Parainfluenza virus infections after hematopoietic stem cell transplantation: risk factors, response to antiviral therapy, and effect on transplant outcome
Parainfluenza virus infections after hematopoietic stem cell transplantation: risk factors, response to antiviral therapy, and effect on transplant outcome
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DOI：
10.1182/blood.v98.3.573
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发表时间：
2001-08-01
期刊：
影响因子：
20.3
通讯作者：
Boeckh, M
中科院分区：
文献类型：
--
作者：
Nichols, WG;Corey, L;Boeckh, M
副流感病毒（PIV）感染可能是干细胞移植患者发病和死亡的重要原因，但关于其对移植相关死亡率影响的数据有限。本研究旨在确定PIV获得和进展为下呼吸道感染的风险因素、其对移植相关死亡率的影响以及抗病毒治疗的有效性。本文对1990 ~ 1999年3577例造血干细胞移植（HSCT）受者进行了研究。253例患者（7.1%）发生PIV感染;其中78%的感染为社区获得性感染。多变量分析确定接受无关移植是PIV感染的唯一风险因素;在同种异体和自体HSCT受者中，PIV感染时皮质类固醇的剂量是与PIV-3肺炎发生相关的主要因素。PIV-3上呼吸道感染和肺炎均与总死亡率相关。从29例（53%）肺炎患者中分离出肺共病原体。死亡率受共病原体的存在和机械通气的需要的高度影响。雾化利巴韦林联合或不联合静脉注射免疫球蛋白似乎并没有改变PIV-3肺炎的死亡率，也没有减少肺炎患者鼻咽部病毒脱落的持续时间。因此，即使在自体HSCT受者中，皮质类固醇给药也以剂量依赖性方式驱动PIV肺炎的发展。上、下尿路PIV感染均是HSCT后死亡率的预测因子。目前可用的抗病毒治疗似乎不足以减少病毒脱落或死亡率，一旦肺炎建立。
Parainfluenza virus (PIV) infections may be significant causes of morbidity and mortality in patients undergoing stem cell transplantation, but data regarding their impact on transplant-related mortality is limited. This study sought to determine the risk factors of PIV acquisition and progression to lower respiratory tract infection, their Impact on transplant-related mortality, and the effectiveness of antiviral therapy. A total of 3577 recipients of hematopoietic stem cell transplantation (HSCT) between 1990 and 1999 were studied. PIV infections occurred in 253 patients (7.1%); 78% of these infections were community acquired. Multivariable analysis identified the receipt of an unrelated transplant as the only risk factor for PIV acquisition; the dose of corticosteroids at the time of PIV infection acquisition was the primary factor associated with the development of PIV-3 pneumonia, both among allogeneic and autologous HSCT recipients. Both PIV-3 upper respiratory infection and pneumonia were associated with overall mortality. Pulmonary copathogens were isolated from 29 patients (53%) with pneumonia. Mortality was highly influenced by the presence of copathogens and the need for mechanical ventilation. Aerosolized ribavirin with or without intravenous immunoglobulin did not appear to alter mortality from PIV-3 pneumonia, nor did such therapy decrease the duration of viral shedding from the nasopharynx among patients with pneumonia. Corticosteroid administration thus drives the development of PIV pneumonia in a dose-dependent fashion, even among autologous HSCT recipients. Both upper and lower tract PIV infections are predictors of mortality after HSCT. Currently available antiviral therapy appears to be inadequate in reducing viral shedding or mortality once pneumonia is established.