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原发性自发性气胸后发生的胸膜炎症的特征

Characterisation of pleural inflammation occurring after primary spontaneous pneumothorax.

作者信息

De Smedt A, Vanderlinden E, Demanet C, De Waele M, Goossens A, Noppen M

机构信息

Respiratory Division and Haematology-Immunology Dept, Academic Hospital, Brussels, Belgium.

出版信息

Eur Respir J. 2004 Jun;23(6):896-900. doi: 10.1183/09031936.04.00079304.

Abstract

The aim of this study was to examine the inflammatory reaction occurring in the pleural space of patients suffering from primary spontaneous pneumothorax (PSP) using pleural lavage, which was performed in patients with PSP and in healthy control subjects (essential hyperhidrosis patients undergoing thoracoscopy for sympathicolysis treatment). Cellular and solute composition of lavage fluid, peripheral blood and parietal pleural biopsies were analysed. PSP lavage fluid showed an increase in all differentiated leucocytes, but most strikingly eosinophils and neutrophils. In the blood of patients with PSP, the total number of leucocytes and the absolute number of eosinophils, neutrophils and monocytes were also significantly increased. The time in which air was present in the pleural space was positively correlated with the increase of eosinophils in lavage fluid, parietal pleura and blood. Eosinophilic cationic protein was elevated after PSP and strongly correlated with the absolute number of lavage eosinophils. Chemo and cytokine analysis in lavage fluid showed differences in concentrations of interleukin (IL)-5, IL-6, IL-8, IL-12p40, tumour necrosis factor-alpha and RANTES, but not of eotaxin. Surprisingly, high levels of lipopolysaccharide binding protein were also measured. Primary spontaneous pnumothorax is associated with a substantial pleural inflammatory reaction. The authors hypothesise that mechanical stretch factors, lipopolysaccharide binding protein/lipopolysaccharide complexes or other environmental components trigger pleural inflammation after primary spontaneous pnumothorax.

摘要

本研究的目的是通过对原发性自发性气胸(PSP)患者及健康对照者(因多汗症接受胸腔镜交感神经切断术治疗的患者)进行胸腔灌洗,来检测PSP患者胸腔内发生的炎症反应。分析了灌洗液、外周血和壁层胸膜活检组织的细胞及溶质成分。PSP灌洗液中所有分化的白细胞均增加,其中嗜酸性粒细胞和中性粒细胞增加最为显著。PSP患者血液中白细胞总数以及嗜酸性粒细胞、中性粒细胞和单核细胞的绝对数量也显著增加。胸腔内存在空气的时间与灌洗液、壁层胸膜和血液中嗜酸性粒细胞的增加呈正相关。PSP后嗜酸性阳离子蛋白升高,且与灌洗嗜酸性粒细胞的绝对数量密切相关。灌洗液中的化学因子和细胞因子分析显示,白细胞介素(IL)-5、IL-6、IL-8、IL-12p40、肿瘤坏死因子-α和调节激活正常T细胞表达和分泌的趋化因子(RANTES)浓度存在差异,但嗜酸性粒细胞趋化因子浓度无差异。令人惊讶的是,还检测到高水平的脂多糖结合蛋白。原发性自发性气胸与显著的胸腔炎症反应相关。作者推测,机械拉伸因素、脂多糖结合蛋白/脂多糖复合物或其他环境成分在原发性自发性气胸后引发胸腔炎症。

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