Patterson Robert N, Johnston Brian T, Ardill Joy E S, Heaney Liam G, McGarvey Lorcan P A
Department of Medicine, Queen's University Belfast, and Regional Respiratory Centre, Belfast City Hospital, Grosvenor Road, Belfast BT12 6BJ, UK.
Thorax. 2007 Jun;62(6):491-5. doi: 10.1136/thx.2006.063982. Epub 2007 Jan 24.
Acid reflux may aggravate airway disease including asthma and chronic cough. One postulated mechanism concerns a vagally-mediated oesophageal-tracheobronchial reflex with airway sensory nerve activation and tachykinin release.
To test the hypothesis that patients with airways disease and reflux have higher airway tachykinin levels than those without reflux.
Thirty-two patients with airways disease (16 with mild asthma and 16 non-asthmatic subjects with chronic cough) underwent 24 h oesophageal pH monitoring. Acid reflux was defined as increased total oesophageal acid exposure (% total time pH<4 of >4.9% at the distal probe). All subjects underwent sputum induction. Differential cell counts and concentrations of substance P (SP), neurokinin A (NKA), albumin and alpha2-macroglobulin were determined.
SP and NKA levels were significantly higher in patients with reflux than in those without (SP: 1434 (680) pg/ml vs 906 (593) pg/ml, p=0.026; NKA: 81 (33) pg/ml vs 52 (36) pg/ml, p=0.03). Significantly higher tachykinin levels were also found in asthmatic patients with reflux than in asthmatic patients without reflux (SP: 1508 (781) pg/ml vs 737 (512) pg/ml, p=0.035; NKA: median (interquartile range 108 (85-120) pg/ml vs 75 (2-98) pg/ml, p=0.02). In patients with asthma there was a significant positive correlation between distal oesophageal acid exposure and SP levels (r=0.59, p=0.01) and NKA levels (r=0.56, p=0.02). Non-significant increases in SP and NKA were measured in patients with cough with reflux (SP: 1534.71 (711) pg/ml vs 1089 (606) pg/ml, p=0.20; NKA: 56 (43) pg/ml vs 49 (17) pg/ml, p=0.71). No significant difference in differential cell counts or any other biochemical parameter was noted between study groups.
This study demonstrates increased airway tachykinin levels in patients with asthma and cough patients with coexistent acid reflux. This suggests airway sensory nerve activation in this population.
胃酸反流可能会加重包括哮喘和慢性咳嗽在内的气道疾病。一种推测的机制涉及迷走神经介导的食管-气管支气管反射,伴有气道感觉神经激活和速激肽释放。
验证气道疾病和反流患者的气道速激肽水平高于无反流患者这一假设。
32例气道疾病患者(16例轻度哮喘患者和16例慢性咳嗽的非哮喘患者)接受了24小时食管pH监测。胃酸反流定义为食管总酸暴露增加(远端探头处pH<4的总时间百分比>4.9%)。所有受试者均进行痰液诱导。测定了细胞分类计数以及P物质(SP)、神经激肽A(NKA)、白蛋白和α2-巨球蛋白的浓度。
反流患者的SP和NKA水平显著高于无反流患者(SP:1434(680)pg/ml对906(593)pg/ml,p = 0.026;NKA:81(33)pg/ml对52(36)pg/ml,p = 0.03)。有反流的哮喘患者的速激肽水平也显著高于无反流的哮喘患者(SP:1508(781)pg/ml对737(512)pg/ml,p = 0.035;NKA:中位数(四分位间距)108(85 - 120)pg/ml对75(2 - 98)pg/ml,p = 0.02)。在哮喘患者中,远端食管酸暴露与SP水平(r = 0.59,p = 0.01)和NKA水平(r = 0.56,p = 0.02)之间存在显著正相关。有反流咳嗽患者的SP和NKA有非显著性升高(SP:1534.71(711)pg/ml对1089(606)pg/ml,p = 0.20;NKA:56(43)pg/ml对49(17)pg/ml,p = 0.71)。研究组之间在细胞分类计数或任何其他生化参数方面未发现显著差异。
本研究表明哮喘患者和同时存在胃酸反流的咳嗽患者的气道速激肽水平升高。这提示该人群存在气道感觉神经激活。