Cure of Helicobacter pylori infection was associated with reflux esophagitis
ACP J Club. 1998 Jan-Feb;128:19. doi:10.7326/ACPJC-1998-128-1-019
Labenz J, Blum AL, Bayerdörffer E, et al. Curing Helicobacter pylori infection in patients with duodenal ulcer may provoke reflux esophagitis. Gastroenterology. 1997 May;112:1442-7.
To determine whether curing Helicobacter pylori infection in patients with duodenal ulcer increases the risk for reflux esophagitis.
Cohort study with mean follow-up of 17.5 months.
9 clinical centers in Germany.
460 adults ≥ 18 years of age (mean age 52 y, 61% men) who had a history of relapsing or complicated duodenal ulcers and an endoscopy-proven cure. Exclusion criteria were concomitant reflux esophagitis; additional gastric ulcer; malignant conditions of the upper gastrointestinal tract; pretreatment with proton-pump inhibitors, bismuth salts, or antibiotics; pregnancy or lactation; need for treatment with potentially ulcerogenic drugs; and suspected poor compliance. 244 patients had been cured of H. pylori infection, and 216 had not been cured.
Assessment of risk factors
Helicobacter pylori status and gastritis were confirmed by biopsy at annual check-ups. Other risk factors evaluated were age, sex, smoking, regular alcohol intake, heartburn before treatment of H. pylori infection, score for antrum, score for body gastritis, and weight gain ≥ 2 kg after cure.
Main outcome measures
Endoscopy-proven reflux esophagitis was defined as an unequivocal visible break of the mucosal surface and was graded into 4 categories from 1 or 2 linear erosions to complicated esophagitis with ulcer, stricture, or Barrett metaplasia. Endoscopists were blinded to H. pylori status.
Reflux esophagitis was identified in 32 patients who did not have H. pylori infection and in 7 patients who did have H. pylori infection. Life-table analysis was used to calculate the 3-year incidence of reflux esophagitis, which was 26% in patients who were cured of H. pylori infection and 13% in patients who had persistent H. pylori infection (P < 0.001). The groups did not differ for heartburn. In patients with reflux esophagitis, 6 were asymptomatic, 6 had mild heartburn, and 20 had marked heartburn. Risk factors associated with the development of reflux esophagitis were a higher score for body gastritis before H. pylori treatment (odds ratio [OR] 5.5, 95% CI 2.8 to 13.6), weight gain > 2 kg after cure (OR 3.2, CI 1.2 to 9.4), and being a man (OR 3.6, CI 1.1 to 10.6). Development of reflux esophagitis was not associated with heartburn before H. pylori treatment, alcohol drinking, age, smoking, and sum score for antral gastritis (all P > 0.1).
Cure of Helicobacter pylori infection in patients with duodenal ulcers was associated with the development of reflux esophagitis.
Source of funding: Not stated.
For article reprint: Dr. J. Labenz, Elisabeth Hospital, Moltkestrasse 61, D-45138 Essen, Germany. FAX 49-201-897-2249.
This important German study supports smaller reports that have suggested the same effect. We, too, have seen patients with reflux esophagitis after treatment for H. pylori infection. The authors speculate that esophagitis might appear after cure of H. pylori in patients with duodenal ulcer because these patients gain weight, no longer produce ammonia from the H. pylori urease, or have changes in gastroesophageal motility.
If the association between reflux esophagitis and cure of H. pylori is confirmed, how should clinical practice be affected? The benefits of eradicating H. pylori from patients with duodenal ulcer are overwhelming and include far fewer painful episodes and incidences of bleeding (1), but perhaps patients should be warned against celebrating their lack of dyspepsia by overeating. We still do not know whether it is beneficial to eradicate H. pylori, if it is present, from persons without ulcers. Does the same association occur between esophagitis and cure in these patients? If so, it might contribute to the frequent persistence of nonulcer symptoms after cure of H. pylori (2) and may help us to withstand the nearly irresistible pressure to treat.
An apocalyptic suggestion is that the decreasing prevalence of H. pylori might underlie the alarming recent increase in cases of adenocarcinoma of the esophagus in western countries (3). This cancer occurs in patients with metaplastic Barrett mucosa, which is caused by reflux of acid into the lower esophagus. This is interesting but highly speculative and should not impinge on clinical practice, particularly because H. pylori is a well-established risk factor for intestinal cancer (4).
John Calam, MD
Imperial College School of Medicine,Hammersmith HospitalLondon, England, United Kingdom