Clin Pediatr Hematol Oncol.
2012 Oct;19(2):92-99.
Polyomavirus Activation in Pediatric Patients with Hemorrhagic Cystitis Following Hematopoietic Stem Cell Transplantation
- Affiliations
-
- 1Department of Pediatrics, Ajou University School of Medicine, Suwon, Korea. pedpje@ajou.ac.kr
- 2Department of Radiation Oncology, Ajou University School of Medicine, Suwon, Korea.
Abstract
- BACKGROUND
Reactivation of the polyomavirus and the use of conditioning regimen may be the causes of hemorrhagic cystitis (HC) following hematopoietic stem cell transplantation (HSCT). However, there are only a few reports on the clinical characteristics of viral reactivation in HC following HSCT in Korea, especially in pediatric population.
METHODS
51 patients who received HSCT in Ajou University Hospital from January 2006 to June 2012 were investigated retrospectively. 16 patients were diagnosed with HC following HSCT and were enrolled in this study. Confirmation of polyomavirus was done by polymerase chain reaction (PCR) method.
RESULTS
Out of the 16 patients diagnosed with HC following HSCT, there were 5 early type HC patients and 11 late type HC patients. Positive PCR results for the BK virus (BKV) and the JC virus were found on 13 and 5 patients, respectively. 4 patients showed positive results for both viruses. For the late type HC, there were 10 patients with positive PCR results for the BKV. Cyclophosphamide was used in 33 patients, and 13 patients eventually developed HC. There was no statistical significance between the incidence of hematuria and the reactivation of the BKV or the conditioning regimens. Most patients were treated conservatively but 4 patients who showed severe hematuria or poor general condition received intravenous cidofovir. After the infusion of cidofovir, hematuria disappeared on average of 65 days and the BKV was undetectable on average of 53 days.
CONCLUSION
In our study, activation of the BKV was common in patients who were diagnosed with HC following HSCT. All patients recovered from HC with conservative management and the BKV became undetectable in the majority of patients who were treated with intravenous cidofovir.