Helicobacter (H.) pylori’s role in gastric ulcer disease and duodenal ulcer disease is firmly established, and it has been widely accepted as a carcinogen in gastric adenocarcinoma and mucosa-associated lymphoid tissue (MALT) lymphoma. Nearly a decade ago, it was first suggested that H. pylori may offer a protective benefit against gastroesophageal reflux disease (GERD), and that its eradication may worsen GERD and theoretically increase the risk of both symptom severity and refluxinduced complications such as Barrett’s metaplasia of the esophagus and esophageal adenocarcinoma.

Does H. pylori Protect Against GERD?
Although the exact mechanism for any potential protective effect remains elusive, multiple theories have been proposed.Perhaps most plausible is where H. pylori induces a severe inflammatory response of the proximal stomach and subsequent damage of the underlying parietal cells, which are predominantly found in this location. This results in diminished overall acid output and thus reduced acid in any potential refluxate. Eradication of H. pylori would then lead to a reversal of the inflammatory process, re-establishment of the parietal cell mass, hyperchlorhydria, and subsequent worsening of GERD in someone with a propensity for gastroesophageal reflux. However, one problem with this theory is that the original study that suggested an increase in incidence after eradication was in duodenal ulcer patients. Eradication of H. pylori in this situation would thus theoretically diminish acid hypersecretion and achieve the opposite effect. Given this discrepancy, other potential mechanisms of action have been proposed. It has been theorized that the ammonia production in this biochemical pathway may contribute to acid neutralization at the level of the gastroesophageal junction.Yet another postulate is based upon the observation that gastrin increases esophageal sphincter pressure; when H. pylori is in an antral predominant distribution, it may be indirectly improving the esophageal barrier to refluxate.

Epidemiological Association
The association between H. pylori and GERD has been explored in several prevalence studies. Earlier data demonstrated that the rate of H. pylori infection in GERD patients was significantly lower than controls.A meta-analysis confirmed these numbers, observing a prevalence of H. pylori infection of 38% in GERD patients compared with 49.5% in controls without GERD. Studies from the Far East, where corpus gastritis (atrophic gastritis) is predominant, concluded that the same negative relationship between infection and esophagitis existed. In addition, certain genotypes, such as vacA S1, have been found to be more prevalent in controls than in GERD patients, suggesting a potential protective role for this genotype against GERD. More recently, with the utilization of more objective measures of GERD severity such as validated symptom-severity scores, endoscopy, and 24-hour esophageal pH-metry, there was a failure to demonstrate any difference in clinical or lab-related severity of GERD between infected and non-infected patients, with underlying GERD.

ERD is thought to possibly lead to lower esophageal metaplasia in certain individuals when left untreated. Since Barrett’s metaplasia is associated with an increased risk of esophageal adenocarcinoma, concern has mounted that eradication of H. pylori may be tantamount to exchanging one risk of malignancy for another. In support, although potentially coincidental, the increasing incidence of esophageal adenocarcinoma over time has paralleled the decreasing prevalence of H. pylori infection. In addition, the rate of cagA+ infection has been found to be lower in those with GERD complications compared with those without complications, highlighting a potential protective effect from this genotype. At this point, the available data do not establish a consistent association between H. pylori infection and malignant complications of GERD.