Relationship of Pretransplantation Polyoma BK Virus Serologic Findings and BK Viral Reactivation after Hematopoietic Stem Cell Transplantation
Identifieur interne : 003803 ( Main/Exploration ); précédent : 003802; suivant : 003804Relationship of Pretransplantation Polyoma BK Virus Serologic Findings and BK Viral Reactivation after Hematopoietic Stem Cell Transplantation
Auteurs : Anders S. Y. Wong [République populaire de Chine] ; Kwok-Hung Chan [République populaire de Chine] ; Vincent C. C. Cheng [République populaire de Chine] ; Kwok-Yung Yuen [République populaire de Chine] ; Yok-Lam Kwong [République populaire de Chine, Hong Kong] ; Anskar Y. H. Leung [République populaire de Chine]Source :
- Clinical Infectious Diseases [ 1058-4838 ] ; 2007.
Abstract
Background. Reactivation of polyoma BK virus (BKV) infection is consistently associated with hemorrhagic cystitis in persons who undergo hematopoietic stem cell transplantation (HSCT). In this study, we examined the relationship of reactivation of BKV infection with pre-HSCT serologic findings of BKV antibody. Methods. Serial urine samples (n = 1118) obtained from 140 HSCT recipients were prospectively obtained, and BKV loads were quantified by quantitative polymerase chain reaction. Pre-HSCT anti-BKV immunoglobulin G (IgG) levels were determined by indirect immunofluorescence. Results. In 68 patients, there was significant peaking (i.e., ⩾3-log increase) in the urine BKV load (median peak, 1.7 ×; 109 copies/mL; range, 1.1 ×; 104 to 3.2 ×; 1014 copies/mL) occurring at a median time of 24.5 days (range, 7–49 days). In 72 patients, low-level BKV viruria occurred without peaking (median BKV load, 10 copies/mL; range, 9.9 ×; 103 to 1.2 ×; 1010 copies/mL) at a median time of 24.5 days (range, 7–49 days). Pre-HSCT anti-BKV IgG was positively related to elevated urine BKV load during HSCT (P < .001). Binary logistic regression revealed that pre-HSCT anti-BKV IgG level was the only statistically significant factor (P = .009) to be associated with a ⩾3-log increase in the peak urine BKV load (positive and negative predictive values, 69% and 68%, respectively). Nine patients developed hemorrhagic cystitis at a median of 56 days (range, 29–160); 7 of these patients were evaluable and were found to have a ⩾3-log increase in the peak BKV load. In binary logistic regression, peaking of the urine BKV load (P = .026) and graft-versus-host disease (P = .033) were found to be statistically significant risks for hemorrhagic cystitis. Conclusions. The identification of the serologic status of BKV as a significant risk factor for BKV viruria suggests that it should be included as an integral part of the pre-HSCT evaluation.
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DOI: 10.1086/511863
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Cheng</name></author><author><name sortKey="Yuen, Kwok Yung" sort="Yuen, Kwok Yung" uniqKey="Yuen K" first="Kwok-Yung" last="Yuen">Kwok-Yung Yuen</name></author><author><name sortKey="Kwong, Yok Lam" sort="Kwong, Yok Lam" uniqKey="Kwong Y" first="Yok-Lam" last="Kwong">Yok-Lam Kwong</name></author><author><name sortKey="Leung, Anskar Y H" sort="Leung, Anskar Y H" uniqKey="Leung A" first="Anskar Y. H." last="Leung">Anskar Y. H. 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Y." last="Wong">Anders S. Y. Wong</name><affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Medicine, University of Hong Kong</wicri:regionArea><wicri:noRegion>University of Hong Kong</wicri:noRegion></affiliation></author><author><name sortKey="Chan, Kwok Hung" sort="Chan, Kwok Hung" uniqKey="Chan K" first="Kwok-Hung" last="Chan">Kwok-Hung Chan</name><affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Microbiology, University of Hong Kong</wicri:regionArea><wicri:noRegion>University of Hong Kong</wicri:noRegion></affiliation></author><author><name sortKey="Cheng, Vincent C C" sort="Cheng, Vincent C C" uniqKey="Cheng V" first="Vincent C. C." last="Cheng">Vincent C. C. Cheng</name><affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Microbiology, University of Hong Kong</wicri:regionArea><wicri:noRegion>University of Hong Kong</wicri:noRegion></affiliation></author><author><name sortKey="Yuen, Kwok Yung" sort="Yuen, Kwok Yung" uniqKey="Yuen K" first="Kwok-Yung" last="Yuen">Kwok-Yung Yuen</name><affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Microbiology, University of Hong Kong</wicri:regionArea><wicri:noRegion>University of Hong Kong</wicri:noRegion></affiliation></author><author><name sortKey="Kwong, Yok Lam" sort="Kwong, Yok Lam" uniqKey="Kwong Y" first="Yok-Lam" last="Kwong">Yok-Lam Kwong</name><affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Medicine, University of Hong Kong</wicri:regionArea><wicri:noRegion>University of Hong Kong</wicri:noRegion></affiliation><affiliation wicri:level="1"><country wicri:rule="url">Hong Kong</country></affiliation><affiliation wicri:level="1"><country wicri:rule="url">Hong Kong</country><wicri:regionArea>Reprints or correspondence: Dr. Y. L. Kwong, University Dept. of Medicine, Professorial Block, Queen Mary Hospital, Pokfulam Rd., Hong Kong</wicri:regionArea><wicri:noRegion>Hong Kong</wicri:noRegion></affiliation></author><author><name sortKey="Leung, Anskar Y H" sort="Leung, Anskar Y H" uniqKey="Leung A" first="Anskar Y. H." last="Leung">Anskar Y. H. Leung</name><affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Medicine, University of Hong Kong</wicri:regionArea><wicri:noRegion>University of Hong Kong</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Clinical Infectious Diseases</title><title level="j" type="abbrev">Clinical Infectious Diseases</title><idno type="ISSN">1058-4838</idno><idno type="eISSN">1537-6591</idno><imprint><publisher>The University of Chicago Press</publisher><date type="published">2007</date><biblScope unit="vol">44</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="830">830</biblScope><biblScope unit="page" to="837">837</biblScope></imprint><idno type="ISSN">1058-4838</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1058-4838</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract">Background. Reactivation of polyoma BK virus (BKV) infection is consistently associated with hemorrhagic cystitis in persons who undergo hematopoietic stem cell transplantation (HSCT). In this study, we examined the relationship of reactivation of BKV infection with pre-HSCT serologic findings of BKV antibody. Methods. Serial urine samples (n = 1118) obtained from 140 HSCT recipients were prospectively obtained, and BKV loads were quantified by quantitative polymerase chain reaction. Pre-HSCT anti-BKV immunoglobulin G (IgG) levels were determined by indirect immunofluorescence. Results. In 68 patients, there was significant peaking (i.e., ⩾3-log increase) in the urine BKV load (median peak, 1.7 ×; 109 copies/mL; range, 1.1 ×; 104 to 3.2 ×; 1014 copies/mL) occurring at a median time of 24.5 days (range, 7–49 days). In 72 patients, low-level BKV viruria occurred without peaking (median BKV load, 10 copies/mL; range, 9.9 ×; 103 to 1.2 ×; 1010 copies/mL) at a median time of 24.5 days (range, 7–49 days). Pre-HSCT anti-BKV IgG was positively related to elevated urine BKV load during HSCT (P < .001). Binary logistic regression revealed that pre-HSCT anti-BKV IgG level was the only statistically significant factor (P = .009) to be associated with a ⩾3-log increase in the peak urine BKV load (positive and negative predictive values, 69% and 68%, respectively). Nine patients developed hemorrhagic cystitis at a median of 56 days (range, 29–160); 7 of these patients were evaluable and were found to have a ⩾3-log increase in the peak BKV load. In binary logistic regression, peaking of the urine BKV load (P = .026) and graft-versus-host disease (P = .033) were found to be statistically significant risks for hemorrhagic cystitis. Conclusions. The identification of the serologic status of BKV as a significant risk factor for BKV viruria suggests that it should be included as an integral part of the pre-HSCT evaluation.</div></front></TEI><affiliations><list><country><li>Hong Kong</li><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Wong, Anders S Y" sort="Wong, Anders S Y" uniqKey="Wong A" first="Anders S. Y." last="Wong">Anders S. Y. Wong</name></noRegion><name sortKey="Chan, Kwok Hung" sort="Chan, Kwok Hung" uniqKey="Chan K" first="Kwok-Hung" last="Chan">Kwok-Hung Chan</name><name sortKey="Cheng, Vincent C C" sort="Cheng, Vincent C C" uniqKey="Cheng V" first="Vincent C. C." last="Cheng">Vincent C. C. Cheng</name><name sortKey="Kwong, Yok Lam" sort="Kwong, Yok Lam" uniqKey="Kwong Y" first="Yok-Lam" last="Kwong">Yok-Lam Kwong</name><name sortKey="Leung, Anskar Y H" sort="Leung, Anskar Y H" uniqKey="Leung A" first="Anskar Y. H." last="Leung">Anskar Y. H. Leung</name><name sortKey="Yuen, Kwok Yung" sort="Yuen, Kwok Yung" uniqKey="Yuen K" first="Kwok-Yung" last="Yuen">Kwok-Yung Yuen</name></country><country name="Hong Kong"><noRegion><name sortKey="Kwong, Yok Lam" sort="Kwong, Yok Lam" uniqKey="Kwong Y" first="Yok-Lam" last="Kwong">Yok-Lam Kwong</name></noRegion><name sortKey="Kwong, Yok Lam" sort="Kwong, Yok Lam" uniqKey="Kwong Y" first="Yok-Lam" last="Kwong">Yok-Lam Kwong</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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