Helicobacter pylori and Symptomatic Relapse of Gastro-esophageal Reflux Disease

Abstract & commentary

Synopsis: This elegant study indicated that a group of international patients with GERD and concomitant infection with Helicobacter pylori had definite GERD improvement when H pylori was successfully eradicated.

Source: Schwizer W, et al. Lancet. 2001;357:1738-1742.

This article addresses the highly controversial relationship between Helicobacter pylori infection and gastroesophageal reflux disease (GERD). Schwizer and colleagues studied 70 GERD patients as defined by either erosive esophagitis and/or abnormal esophageal acid exposure. All patients received lansoprazole 30 mg b.i.d. for 10 days, followed by 30 mg daily for an additional 8 weeks. Patients with documented H pylori infections were randomized to receive placebo or antibiotics for the first 10 days (clarithromycin 500 mg b.i.d. and amoxicillin 1000 mg b.i.d.). Clinical follow-up was performed for 6 months at 2-week intervals, and endoscopy and pH monitoring were again performed at the end of the study. A total of 58 patients completed the trial, and 16 patients were H pylori positive at the study conclusion (14 placebo recipients and 2 eradication failures). Thirteen patients were negative due to successful H pylori eradication and there were 29 controls who completed the study. The H pylori-positive patients relapsed earlier (54 days) than those in whom H pylori had been eradicated (100 days; P = .046). H pylori-negative controls relapsed after the longest interval (110 days). Esophagitis grade also affected relapse. Those with no esophagitis relapsed in 127 days and grade III or IV esophagitis led to relapse after only 18 days. Corrected by esophagitis grade, H pylori-positive patients relapsed earlier than H pylori-negative patients and controls. (P = .001).

Comment by Malcolm Robinson, MD, FACP, FACG

Gastroesophageal reflux is clearly caused by acid contact with esophageal mucosa although the pathophysiology is complex, including motility and acid secretory factors as well as local mucosal defenses. Some previous studies have suggested that H pylori might protect against both GERD and its more severe complications. Eradication of H pylori in duodenal ulcer disease has led to development of GERD in one study although other studies suggest that GERD symptoms might improve after cure of H pylori infection. Issues that could be involved in such divergent outcomes might include differing H pylori strains, their differing intragastric distributions, and the varying severities of accompanying gastritis.

The present study does not allow us to answer the basic question of how H pylori will affect reflux disease that already exists or the triggering of new GERD symptoms or damage by either its presence or its eradication. It is unfortunate that this study was small and that it did not permit subdivision of possible organism virulence and anatomic involvement characteristics. It seems likely that patients who relapsed sooner in conjunction with H pylori infection eradication must have had relative hypersecretion of acid, well known to occur in a subgroup of H pylori infections. Had other patients been included with gastritis and impaired acid secretion resulting from H pylori infections, eradication would have produced the opposite result. Schwizer et al found little gastric atrophy in patients entering or leaving this study. Although Schwizer et al recommend H pylori eradication in patients with GERD, this applies only to the specific patient population and characteristics involved in this study. Other patients probably would demonstrate quite different results, and many experts (including this one) still believe that the only rational approach to H pylori in patients presenting with GERD signs or symptoms should remain, "Don’t ask, don’t tell."