Abstract

Most gastro-oesophageal reflux events are triggered by transient lower oesophageal sphincter relaxations (TLOSRs). Acid-related reflux disease with typical heartburn and reflux oesophagitis generally responds well to acid suppression with proton pump inhibitors (PPI), but treating non-acid and mixed gaseous reflux has proven more challenging.

Highlights

  • The pathophysiology of typical gastro-oesophageal reflux disease (GORD) symptoms and reflux oesophagitis is associated with excess acid reflux, but both refractory GORD and laryngopharyngeal reflux (LPR) have strong links with functional gut disorders [1,2,3]

  • In more severe or refractory cases where the proximal colon remains full on abdominal x-ray (AXR) despite laxative therapy, adding prucalopride may prove invaluable as it has been shown to preferentially improve proximal colonic motility [65] in addition to improving gastric emptying and reducing oesophageal acid exposure and proximal oesophageal reflux in healthy subjects [66], all of which are beneficial in controlling both refractory GORD and LPR

  • As our study demonstrated a strong correlation between improvement of functional colonic and upper gut, refractory GORD and LPR symptoms with treatment as the colon decompresses [18], prompt improvement in cough, reflux or dyspeptic symptoms with bowel cleansing suggests that a good longterm response on maintenance therapy is achievable

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Summary

Introduction

The pathophysiology of typical gastro-oesophageal reflux disease (GORD) symptoms and reflux oesophagitis is associated with excess acid reflux, but both refractory GORD and laryngopharyngeal reflux (LPR) have strong links with functional gut disorders [1,2,3]. IBS subjects are known to have increased sensitivity to colonic distension causing pain and increased contractility [5], but colonic distension has been found to affect upper gut motility [6,7,8,9] and increase reflux events in physiological studies [10]. We hypothesised that reducing colonic distension mainly with simple osmotic laxative therapy would improve colonic symptoms and LPR, refractory GORD and functional upper gut symptoms

Pathophysiology of GORD
Limitations of PPI Therapy for GORD and LPR
Optimising Management of Refractory GORD and LPR
IBS Increasing
Findings
Conclusion
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