Delayed Gastric Emptying Neither Contributes to Gastroesophageal Reflux nor Disease Severity in Patients With Respiratory Disease
Year: 2025
Type: article
Study design: Observational Study
Abstract: Background and Aims: Gastroesophageal reflux (GER) is common and thought to contribute to disease progression in patients with respiratory disease. Delayed gastric emptying (DGE) can increase GER in patients with GER disease, but its effect in patients with respiratory disease, and how differing lung structure (eg, scarring, inflammation) and mechanics (eg, decreased thoracic pressure in restrictive disease, increased abdominal pressure in obstructive disease) influences this is unknown. Our aim was to understand these interrelationships and association with pulmonary function in patients with chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF) and non-IPF interstitial lung disease (non-IPF ILD). Methods: We prospectively recruited 22 COPD (aged 34-75 years), 33 IPF (45-74 years), and 19 non-IPF ILD (37-74 years) patients who underwent gastric emptying studies, high resolution impedance manometry, 24-hr pH-impedance, and pulmonary function testing, as part of routine lung transplantation assessment. Results: < .02 compared with other groups). DGE irrespective of disease type was not associated with increased acid exposure time, total bolus exposure time or number of reflux events. Furthermore, DGE was not associated with higher intra-abdominal pressure, specific esophageal dysmotility, or worse pulmonary function in any of the respiratory diseases. Conclusion: Significantly more NSIP patients have DGE compared with other respiratory diseases. Irrespective of this, DGE had little effect on GER or pulmonary function in any of the respiratory diseases.
Source: Gastro Hep Advances
Authors: Jessica Bradley, Caroline Olson, Ali Alghubari, Ramsah Cheah, Sadia Z. Shah, Augustine S. Lee, Kenneth R. DeVault, Lesley A. Houghton
Language: English
Subfield: Gastroenterology
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $2,000
Funder: United Therapeutics Corporation
OpenAlex ID: W4411499839
