Introduction IPF is a chronic, irreversible, and progressive lung disease, with survival from diagnosis of only 2–5 years. It is characterised by excessive extracellular matrix deposition and remodelling within lung tissue, initiated by repetitive alveolar epithelial cell injury. One trigger of injury is believed to be micro-aspiration of gastroesophageal reflux. However, there is limited or no data on objective measures of reflux, and how it relates to oesophageal motility, lung mechanics and pulmonary function. This study used high resolution impedance manometry, 24 hr pH-impedance and pulmonary function testing to address these questions.
Methods A prospective cohort study of 32 patients with IPF (aged 53–75 yr; 25 male) assessed between Dec. 2018 and Dec. 2019 at Mayo Clinic, USA and Leeds Teaching Hospital Trust.
Results Twenty (63%) patients exhibited dysmotility (Chicago Classification v3.0 (CC)); 14(70%) hypo-contractility (eg ineffective oesophageal motility, fragmented peristalsis, occurring in ≥50% swallows, and absent contractility) and 6(30%) oesophagogastric junction outflow obstruction (EGJOO). Abnormal reflux bolus exposure time was identified in 9(28%) patients, in whom 5/9, and one patient with normal reflux, had an abnormal number of events reaching the proximal oesophagus. 30%(13–48%) (median(IQR)) of all events reached the proximal oesophagus. 4/14 patients with hypo-contractility, 5/12 with normal motility and 0/6 with EGJOO (CC) exhibited abnormal reflux. Interestingly, 4 patients with normal motility (CC) did have ineffective swallows (<40% swallows), and the removal of these patients, resulted in the redefined cohort having no abnormal proximal reflux. Across all patients reflux bolus exposure time correlated with gastroesophageal pressure gradient (GEPG) (r=0.479;p=0.009), which became stronger when only patients with normal motility were examined (CC: r=0.664;p=0.018; redefined: r=0.881;p=0.004). There was no association in hypo-contractility, likely due to the presence of ineffective motility, which correlated with reflux bolus exposure time (r=0.422;p=0.133). Patients with hypo-contractility had a lower Forced Vital Capacity percent predicted (49%(40–68)%) than patients with normal motility (67%(61–72)%;p=0.04).
Conclusions Ineffective oesophageal motility was associated with increased reflux exposure, with many events reaching the proximal oesophagus, irrespective of whether patients had hypo- or normal motility; likely driven in part by increased GEPG. Furthermore, such motility abnormalities appear to associate with pulmonary dysfunction.
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