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DOI 10.1111/j.1365-2036.2007.03281.x

Медицинская библиотека · Alimentary pharmacology & therapeutics · 2007

Review article: 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

СтатьяПоддержка исследования: вне правительства СШАОбзорПеревод в очереди

Аннотация

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.

Для цитирования: Sifrim D, Mittal R, Fass R, Smout A, Castell D, Tack J, Gregersen H. Review article: acidity and volume of the refluxate in the genesis of gastro-oesophageal reflux disease symptoms.. Alimentary pharmacology & therapeutics. 2007. DOI: 10.1111/j.1365-2036.2007.03281.x.

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