Stomach Flu

Summary text
While GERD symptoms are generally considered to be caused by acid reflux, data indicate that other mechanisms, such as weakly acidic reflux, bile, reflux volume and esophageal distension may play a role. Baclofen therapy and surgical or endoscopic procedures have been shown to reduce weakly acidic reflux.

Key findings

Mechanisms other than acid reflux are involved in the generation of GERD symptoms.Weakly acidic reflux is associated with heartburn and atypical GERD symptoms (chest pain and cough).The association between weakly acidic reflux and GERD symptoms appears to be most evident among patients “on”, rather than “off”, PPI therapy.Initial data indicate that baclofen treatment and surgical or endoscopic procedures may reduce weakly acidic reflux.
Extended abstract

Background: The symptoms of gastroesophageal reflux disease (GERD) are usually thought to be caused by acid reflux (esophageal pH <4). However, symptoms may persist in some patients receiving acid-suppressive therapy. It has been suggested that other mechanisms, such as weakly acidic acid reflux (pH 4–7) or esophageal distension, may be involved in GERD symptom generation.

Aim: To assess the importance of mechanisms other than acid reflux in the generation of GERD symptoms.

Methods: Data are based on presentations given at a workshop, at which specialists in the field discussed current available data related to the mechanisms of symptom generation in GERD.

Discussion: While heartburn has traditionally been considered as being an acid-mediated event, ambulatory pH monitoring studies have demonstrated that as many as 30% of symptoms in patients with GERD may be associated with reflux episodes with a pH of 4–7, suggesting that the threshold of pH <4 for esophageal symptom generation may need to be revisited.
Studies using pH impedance monitoring demonstrate that the relationship between symptoms and weakly acidic reflux differs between patients “on”, and those “off”, proton pump inhibitor (PPI) therapy. In the former, heartburn and acid regurgitation episodes were more commonly associated with weakly acidic than with acid reflux. In the latter, heartburn and acid regurgitation episodes were more commonly preceded by acid reflux than by weakly acidic reflux. In both groups of patients, weakly acidic reflux was associated with regurgitation and atypical GERD symptoms, such as chest pain and cough.
Some studies have suggested that acid-sensitive chemoreceptors may react to a change in pH. In terms of non-acidic stimuli, data indicate that bile may have a role in generating heartburn. The role of pepsin and trypsin in GERD symptom generation is unclear.
In terms of mechanical stimuli, reflux volume is likely to be clinically relevant in GERD patients; high proximal extent of reflux and slow acid and volume clearance may be indirect markers of high reflux volume. Esophageal distension, measured using high frequency intraluminal ultrasonography, is unaffected by PPI treatment, suggesting that persistent GERD symptoms in patients “on” PPI therapy may result from esophageal distension by non-acidic refluxate. Balloon distensions in the proximal or distal esophagus elicit typical heartburn symptoms in both healthy volunteers and GERD patients, supporting the theory that a variety of intra-esophageal stimuli can induce similar perceptual responses. Non-acid-related heartburn can be induced by exaggerated longitudinal muscle contraction.
Initial data indicate that surgical or endoscopic procedures effectively reduce the number, volume and proximal extent of weakly acidic reflux episodes. In small studies in healthy volunteers and GERD patients “off” PPI therapy, baclofen effectively reduced the number of acid and weakly acidic reflux episodes, and improved reflux-related symptoms. When baclofen 20 mg three times daily was administered with PPIs to patients with GERD symptoms refractory to standard-dose PPI therapy and with persistent duodenogastrooesophageal reflux (DGER), acid exposure was similar but DGER decreased significantly. The number of duodenal reflux episodes and long-lasting duodenal reflux episodes (>5 min) decreased, as did the cumulative severity score for 14 reflux symptoms.

Conclusions: Mechanisms other than acid reflux, including weakly acidic reflux and esophageal distension, may contribute to the generation of GERD symptoms. Preliminary data indicate that baclofen therapy and surgical and endoscopic antireflux procedures may reduce weakly acidic reflux. Controlled clinical studies are required to determine the effects of these therapies on GERD symptoms, particularly in patients with persistent symptoms associated with weakly acidic reflux while receiving PPI treatment.

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