Aksu Oğuzhan, Songür Necla, Songür Yıldıran, Öztürk Önder, Adiloğlu Ali Kudret, Kapucuoğlu Nilgün, Akın Mete
Department of Internal Medicine, Süleyman Demirel University Faculty of Medicine, Isparta, Turkey.
Turk J Gastroenterol. 2014 Dec;25 Suppl 1:48-53. doi: 10.5152/tjg.2014.4018.
BACKGROUND/AIMS: Previous studies have shown that the prevalence of abnormal acid reflux in fibrotic lung disease patients is high, and in particular, patients with secondary pulmonary fibrosis show higher esophageal acid exposure than normal controls. There are also some findings that, in patients with pathological reflux, pulmonary fibrosis may develop. The aim of this study is to investigate if pulmonary fibrosis is involved in the pathogenesis of chronic cough due to Gastroesophageal Reflux.
A prospective study was performed in twenty-one patients with chronic cough due to gastroesophageal reflux who was diagnosed as reflux esophagitis by upper gastrointestinal endoscopy, histology, and in ten healthy controls without GER or any lung disease. All participitants underwent laryngoscopic examination and gastroesophageal scintigraphy with late lung imaging. Bronchoalveolar lavage fluid total and differential cell counts, T and B cell subsets, and the concentrations of IL- 1β and TNF-α were measured.
Reflux extending into the proximal esophagus was noted in 52.5%, and posterior laryngitis was present in 90.5% of the patients. No evidence of pulmonary aspiration was noted in the patients with reflux on scintigraphic examination. No significant difference was found between the GER and control groups in terms of cellular content, IL-1β and TNF-α levels or mean T cell subsets and B cell counts in bronchoalveolar lavage fluid. Forced expiratory volume in one second, forced vital capacity FEV1/FVC, total lung capacity, and carbon monoxide diffusion capacity values were within normal limits in the gastroesophageal reflux group.
Our findings do not support the hypothesis that gastroesophageal reflux leads to chronic cough by triggering alveolar epithelial injury and subsequent pulmonary fibrosis.
背景/目的：既往研究表明，纤维化肺病患者中异常酸反流的患病率较高，尤其是继发性肺纤维化患者的食管酸暴露高于正常对照组。也有一些研究发现，在病理性反流患者中，可能会发生肺纤维化。本研究的目的是调查肺纤维化是否参与胃食管反流所致慢性咳嗽的发病机制。
对21例因胃食管反流导致慢性咳嗽且经上消化道内镜检查、组织学检查确诊为反流性食管炎的患者，以及10例无胃食管反流或任何肺部疾病的健康对照者进行了一项前瞻性研究。所有参与者均接受了喉镜检查和胃食管闪烁显像及肺部延迟显像。检测支气管肺泡灌洗液中的细胞总数和分类计数、T细胞和B细胞亚群以及白细胞介素-1β和肿瘤坏死因子-α的浓度。
52.5%的患者反流延伸至食管近端，90.5%的患者存在后喉炎。闪烁显像检查显示反流患者未发现肺误吸的证据。胃食管反流组和对照组在细胞成分、白细胞介素-1β和肿瘤坏死因子-α水平、支气管肺泡灌洗液中T细胞亚群均值和B细胞计数方面无显著差异。胃食管反流组的一秒用力呼气量、用力肺活量、FEV1/FVC、肺总量和一氧化碳弥散量值均在正常范围内。
我们的研究结果不支持胃食管反流通过触发肺泡上皮损伤及随后的肺纤维化导致慢性咳嗽这一假说。
