Background: BK virus–associated hemorrhagic cystitis can occur in posttransplant phase owing to reactivation of BK virus after loss of immune function. The purpose of this study was to examine risk factors for BKV-associated hemorrhagic cystitis (BKV-HC) in hematopoietic stem cell transplant (HSCT) recipients.
Methods: Fifteen patients who received HSCT were enrolled as BKV-positive cases along with 37 controls who were HSCT recipients who had not developed BKV-HC in the posttransplant period. A retrospective review of risk factors was done using information from medical notes and the Laboratory Information System.
Results: The only statistically significant differences were seen in the white cell, platelet, neutrophil, and lymphocyte counts on the day of the positive test for BK or day 60 for the controls. With regard to the use of immunosuppression and chemotherapy agents, the only statistical difference was that there were more patients in the BKV case group on cyclosporin posttransplant than in the control group (χ2 = 3.77; P = 0.05). There was a trend toward a higher rate of graft versus host disease in the BKV case group (12/12 vs. 22/29, mid P exact = 0.07).
Discussion: This study has shown that the myelosuppression on the day of the positive BKV test result is greater in the BKV-HC group than in the control group, which suggests that prolonged immunosuppression posttransplant is a major risk factor for development of BKV-HC.
The purpose of this study was to examine risk factors for BK-haemorrhagic cystitis in stem cell transplant recipients. It was found that significant differences in laboratory parameters were seen in the white cell, platelet, neutrophil and lymphocyte counts on the day of the positive test for BKV-HC cases in comparison to the control group. This is in keeping with the hypothesis that BKV-HC is due to reactivation of latent BKV when patients experience prolonged immunosuppression.
From the *Sir Patrick Dun Translational Research Laboratory, Dept. of Clinical Microbiology, Trinity College Dublin, Dublin, Ireland; †Department of Haematology; and ‡Department of Clinical Microbiology, St James’s Hospital, Dublin, Ireland.
Correspondence to: Richard John Drew, MD, FRCPath, Alder Hey Children’s NHS Foundation Trust, Liverpool, UK. E-mail: firstname.lastname@example.org.
The authors have no funding or conflicts of interest to disclose.
Author Contributions: RJ Drew: concept/design, data analysis/interpretation, drafting article, data collection, and approval of article; E Conneally: concept/design, critical revision of article, approval of article; B Crowley: concept/design, critical revision of article, approval of article.