</topic><topic>Humans</topic><topic>Malaria</topic><topic>Multivariate analysis</topic><topic>Pediatrics</topic><topic>Sickle cell disease</topic><topic>Survival</topic><topic>Transfusion</topic><topic>Vector-borne diseases</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yee, Marianne E.</creatorcontrib><creatorcontrib>Francis, Richard O.</creatorcontrib><creatorcontrib>Luban, Naomi L. C.</creatorcontrib><creatorcontrib>Easley, Kirk A.</creatorcontrib><creatorcontrib>Lough, Christopher M.</creatorcontrib><creatorcontrib>Roback, John D.</creatorcontrib><creatorcontrib>Josephson, Cassandra D.</creatorcontrib><creatorcontrib>Fasano, Ross M.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Transfusion (Philadelphia, Pa.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yee, Marianne E.</au><au>Francis, Richard O.</au><au>Luban, Naomi L. C.</au><au>Easley, Kirk A.</au><au>Lough, Christopher M.</au><au>Roback, John D.</au><au>Josephson, Cassandra D.</au><au>Fasano, Ross M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Glucose‐6‐phosphate dehydrogenase deficiency is more prevalent in Duffy‐null red blood cell transfusion in sickle cell disease</atitle><jtitle>Transfusion (Philadelphia, Pa.)</jtitle><addtitle>Transfusion</addtitle><date>2022-03</date><risdate>2022</risdate><volume>62</volume><issue>3</issue><spage>551</spage><epage>555</epage><pages>551-555</pages><issn>0041-1132</issn><eissn>1537-2995</eissn><abstract>Background
Resistance to malaria infection may be conferred by erythrocyte genetic variations including glucose‐6‐phosphate dehydrogenase (G6PD) deficiency and lack of Duffy antigens. In red blood cell (RBC) transfusion, G6PD deficiency may shorten transfusion survival. Because Duffy‐null units are commonly transfused in sickle cell disease (SCD) due to antigen matching protocols, we examined whether Duffy‐null donor RBC units have a higher prevalence of G6PD deficiency.
Materials and methods
Pediatric patients with SCD on chronic transfusion therapy were followed prospectively for multiple transfusions. RBC unit segments were collected to measure G6PD activity and RBC genotyping. The decline in donor hemoglobin (ΔHbA) following transfusion was assessed from immediate posttransfusion estimates and HbA measurements approximately 1 month later.
Results
Of 564 evaluable RBC units, 59 (10.5%) were G6PD deficient (23 severe, 36 moderate deficiency); 202 (37.6%) units were Duffy‐null. G6PD deficiency occurred in 40 (19.8%) Duffy‐null units versus 15 (4.5%) Duffy‐positive units (p < .0001). In univariate analysis, the fraction of Duffy‐null RBC units per transfusion was associated with greater decline in HbA (p = .038); however, in multivariate analysis, severe G6PD deficiency (p = .0238) but not Duffy‐null RBC (p = .0139) were associated with ΔHbA.
Conclusion
Selection of Duffy‐null RBC units may result in shorter in vivo survival of transfused RBCs due to a higher likelihood of transfusing units from G6PD deficient donors.</abstract><cop>Hoboken, USA</cop><pub>John Wiley & Sons, Inc</pub><pmid>35044697</pmid><doi>10.1111/trf.16806</doi><tpages>5</tpages><orcidid>https://orcid.org/0000-0001-6082-8385</orcidid><orcidid>https://orcid.org/0000-0001-8692-4041</orcidid><orcidid>https://orcid.org/0000-0003-2543-991X</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Transfusion (Philadelphia, Pa.), 2022-03, Vol.62 (3), p.551-555 |
| issn | 0041-1132 1537-2995 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_8940658 |
| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | Anemia, Sickle Cell - genetics Anemia, Sickle Cell - therapy Antigens Blood Transfusion Child Dehydrogenase Dehydrogenases Disease resistance Duffy antigen Erythrocyte Transfusion - adverse effects Erythrocytes Genetic diversity Genotyping Glucose Glucose 6 phosphate dehydrogenase Glucosephosphate Dehydrogenase Glucosephosphate Dehydrogenase Deficiency - epidemiology Glucosephosphate Dehydrogenase Deficiency - genetics glucose‐6‐phosphate dehydrogenase deficiency Hemoglobin Humans Malaria Multivariate analysis Pediatrics Sickle cell disease Survival Transfusion Vector-borne diseases |
| title | Glucose‐6‐phosphate dehydrogenase deficiency is more prevalent in Duffy‐null red blood cell transfusion in sickle cell disease |
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