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Home > Medicine & Health Science textbooks > Medicine: general issues > The Pathogenetic Link Between Severe Hemorrhagic Cystitis After Hematopoietic Stem Cell Transplantation and Polyoma B.K. Virus Reactivation
The Pathogenetic Link Between Severe Hemorrhagic Cystitis After Hematopoietic Stem Cell Transplantation and Polyoma B.K. Virus Reactivation

The Pathogenetic Link Between Severe Hemorrhagic Cystitis After Hematopoietic Stem Cell Transplantation and Polyoma B.K. Virus Reactivation


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About the Book

This dissertation, "The Pathogenetic Link Between Severe Hemorrhagic Cystitis After Hematopoietic Stem Cell Transplantation and Polyoma B.K. Virus Reactivation" by Y H, Anskar, Leung, 梁如鴻, was obtained from The University of Hong Kong (Pokfulam, Hong Kong) and is being sold pursuant to Creative Commons: Attribution 3.0 Hong Kong License. The content of this dissertation has not been altered in any way. We have altered the formatting in order to facilitate the ease of printing and reading of the dissertation. All rights not granted by the above license are retained by the author. Abstract: Abstract of thesis entitled The pathogenetic link between severe hemorrhagic cystitis after hematopoietic stem cell transplantation and polyoma B.K. virus reactivation Submitted by Dr. Anskar Y.H.Leung for the degree of Doctor of Medicine at The University of Hong Kong in March, 2006 Hemorrhagic cystitis (HC) is a distinct clinical disorder of multiple aetiologies characterized by painful hematuria due to hemorrhagic inflammation of the urinary bladder mucosa. In this project, we characterized the clinicopathologic features of HC after hematopoietic stem cell transplantation (HSCT) with particular reference to the role of polyoma BK virus (BKV) reactivation in its pathogenesis. The study involved retrospective analysis of clinical records, prospective quantification of BKV and adenovirus (ADV) viral load in urine and plasma as well as an open label study on the role of ciprofloxacin on BKV viral load in HSCT patients. In-vitro virologic studies on the role of quinolone antibiotics were also performed to ascertain their suppressive effects on BKV replication. Using the donor HSC engraftment as a cut-off, we defined two types of HC with distinct clinical features. HC that occurs before donor HSC engraftment is transient and self-limiting. However, HC after donor engraftment is severe and sometimes life-threatening and is a major morbidity after HSCT. Using real-time quantitative polymerase chain reaction (Q-PCR), we demonstrated that urinary load of BKV is significantly associated with the occurrence of HC. Moreover, a peak in BKV viruria invariably precedes the onset of severe HC. Such associations do not exist for plasma BKV viremia or adenovirus reactivation suggesting that BKV reactivation in the urinary tract plays a unique role in the pathogenesis of severe HC. BKV reactivation occurs similarly in autologous HSCT patients in whom severe HC is a rare occurrence. These observations, together with the clinical experience that severe HC is significantly associated with graft-versus-host disease, underscore the role of allo-immunity in the pathogenesis of severe HC. We further demonstrated that ciprofloxacin, a quinolone antibiotic with inhibitory effects on prokaryotic DNA gyrase, reduces the replication and cytopathic effects of BKV in a human cell- line derived from embryonic lung fibroblasts. This was confirmed clinically, and HSCT patients taking standard dose of ciprofloxacin have less BKV viruria and reduced risk of BKV reactivation. We postulate a pathogenetic model incorporating BKV reactivation in the urothelium and subsequent allo-immunity targeting at BKV infected urothelial cells. Such a model may provide a theoretical framework for the formulation and testing of strategies in the prevention and treatment of HC. Word Count: 365 M.D. Candidate: ___________________________ (Anskar Y.H. Leung) DOI: 10.5353/th_b3738318 Subjects: Cystitis - Pathogenesis Hematopoietic stem cells - Transplantation Polyomaviruses


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Product Details
  • ISBN-13: 9781374664050
  • Publisher: Open Dissertation Press
  • Publisher Imprint: Open Dissertation Press
  • Height: 279 mm
  • No of Pages: 126
  • Weight: 590 gr
  • ISBN-10: 1374664057
  • Publisher Date: 27 Jan 2017
  • Binding: Hardback
  • Language: English
  • Spine Width: 10 mm
  • Width: 216 mm


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