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慢性阻塞性肺疾病的一种特殊表型:由生物燃料烟雾引起的COPD

2017/09/29

   摘要
   目的:探讨生物燃料烟雾引起COPD患者临床表型。
   方法:根据暴露的危险因素对受试者进行分组:①由生物燃料烟雾(BSCOPD)引起的COPD组,②由香烟烟雾引起的COPD组(CSCOPD),③生物燃料烟雾暴露下的正常对照组(BSNormal),④香烟烟雾暴露下的正常对照组组(CSNormal)。所有受试者完成了有关人口统计学、症状和环境暴露相关的问卷调查,并进行了肺功能,胸部HRCT,支气管粘膜活检和支气管肺泡灌洗液(BALF)检测。。
   结果:共纳入BSCOPD共29例,CSCOPD 31例,BSNormal 12例,CSNormal 10例。肺功能:BSCOPD的VCmax%pred和FVC%pred大于CSCOPD(P = 0.013)。 BSCOPD中PEF25,PEF50,PEF75,MMEF均低于CSCOPD(P <0.05)。 PEF25,PEF50,PEF75,MMEF,MMEF%pred在BSCOPD和CSCOPD均低于对照组(p <0.01)。 BSCOPD和CSCOPD中FEV1%pred和FEV1 / FVC均低于对照组(P <0.05),但BSCOPD与CSCOPD无显着性差异。 HRCT:BSCOPD中的EI和GVin%明显低于CSCOPD(P <0.01)。 BSCOPD和CSCOPD中的EI和GV%显着高于对照组(p <0.05)。 BSCOPD中RVC-860〜950HU明显低于CSCOPD(P <0.01)。病理特征:BSCOPD基底膜厚度明显大于CSCOPD和对照组(P <0.01)。 CSCOPD基底膜厚度与对照组无显着性差异(P> 0.05)。 BSCOPD支气管镜下色素沉着明显高于CSCOPD(P <0.05)。 BSCOPD中BALF的巨噬细胞和淋巴细胞比例明显高于CSCOPD。 BSCOPD中BALF中性粒细胞比例明显低于CSCOPD组(P <0.05)。
   结论:生物燃料烟雾引起的COPD与香烟烟雾引起的COPD相比,具有不同的临床表现,放射学,病理学和生理学特征。
   临床意义:与吸烟引起的COPD相比,生物燃料烟雾引起的COPD可能具有不同的预后或治疗特征。

 
(中日友好医院呼吸与危重症医学科 王圆方 摘译 林江涛 审校)
( Chest, 2016, 149(4):A399-A399.)
 
 
 

A Distinct Phenotype in Chronic Obstructive Pulmonary Disease: COPD Caused by Biomass Smoke


Zhao D, Zhou Y, Jiang C, et al.A Distinct Phenotype in Chronic Obstructive Pulmonary Disease: COPD Caused by Biomass Smoke[J]. 

Abstract
PURPOSE: To investigate the clinical phenotype in patients with COPD caused by biomass smoke.
METHODS: The subjects were grouped according to the risk factors exposured: ① COPD group caused by biomass smoke (BSCOPD), ② COPD group caused by cigarette smoke (CSCOPD), ③ Normal control group exposed by biomass smoke (BSNormal), ④ Normal control group exposed by cigarette smoke (CSNormal). All subjects completed a questionnaire regarding demographic data, symptoms, and environmental exposure and underwent spirometry, HRCT of the chest, bronchial mucosal biopsies and bronchoalveolar lavage fluid (BALF). The clinical variables of four groups were compared.
RESULTS: There were 29 subjects in BSCOPD,31 in CSCOPD,12 in BSNormal and 10 in CSNormal. Phenotype of pulmonary function:Vcmax% pred and FVC% pred in BSCOPD were greater than that in CSCOPD (P=0.013). PEF25, PEF50, PEF75, MMEF in BSCOPD were less than those in CSCOPD (P<0.05). PEF25, PEF50, PEF75, MMEF, MMEF% pred in BSCOPD and CSCOPD were less than those in control groups (p<0.01). FEV1% pred and FEV1/FVC in BSCOPD and CSCOPD were less than those in control groups (p<0.05) but there was no significant difference between BSCOPD and CSCOPD. Phenotype of HRCT: EI and GVin% in BSCOPD were significantly less than those in CSCOPD (P<0.01). EI and GV in% in BSCOPD and CSCOPD were significantly greater than those in control groups (p<0.05). RVC-860to-950HU in BSCOPD was significantly less than that in CSCOPD (P<0.01). Pathological features:basement membrane thickness of BSCOPD was significantly thicker than CSCOPD and control groups (P<0.01). The basement membrane thickness of CSCOPD had no significant difference with control groups (P>0.05). Endobronchial pigmentation in BSCOPD was significantly more than that in CSCOPD (P<0.05). The proportions of macrophages and lymphocytes of BALF in BSCOPD were significantly greater than those in CSCOPD. The proportion of neutrophils of BALF in BSCOPD was significantly less than that in CSCOPD (P<0.05).
CONCLUSIONS: COPD caused by biomass smoke is a distinct phenotype of COPD, with different clinical, radiological, pathological and physiological characteristics compared with COPD caused by cigarette smoke.
CLINICAL IMPLICATIONS: COPD caused by biomass smoke maybe have different prognosis or treatment characteristics compared with COPD caused by cigarette smoke.
 


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