Chinese medical journal · 2007
Hemorrhagic cystitis following hematopoietic stem cell transplantation: incidence, risk factors and association with CMV reactivation and graft-versus-host disease.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Xu Lan-ping, Zhang Hong-yu, Huang Xiao-jun, Liu Kai-yan, Liu Dai-hong, Han Wei, Chen Huan, Chen Yu-hong, Gao Zhi-yong, Zhang Yao-chen, Lu Dao-pei
Аннотация
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 determined the incidence and risk 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 allo-HSCT all based on busulfan/cyclophosphamide (BU/CY) myloablative regimens. The incidence, etiology, risk factors and clinical management of HC were investigated.
RESULTS: 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 incidence of later onset HC (LOHC); however, only 9 out of 15 patients with CMV viruria actually developed LOHC. Multiple regression analysis identified grade II - IV acute GVHD (RR = 2.75; 95% CI 1.63 +/- 4.66; P < 0.01) and grafts from MUD or MMRD (RR = 2.60; 95% CI 1.52 +/- 5.20; P < 0.01) as independent risk factors for HC. Event sequence analysis indicated a majority 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.
METHODS: We retrospectively studied 250 patients at high risk for CMV disease who underwent allo-HSCT all based on busulfan/cyclophosphamide (BU/CY) myloablative regimens. The incidence, etiology, risk factors and clinical management of HC were investigated.
RESULTS: 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 incidence of later onset HC (LOHC); however, only 9 out of 15 patients with CMV viruria actually developed LOHC. Multiple regression analysis identified grade II - IV acute GVHD (RR = 2.75; 95% CI 1.63 +/- 4.66; P < 0.01) and grafts from MUD or MMRD (RR = 2.60; 95% CI 1.52 +/- 5.20; P < 0.01) as independent risk factors for HC. Event sequence analysis indicated a majority 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.