HEMORRHAGIC CYSTITIS IN PEDIATRIC BONE-MARROW TRANSPLANT PATIENTS - AN ASSOCIATION WITH INFECTIVE AGENTS, GVHD AND PRIOR CYCLOPHOSPHAMIDE

Citation
Sj. Russell et al., HEMORRHAGIC CYSTITIS IN PEDIATRIC BONE-MARROW TRANSPLANT PATIENTS - AN ASSOCIATION WITH INFECTIVE AGENTS, GVHD AND PRIOR CYCLOPHOSPHAMIDE, Bone marrow transplantation, 13(5), 1994, pp. 533-539
Citations number
30
Categorie Soggetti
Hematology,Oncology,Immunology
Journal title
ISSN journal
02683369
Volume
13
Issue
5
Year of publication
1994
Pages
533 - 539
Database
ISI
SICI code
0268-3369(1994)13:5<533:HCIPBT>2.0.ZU;2-2
Abstract
The frequency of haemorrhagic cystitis (HC) is evaluated in a paediatr ic population undergoing bone marrow transplantation (BMT) and its rel ationship to therapy with cyclophosphamide (CY) prior to conditioning for BMT (prior CY), infectious agents and graft-versus-host disease (G VHD) assessed. HC was defined as macroscopic haematuria with early ons et HC occurring within 2 days of and delayed onset beyond 2 days from CY infusion. Sixty-three children received a total of 65 BMTs between July 1988 and January 1991, with 60 children receiving CY and 31/m(2)/ 24 h of post-hydration fluid post-CY as part of their conditioning. Th ere were no cases of early onset HC. Eleven (17%) children had a total of 19 episodes of delayed onset HC. Overall, an infective agent was i dentified in the urine at the time of 17 of 19 (89%) episodes of HC. W hile papovavirus was the most common organism (12 episodes), adenoviru s (2), cytomegalovirus (1) and bacteria (3) were also identified. The frequency of HC in transplants complicated by acute GVHD grade II-IV w as 40% (p = 0.016), in children who had received prior CY was 43% (p < 0.001) and in mismatched transplants was 32% (p = 0.06). Four childre n who developed GVHD had exacerbations of symptoms associated with the use of high-dose steroid therapy. Our results suggest that most cases of delayed onset HC are temporally associated with an infective organ ism, predominantly papovavirus, and identify GVHD and prior CY as risk factors. Increased symptomatology was associated with acute GVHD and its treatment and this may be explained by the added immune suppressio n, resulting in greater viral reactivation and further mucosal damage.