Obstructive sleep apnea does not promote esophageal reflux in fibrosing interstitial lung disease

Abstract

Background In patients with fibrosing interstitial lung disease (fILD), gastroesophageal reflux (GER) is highly prevalent, perhaps because of the effects of lung fibrosis on altering intrathoracic pressure, diaphragm morphology and lower esophageal sphincter (LES) function. For unclear reasons, obstructive sleep apnea (OSA) is also highly prevalent among patients with fILD. We conducted this study to test our hypothesis that, in patients with fILD, OSA would exacerbate diaphragm/LES dysfunction and increase the propensity for—and severity of—GER. Methods We identified patients with fILD who underwent screening polysomnogram and pH or pH/impedence probe at our center during the same week. We examined the association between OSA and GER and used logistic regression to determine independent predictors of OSA or GER. Results In 54 included subjects, neither OSA (dichotomous) nor apnea hypopnea index (continuous) predicted the presence of GER. Regardless of body position (upright, recumbent), GER was no more frequent or severe among subjects with OSA vs. those without OSA. Subjects with idiopathic pulmonary fibrosis (IPF) had an odds of GER nearly seven-fold greater than subjects with other forms of fILD (odds ratio=6.84, 95% confidence interval 1.36–34.43, p=0.02). For the entire cohort and the subgroup with IPF, there was no correlation between pulmonary physiology and GER. Conclusions In fILD, OSA does not appear to promote GER. Research is needed to determine if compensatory mechanisms emanating from the crural diaphragm prevent GER in fILD patients with OSA and to sort out whether GER has a role in the pathogenesis of certain forms of fILD.

Comorbidities in interstitial lung diseases

“…Worse outcomes observed in IPF patients who do not comply with CPAP are inconclusive in this regard because difficulties with the use of CPAP machines may be more prevalent in advanced IPF [143]. An increase in mortality in IPF patients with OSA might, in theory, be linked to the promotion of GOR but this view is not supported by a study of 54 patients in which GOR promotion by OSA was definitively refuted [144]. Failure to treat OSA might, in principle, lead to worsening PH, triggered by the severity of desaturation, but if so, it is entirely uncertain whether this danger might be alleviated, at least in some patients, by nocturnal oxygen supplementation alone, without the need for routine institution of CPAP.…”

Cough in idiopathic pulmonary fibrosis

“…Gastro-oesophageal reflux disease (GORD) is highly prevalent in IPF, yet classical symptoms are often absent [37,38]. GORD-associated microaspiration of acid and non-acid reflux in the airway is thought to induce epithelial damage and may cause fibrosis [45].…”

“…GORD-associated microaspiration of acid and non-acid reflux in the airway is thought to induce epithelial damage and may cause fibrosis [45]. Traction caused by lung fibrosis also can result in a weakened lower oesophageal sphincter, leading to gastro-oesophageal reflux and microaspiration [38,46]. Cough receptors could be directly stimulated through aspiration of gastric secretions in the larynx and the upper airways [6].…”

“…1: traction leading to a weaker lower oesophageal sphincter tonus [45]; 2: microaspiration inducing epithelial damage [38,46]; 3: restriction inducing instability of the upper airway [39]; 4: intermitted hypoxaemia promoting profibrotic mechanisms [49]; 5: increased cough reflex sensitivity [22][23][24][25][26][27][28][29][30][31]; 6: pressure causing stretch injury and activation of fibrotic mechanisms [31]; 7: microaspiration causing an inflammatory reaction blocking the airway [53]; 8: obstruction increasing trans-diaphragmatic pressure [51,52]; 9: aspiration directly and acid reflux indirectly stimulate the cough reflex [6,47]; 10: cough increasing trans-diaphragmatic pressure [47]; 11: less central inhibition and inflammation increasing cough reflex sensitivity [54]. sensory nerves.…”

Cough, sarcoidosis and idiopathic pulmonary fibrosis: raw nerves and bad vibrations

“…However, not all evidence supports this ‘triad’ as a pathogenetic mechanism. A recent multivariate analysis in 54 patients with fibrosing interstitial lung disease found no relationship between the presence or severity of OSA and GORD and that acid reflux was no more frequent or severe in subjects with OSA compared to those without [37]. Also, a small prospective study found no difference in pepsin levels of exhaled breath condensate between patients with IPF and normal controls [38].…”