Acidity and volume of the refluxate in the genesis of gastro-oesophageal reflux disease symptoms

SIFRIM, D.
MITTAL, R.
FASS, R.
SMOUT, A.
CASTELL, D.
TACK, J.
GREGERSEN, H.

^*Center for Gastroenterological Research, Catholic University of Leuven, Leuven, Belgium
^†Division of Gastroenterology, University of California, San Diego, CA, USA
^‡Neuro-Enteric Clinical Research Group, Department of Medicine, Section of Gastroenterology, Southern Arizona VA Health Care System, Tucson, AZ, USA
^§Department of Gastroenterology, University Medical Center, Utrecht, the Netherlands
^¶Division of Gastroenterology/Hepatology, Medical University of South Carolina, Charleston, SC, USA
^**Center of Excellence in Visceral Biomechanics and Pain, Aalborg Hospital and Center of Sensory-Motor Interaction, Aalborg University, Aalborg, Denmark

Dr D. Sifrim, Faculty of Medicine K.U. Leuven, Lab G-I Physiopathology, O&N Gasthuisberg, 7th floor, Herestraat 49, 3000 Leuven, Belgium. E-mail: [email protected]

Publication data Submitted 2 November 2006, First decision 20 November 2006, Resubmitted 13 December 2006, Resubmitted 18 December 2006, Accepted 20 December 2006

Alimentary Pharmacology & Therapeutics 25(9):p 1003-1017, May 1, 2007.

SUMMARY

Background

A number of mechanisms, other than acid reflux, may be responsible for the symptoms of gastro-oesophageal reflux disease.

Aim

To assess the importance of non-acid reflux mechanisms.

Methods

This review is based on presentations and discussion at a workshop, where specialists in the field analysed data relating to these mechanisms.

Results

Weakly acidic reflux, pH (4–7), detected with impedance–pHmetry is associated with regurgitation and atypical gastro-oesophageal reflux disease symptoms. It is not clear whether pepsin and trypsin can elicit symptoms, but bile can elicit heartburn. The magnitude of reflux-induced oesophageal distension can be determined by high frequency ultrasonography and is not reduced by proton pump inhibition, suggesting that persisting symptoms ‘on’ a proton pump inhibitor may still be due to oesophageal distension by non-acidic reflux. Exaggerated longitudinal muscle contraction can induce non-acid-related heartburn. Preliminary studies showed a positive effect of baclofen, surgery or endoscopic procedures to reduce weakly acidic reflux.

Conclusion

Mechanisms other than acid reflux are involved in some of the symptoms of gastro-oesophageal reflux disease. Controlled outcome studies are needed to clarify their roles and the indications for antireflux procedures in patients with persistent symptoms whilst ‘on’ a proton pump inhibitor.