Alimentary TractGastro-oesophageal reflux and interstitial lung disease
Introduction
Gastro-oesophageal reflux (GER) is thought to be potentially implicated in the pathogenesis of different forms of pulmonary disorders, including asthma [1], chronic obstructive pulmonary disease (COPD) [2], chronic cough [3], pneumonia [4], obstructive sleep apnoea [5] and interstitial lung disease (ILD) [6], [7], [8]. Evidences on acid aspiration-induced lung injury date several decades [9] and this is believed to be the main noxious trigger to pulmonary diseases together with vago-vagal reflexes [10]. However, the role of GER as concomitant or causal is far to be elucidated in many of these conditions including ILD.
ILD encompasses a heterogeneous group of acute and chronic disorders characterised by diffuse pulmonary infiltrates with histologic features of pulmonary inflammation, exertional dyspnoea and restrictive lung patterns [11]. Pulmonary fibrosis results from a variety of insults to the lung, including toxic, autoimmune, drug-induced, infectious, or traumatic injuries. Exposure to a known aetiological factor does not always lead to fibrosis and the existence of familial forms of lung fibrosis suggests a genetic predisposition [12]. When the aetiology of ILD is unknown, the disease is classified as idiopathic pulmonary fibrosis (IPF), which is a progressive and fatal syndrome. It usually affects adults in the fifth decade and mortality rates are high, with median survival at the time of diagnosis of 4–5 years [13]. We defined cases with recognisable underlying causes as secondary pulmonary fibrosis (SPF).
Only scant evidences exist suggesting a high prevalence of increased oesophageal acid reflux in patients with pulmonary fibrosis [6], [7], [8], [14]. The aims of our study were to prospectively evaluate GER in consecutive patients with ILD and to define acid reflux patterns in patients with idiopathic and secondary forms of pulmonary fibrosis.
Section snippets
Patients
Twenty-eight consecutive patients diagnosed as being affected by ILD according to predefined criteria [15] were evaluated by thorough medical history, pulmonary function tests, high resolution computed tomography (HRCT), oesophageal manometry and oesophago-gastric pH monitoring. Each patient completed a modified version of the Bowel Disease Questionnaire (BDQ) that is commonly used in our laboratory to evaluate digestive symptoms [16], [17].
Pulmonary function tests
Flow–volume studies, lung volumes, carbon monoxide
Demographics and function pulmonary tests
All patients showed grade III at HRCT (see Section 2). Demographic features, function pulmonary tests and HRCT findings of ILD patients (n = 28, 15 M, 66 years, IQR 60–71) are listed in Table 1. Eighteen patients were diagnosed as being affected by IPF (10 M, 70 years, IQR 61–72) and 10 by SPF, (5 M, 63 years, IQR 55–67). SPF was diagnosed as secondary to extrinsic allergic alveolitis (n = 2), connective tissue disease (n = 5), non-specific interstitial pneumonia (n = 3).
No differences in function
Discussion
A potential causative role of GER in a variety of pulmonary diseases [1], [2], [3], [4], [5], [6], [23], [24] including ILD [25] has long been hypothesised. An increased prevalence of hiatal hernia and GER has been reported in IPF compared with SPF [12]. Studies on correlations between lung function tests and oesophageal dysmotility in ILDs and between DLCO and pH monitoring, have provided controversial results [26]. Experimental models showed that pulmonary fibrosis can occur after acid
Conflict of interest statement
None declared.
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