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综述：
毛细支气管炎的临床研究进展
国内外研究现状[1-3]：毛细支气管炎又称为喘憋性肺炎，不同于
普通肺炎，重症患儿气喘气急明显，伴发作性喘憋。患儿年龄小，代偿能力差，易合并急性充血性心力衰竭。从而危及患儿健康和生命，是住院患儿死亡的首位原因。近年来，国内外对其发病机制、诊治和预防进行了大量研究[4-7]。毛细支气管炎主要由于呼吸道合胞病毒（RSV）感染引起，在RSV感染时有大量的细胞因子释放导致炎症与组织破坏[4,6]。TNF-α是一种具有广泛活性的细胞因子，可作为致炎症介质参与机体免疫和炎症反应的调节，TNF-α也是重要的促炎细胞因子，可诱发心肌细胞凋亡，促进心肌重构，降低心肌收缩力[7]。VEGF是一种具有广泛活性的缺氧诱导因子，参与急性心衰的发病过程[8]。目前，国内外文献对于毛细支气管炎合并心力衰竭时TNF-α、VEGF的临床研究报道很少[9-11]。我们可通过检测毛细支气炎合并心力衰竭患儿血清TNF-α、VEGF在治疗前后的变化来判断病情严重
程度及估计预后，并探讨新的心肌损害指标。 对毛细支气管炎的认识进展: 1. 危险因素
RSV所以引起的毛细支气管炎的宿主危险因素主要有营养不良、早产、出生后感染、慢性肺疾患、先天性心脏病以及应用免疫抑制剂等[12]。此外不良的环境因素也可能造成婴幼儿毛细支气管炎的感染，包括居住环境差，医疗卫生水平低以及长期被动吸烟[13]等。而在社会因素中，父母受教育程度低、多胎妊娠、特应性家族史以及缺乏母乳喂养都可增加感染的风险[14]。在我国早期的研究中发现，患有肺动脉高压的婴幼儿感染RVS的死亡率达到40%，患有青紫型先天性心脏病的患儿死亡率达到35%[15]。如今，随着重症监护技术的不断进步，其死亡率也大大降低[16]。 2. 流行病学
RSV是一种极不稳定的病毒,可用肥皂，消毒剂或水灭活。通过飞沫或呼吸道分泌物传播。主演传染源是被感染的患者或者物体[17]。流行病学显示[18]毛细支气管炎患儿通常在2岁之前初次感染RSV病毒，在患儿2到8个月时达到高峰。我国调查结果发现[19]，我国毛细支气管炎患儿发病多见于2岁以下婴幼儿，发病高峰期在2-6个月。发病率男女相似,男婴重症较多。而美国流行病学研究显示[20]，美国毛细支气管炎患儿的年龄在六周到六个月内。住院率达到60.8%。 RSV感染具有明显的季节性,多见于冬季，在热带则主要发生在雨季。在我国，北方多发病在冬春季节，而南方多方病于春季或秋季[21]。