Effect of acid suppression therapy on gastroesophageal reflux and cough in idiopathic pulmonary fibrosis: an intervention study

Abstract

BackgroundChronic cough affects more than 70 percent of patients with Idiopathic Pulmonary Fibrosis and causes significant morbidity. Gastroesophageal reflux is the cause of some cases of chronic cough; and also has a postulated role in the aetiology of Idiopathic Pulmonary Fibrosis. A high prevalence of acid; and more recently non-acid, reflux has been observed in Idiopathic Pulmonary Fibrosis cohorts. Therefore, gastroesophageal reflux may be implicated in the pathogenesis of cough in Idiopathic Pulmonary Fibrosis.MethodsEighteen subjects with Idiopathic Pulmonary Fibrosis underwent 24-hour oesophageal impedance and cough count monitoring after the careful exclusion of causes of chronic cough other than gastroesophageal reflux. All 18 were then treated with high dose acid suppression therapies. Fourteen subjects underwent repeat 24-hour oesophageal impedance and cough count monitoring after eight weeks.ResultsTotal reflux and acid reflux frequencies were within the normal range in the majority of this cohort. The frequencies of non-acid and proximal reflux events were above the normal range. Following high dose acid suppression therapy there was a significant decrease in the number of acid reflux events (p = 0.02), but an increase in the number of non-acid reflux events (p = 0.01). There was no change in cough frequency (p = 0.70).ConclusionsThis study confirms that non-acid reflux is prevalent; and that proximal oesophageal reflux occurs in the majority, of subjects with Idiopathic Pulmonary Fibrosis. It is the first study to investigate the effect of acid suppression therapy on gastroesophageal reflux and cough in patients with Idiopathic Pulmonary Fibrosis. The observation that cough frequency does not improve despite verifiable reductions in oesophageal acid exposure challenges the role of acid reflux in Idiopathic Pulmonary Fibrosis associated cough. The finding that non-acid reflux is increased following the use of acid suppression therapies cautions against the widespread use of acid suppression in patients with Idiopathic Pulmonary Fibrosis given the potential role for non-acid reflux in the pathogenesis of cough and Idiopathic Pulmonary Fibrosis itself.Study registrationThe study was registered with the Cardiff and Vale University Local Health Board Research and Development Committee (09/CMC/4619) and the South East Wales Ethics Committee (09/WSE04/57).

Cough in idiopathic pulmonary fibrosis

“…Moreover, the presence of acid in the distal oesophagus may induce cough, probably through an oesophageal-tracheobronchial reflex [47]. Disappointingly, a study by KILDUFF et al [48] showed no improvement of cough by anti-acid treatments, but a paradoxical increase in non-acid reflux. It might well be that non-acid reflux is influencing cough more than acidic reflux [48].…”

“…Disappointingly, a study by KILDUFF et al [48] showed no improvement of cough by anti-acid treatments, but a paradoxical increase in non-acid reflux. It might well be that non-acid reflux is influencing cough more than acidic reflux [48]. Unfortunately, cough itself may also increase trans-diaphragmatic pressure and promote GORD [47].…”

“…Caution is warranted as opiates may influence the protective mechanism of cough, but might be a useful option for palliation of severe cough in patients with advanced IPF. With respect to GORD, no good evidence on the work-up and treatment of GORD-related cough in IPF exists, while the effect of proton pump inhibitors on cough is debated [48,61].…”

Antitussive effect of carcainium chloride in patients with chronic cough and idiopathic interstitial pneumonias: A pilot study

“…For instance, more than 50% of patients with interstitial lung disease could have cough caused by other causes such as asthma, rhinitis or gastro-oesophageal reflux [18,19]. However, IIP may directly cause cough as inflammation is not limited to the parenchyma, and disrupted airway epithelium [20] with inflammatory mediators known to provoke cough having been detected in such patients [17,18].…”

Idiopathic pulmonary fibrosis: a holistic approach to disease management in the antifibrotic age

“…Gastro-oesophageal reflux disease (GORD) has been suggested as a potential contributor to the pathophysiology of IPF and cough (40). However, in one study the use of acid-suppressing medication did not improve cough and led to a paradoxical increase in non-acid reflux (41). Corticosteroids have been shown to improve cough in one small RCT and may be used at a tapering dose if beneficial (34).…”