Lehtonen Hannele, Oksa Panu, Lehtimäki Lauri, Sepponen Anna, Nieminen Riina, Kankaanranta Hannu, Saarelainen Seppo, Järvenpää Ritva, Uitti Jukka, Moilanen Eeva
Medical School/Pharmacology, 33014 University of Tampere, Finland.
Thorax. 2007 Jul;62(7):602-7. doi: 10.1136/thx.2006.067868. Epub 2007 Jan 24.
Inhaled asbestos fibres can cause inflammation and fibrosis in the lungs called asbestosis. However, there are no non-invasive means to assess and follow the severity of the inflammation. Exhaled nitric oxide (NO) measured at multiple exhalation flow rates can be used to assess the alveolar NO concentration and bronchial NO flux, which reflect inflammation in the lung parenchyma and airways, respectively. The aim of the present study was to investigate whether exhaled NO or markers in exhaled breath condensate could be used to assess inflammation in asbestosis.
Exhaled NO and inflammatory markers (leukotriene B(4) and 8-isoprostane) in exhaled breath condensate were measured in 15 non-smoking patients with asbestosis and in 15 healthy controls. Exhaled NO concentrations were measured at four constant exhalation flow rates (50, 100, 200 and 300 ml/s) and alveolar NO concentration and bronchial NO flux were calculated according to the linear model of pulmonary NO dynamics.
The mean (SE) alveolar NO concentration was significantly higher in patients with asbestosis than in controls (3.2 (0.4) vs 2.0 (0.2) ppb, p = 0.008). There was no difference in bronchial NO flux (0.9 (0.1) vs 0.9 (0.1) nl/s, p = 0.93) or NO concentration measured at ATS standard flow rate of 50 ml/s (20.0 (2.0) vs 19.7 (1.8) ppb, p = 0.89). Patients with asbestosis had increased levels of leukotriene B4 (39.5 (6.0) vs 15.4 (2.9) pg/ml, p = 0.002) and 8-isoprostane (33.5 (9.6) vs 11.9 (2.8) pg/ml, p = 0.048) in exhaled breath condensate and raised serum levels of C-reactive protein (2.3 (0.3) vs 1.1 (0.2) mug/ml, p = 0.003), interleukin-6 (3.5 (0.5) vs 1.7 (0.4) pg/ml, p = 0.007) and myeloperoxidase (356 (48) vs 240 (20) ng/ml, p = 0.034) compared with healthy controls.
Patients with asbestosis have an increased alveolar NO concentration and high levels of leukotriene B4 and 8-isoprostane in exhaled breath. Measurement of exhaled NO at multiple exhalation flow rates and analysis of inflammatory markers in exhaled breath condensate are promising non-invasive means for assessing inflammation in patients with asbestosis.
吸入石棉纤维可导致肺部炎症和纤维化,即石棉沉着病。然而,目前尚无评估和跟踪炎症严重程度的非侵入性方法。在多个呼气流量下测量呼出一氧化氮(NO)可用于评估肺泡NO浓度和支气管NO通量,它们分别反映肺实质和气道的炎症情况。本研究的目的是探讨呼出NO或呼出气冷凝物中的标志物是否可用于评估石棉沉着病中的炎症。
对15名非吸烟石棉沉着病患者和15名健康对照者测量呼出气冷凝物中的呼出NO和炎症标志物(白三烯B4和8-异前列腺素)。在四个恒定呼气流量(50、100、200和300 ml/s)下测量呼出NO浓度,并根据肺NO动力学的线性模型计算肺泡NO浓度和支气管NO通量。
石棉沉着病患者的平均(SE)肺泡NO浓度显著高于对照组(3.2(0.4)对2.0(0.2)ppb,p = 0.008)。支气管NO通量(0.9(0.1)对0.9(0.1)nl/s,p = 0.93)或在ATS标准流量50 ml/s下测量的NO浓度(20.0(2.0)对19.7(1.8)ppb,p = 0.89)无差异。与健康对照相比,石棉沉着病患者呼出气冷凝物中的白三烯B4(39.5(6.0)对15.4(2.9)pg/ml,p = 0.002)和8-异前列腺素(33.5(9.6)对11.9(2.8)pg/ml,p = 0.048)水平升高,血清C反应蛋白(2.3(0.3)对1.1(0.2)μg/ml,p = 0.003)、白细胞介素-6(3.5(0.5)对1.7(0.4)pg/ml,p = 0.007)和髓过氧化物酶(356(48)对240(20)ng/ml,p = 0.034)水平升高。
石棉沉着病患者的肺泡NO浓度升高,呼出气中的白三烯B4和8-异前列腺素水平较高。在多个呼气流量下测量呼出NO以及分析呼出气冷凝物中的炎症标志物是评估石棉沉着病患者炎症的有前景的非侵入性方法。