Hemorrhagic cystitis following hematopoietic stem cell transplantation:incidence,risk factors and as

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Background The definite pathogenesis of hemorrhagic cystitis(HC)after allogenic hematopoietic stem celltransplantation (allo-HSCT) has not been well elucidated.The role of cytomegalovirus (CMV) reactivation andgraft-versus-host disease (GVHD) in the development of HC remains obscure.This study determined the incidence andrisk factors for HC after allo-HSCT and analyzed its association with CMV reactivation and GVHD.Methods We retrospectively studied 250 patients at high risk for CMV disease who underwent alIo-HSCT all based onbusulfan/cyclophosphamide (BU/CY) myloablative regimens.The incidence,etiology,risk factors and clinicalmanagement of HC were investigated.Results HC developed within 180 days of transplant in 72 patients,with an overall incidence of 28.8% and an incidenceof 12.6% in patients with HLA-matched related donors(MRD),34.38% in those with HLA-matched unrelated donors(MUD),49.45% in those with mismatched related donors(MMRD).CMV-viremia significantly increased the incidence oflater onset HC (LOHC);however,only 9 out of 15 patients with CMV viruria actually developed LOHC.Multipleregression analysis identified grade Ⅱ-Ⅳ acute GVHD (RR=2.75;95% C/ 1.63-4.66;P<0.01) and grafts from MUD orMMRD (RR=2.60;95% C/ 1.52-5.20;P<0.01) as independent risk factors for HC.Event sequence analysis indicated amajority of HC episodes began around GVHD initiation.Conclusions CMV-viremia is a high risk factor for LOHC.Our data also showed a correlation between acute GVHDand HC,which suggested that alloimmunity may be involved in the pathogenesis of HC.Chin Med J 2007;120(19):1666-1671 Background The definite pathogenesis of hemorrhagic cystitis (HC) after allogenic hematopoietic stem cell transplantation (allo-HSCT) has not been well elucidated. The role of cytomegalovirus (CMV) reactivation and graft-versus-host disease (GVHD) in the development of HC remains obscure . This study determines the incidence andrisk factors for HC after allo-HSCT and analyzed its association with CMV reactivation and GVHD. Methods We retrospectively studied 250 patients at high risk for CMV disease who underwent alIo-HSCT all based onbusulfan / cyclophosphamide (BU / CY Results of HC developed within 180 days of transplant in 72 patients, with an overall incidence of 28.8% and an incidence of 12.6% in patients with HLA-matched related donors (MRD), 34.38% in those with HLA-matched unrelated donors (MUD), 49.45% in those with mismatched related donors (MMRD) .CMV-viremia significantly increased the incide nce oflater onset HC (LOHC); however, only 9 out of 15 patients with CMV viruria actually developed LOHC.Multipleregression analysis identified grade II-IV acute GVHD (RR = 2.75; 95% C / 1.63-4.66; P <0.01) and grafts from MUD or MMRD (RR = 2.60; 95% C / 1.52-5.20; P <0.01) as independent risk factors for HC. Event sequence analysis indicated amajority of HC episodes began around GVHD initiation. Conclusions CMV-viremia is a high risk factor for LOHC.Our data also showed a correlation between acute GVHD and HC, which suggested that alloimmunity may be involved in the pathogenesis of HC. Chin Med J 2007; 120 (19): 1666-1671
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