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Anti-relaxation therapy in GORD
  1. J Tack,
  2. D Sifrim
  1. Centre for Gastroenterological Research, University of Leuven, Leuven, Belgium
  1. Correspondence to:
    Dr J Tack, Department of Internal Medicine, Division of Gastroenterology, University Hospital Gasthuisberg, Herestraat 49, B-3000 Leuven, Belgium;

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Reducing transient LOS relaxations in patients with gastro-oesophageal reflux disease

Gastro-oesophageal reflux disease (GORD), defined as the presence of symptoms or lesions that can be attributed to the reflux of gastric contents into the oesophagus, is one of the most common disorders affecting the gastrointestinal tract. Gastric acid is essential in the development of GORD and the duration of oesophageal acid exposure is a major determinant of the severity of reflux oesophagitis.1 This is the reason why proton pump inhibitors, with their strong acid suppressing action, have brought relief to the majority of these patients, although most GORD patients do not have increased gastric acid secretion.2

The pathophysiology of GORD is multifactorial, including alterations in the volume, composition, or distribution of gastric contents, anatomical and/or motor dysfunction of the antireflux barrier at the gastro-oesophageal junction, impaired clearance mechanisms, and defective resistance to injury at the mucosal level. Acid suppressive therapy addresses one of the pathophysiological mechanisms—that is, gastric acid volume—without affecting others such as the non-acid component of the gastric contents or the function of the antireflux barrier. In spite of the efficacy of acid suppressive therapy, there have been many attempts to target other aspects of GORD pathophysiology, such as basal lower oesophageal sphincter (LOS) pressure, oesophageal body motility, or gastric emptying. Unfortunately, most of these approaches have been clinically disappointing.

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