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Conference Paper: Quantification of polyoma BK viruria in hemorrhagic cystitis complicating bone marrow transplantation

TitleQuantification of polyoma BK viruria in hemorrhagic cystitis complicating bone marrow transplantation
Authors
Issue Date2001
PublisherAmerican Society of Hematology. The Journal's web site is located at http://bloodjournal.hematologylibrary.org/
Citation
The 43rd Annual Meeting of American Society of Hematology (ASH 2001), Orlando, FL., 7-11 December 2001. In Blood, 2001, v. 98 n. 6, p. 1971-1978 How to Cite?
AbstractPolyoma BK virus (BKV) is frequently identified in the urine of bone marrow transplantation (BMT) patients with hemorrhagic cystitis (HC). However, viruria is common even in asymptomatic patients, making a direct causative role of BKV difficult to establish. This study prospectively quantified BK viruria and viremia in 50 BMT patients to define the quantitative relationship of BKV reactivation with HC. Adenovirus (ADV) was similarly quantified as a control. More than 800 patient samples were quantified for BKV VP1 gene with a real-time quantitative polymerase chain reaction. Twenty patients (40%) developed HC, 6 with gross hematuria (HC grade 2 or higher) and 14 with microscopic hematuria (HC grade 1). When compared with asymptomatic patients, patients with HC had significantly higher peak BK viruria (6 × 1012 versus 5.7 × 107 genome copies/d, P < .001) and larger total amounts of BKV excreted during BMT (4.9 × 1013 versus 7.7 × 108 genome copies, P < .001). There was no detectable increase in BK viremia. Binary logistic regression analysis showed that BK viruria was the only risk factor, with HC not related to age, conditioning regimen, type of BMT, and graft-versus-host disease. Furthermore, the levels of ADV viruria in patients with or without HC were similar and comparable with those of BK viruria in patients without HC, suggesting that the significant increase in BK viruria in HC patients was not due to background viral reactivation or damage to the urothelium. BK viruria was quantitatively related to the occurrence of HC after BMT. © 2001 by The American Society of Hematology.
Persistent Identifierhttp://hdl.handle.net/10722/77052
ISSN
2023 Impact Factor: 21.0
2023 SCImago Journal Rankings: 5.272
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLeung, AYHen_HK
dc.contributor.authorSuen, CKMen_HK
dc.contributor.authorLie, AKWen_HK
dc.contributor.authorLiang, RHSen_HK
dc.contributor.authorYuen, KYen_HK
dc.contributor.authorKwong, YLen_HK
dc.date.accessioned2010-09-06T07:27:45Z-
dc.date.available2010-09-06T07:27:45Z-
dc.date.issued2001en_HK
dc.identifier.citationThe 43rd Annual Meeting of American Society of Hematology (ASH 2001), Orlando, FL., 7-11 December 2001. In Blood, 2001, v. 98 n. 6, p. 1971-1978en_HK
dc.identifier.issn0006-4971en_HK
dc.identifier.urihttp://hdl.handle.net/10722/77052-
dc.description.abstractPolyoma BK virus (BKV) is frequently identified in the urine of bone marrow transplantation (BMT) patients with hemorrhagic cystitis (HC). However, viruria is common even in asymptomatic patients, making a direct causative role of BKV difficult to establish. This study prospectively quantified BK viruria and viremia in 50 BMT patients to define the quantitative relationship of BKV reactivation with HC. Adenovirus (ADV) was similarly quantified as a control. More than 800 patient samples were quantified for BKV VP1 gene with a real-time quantitative polymerase chain reaction. Twenty patients (40%) developed HC, 6 with gross hematuria (HC grade 2 or higher) and 14 with microscopic hematuria (HC grade 1). When compared with asymptomatic patients, patients with HC had significantly higher peak BK viruria (6 × 1012 versus 5.7 × 107 genome copies/d, P < .001) and larger total amounts of BKV excreted during BMT (4.9 × 1013 versus 7.7 × 108 genome copies, P < .001). There was no detectable increase in BK viremia. Binary logistic regression analysis showed that BK viruria was the only risk factor, with HC not related to age, conditioning regimen, type of BMT, and graft-versus-host disease. Furthermore, the levels of ADV viruria in patients with or without HC were similar and comparable with those of BK viruria in patients without HC, suggesting that the significant increase in BK viruria in HC patients was not due to background viral reactivation or damage to the urothelium. BK viruria was quantitatively related to the occurrence of HC after BMT. © 2001 by The American Society of Hematology.en_HK
dc.languageengen_HK
dc.publisherAmerican Society of Hematology. The Journal's web site is located at http://bloodjournal.hematologylibrary.org/en_HK
dc.relation.ispartofBlooden_HK
dc.subject.meshAdenoviridae - genetics - isolation & purificationen_HK
dc.subject.meshAdolescenten_HK
dc.subject.meshAdulten_HK
dc.subject.meshAgeden_HK
dc.subject.meshBK Virus - genetics - isolation & purificationen_HK
dc.subject.meshBone Marrow Transplantation - adverse effectsen_HK
dc.subject.meshCystitis - diagnosis - etiology - virologyen_HK
dc.subject.meshDNA, Viral - analysisen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHematuria - diagnosis - etiology - virologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshPapillomavirus Infections - diagnosis - etiology - virologyen_HK
dc.subject.meshPolymerase Chain Reactionen_HK
dc.subject.meshProspective Studiesen_HK
dc.subject.meshUrine - virologyen_HK
dc.titleQuantification of polyoma BK viruria in hemorrhagic cystitis complicating bone marrow transplantationen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0006-4971&volume=98&spage=1971&epage=8&date=2001&atitle=Quantification+of+polyoma+BK+viruria+in+hemorrhagic+cystitis+complicating+bone+marrow+transplantation.en_HK
dc.identifier.emailLeung, AYH:ayhleung@hku.hken_HK
dc.identifier.emailLiang, RHS:rliang@hku.hken_HK
dc.identifier.emailYuen, KY:kyyuen@hkucc.hku.hken_HK
dc.identifier.emailKwong, YL:ylkwong@hku.hken_HK
dc.identifier.authorityLeung, AYH=rp00265en_HK
dc.identifier.authorityLiang, RHS=rp00345en_HK
dc.identifier.authorityYuen, KY=rp00366en_HK
dc.identifier.authorityKwong, YL=rp00358en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1182/blood.V98.6.1971en_HK
dc.identifier.pmid11535537-
dc.identifier.scopuseid_2-s2.0-0035885944en_HK
dc.identifier.hkuros66648en_HK
dc.identifier.hkuros66907-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035885944&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume98en_HK
dc.identifier.issue6en_HK
dc.identifier.spage1971en_HK
dc.identifier.epage1978en_HK
dc.identifier.isiWOS:000170947800051-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLeung, AYH=7403012668en_HK
dc.identifier.scopusauthoridSuen, CKM=7102317262en_HK
dc.identifier.scopusauthoridLie, AKW=24284842400en_HK
dc.identifier.scopusauthoridLiang, RHS=26643224900en_HK
dc.identifier.scopusauthoridYuen, KY=36078079100en_HK
dc.identifier.scopusauthoridKwong, YL=7102818954en_HK
dc.identifier.issnl0006-4971-

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