The association between Helicobacter pylori infection and gastroesophageal reflux disease (GERD) remains controversial, with geographical location being a strong contributor to the heterogeneity of results in different studies.1,2 Studies from Western countries have shown an inconsistent association between GERD and H. pylori.3-5 In contrast, a negative association between reflux esophagitis and H. pylori has been shown in most of the studies from East Asia.6-8 A prospective cohort study with large scale in Korea showed that H. pylori infection had a strong negative association with reflux esophagitis and eradication of H. pylori increased the risk of reflux esophagitis.9 However, there are few reports about the relationship between the severity of reflux esophagitis and H. pylori. Presence of H. pylori was associated with reduced severity across the spectrum of GERD, especially in Indians.8
In the current issue of the Journal, Chung et al9 assessed the effect of H. pylori infection on the risk of reflux esophagitis in general population. They found that H. pylori seropositivity reduced the risk of reflux esophagitis (adjusted OR, 0.44; 95% CI, 0.39-0.49) after adjusting for potential confounders. This OR is similar with OR (adjusted OR 0.42; 95% CI, 0.34-0.51) from the previous Korean study.10 Epidemiological evidence for the association between H. pylori infection and reflux esophagitis has been inconsistent, according to the study places.2 In a study from a population-based setting in Northern Europe, H. pylori infection, irrespective of cytotoxin associated gene A (cagA) status, did not affect reflux symptoms.3 However, the results of recent population-based studies performed in Western countries showed an inverse relation between H. pylori seropositivity and reflux esophagitis.4,11 In contrast, the negative association between reflux esophagitis and H. pylori has been shown in most of the studies from East Asia.6-8,10
H. pylori seems to have a protective effect against GERD mainly through the development of atrophic gastritis and thereby decreased gastric acid secretion.6,7 The more virulent type of H. pylori such as cagA-positive strain was postulated to promote the more intense gastric inflammation, exemplifying the risk of atrophy and thereby the further reduction in GERD risk.12,13 However, H. pylori had a negative association with GERD even in atrophy-negative subjects, suggesting that H. pylori might protect GERD not only by atrophy-related low acid production but also by other mechanisms.4 Intragastric urease, which is produced by H. pylori, increases the gastric pH.14 Ammonia, which serves as an acid neutralizer, is one of the products of H. pylori. The development of reflux esophagitis was significantly inhibited by ammonia in a dose-dependent manner in the rat experiments.15 That study indicates that ammonia protects against development of reflux esophagitis. A decreased amount of ammonia in the stomach might be related to the development of reflux esophagitis after H. pylori eradication. Actually, compared with the prevalence of reflux esophagitis in the persistent infection group, the prevalence of reflux esophagitis increased after a successful H. pylori eradication (OR, 2.34; 95% CI, 1.45-3.76; P < 0.001), which was comparable to that of the H. pylori-negative group (OR, 2.42; 95% CI, 1.73-3.36; P < 0.001) in a previous Korean study.10
In the large case-control study from Chung et al,9 H. pylori seropositivity was inversely associated with the severity of reflux esophagitis with adjusted ORs of 0.63 in Los Angeles-M (LA-M), 0.36 in LA-A or B and 0.20 in LA-C or D (P < 0.001). Although there are many evidences about the inverse relationship between reflux esophagitis and H. pylori, there are few reports about the association between severity of GERD and H. pylori. Presence of H. pylori was associated with reduced severity across the spectrum of GERD, especially in Indians, who had the highest H. pylori prevalence among multiethnic Asian populations.8 In a small case-control study, compared with the prevalence of H. pylori infection in the non-reflux group, the prevalence in the mild and severe reflux groups was significantly lower (60.7%, 47.8% and 14.8%, respectively; P < 0.05).7 was significantly lower.7 Barrett's esophagus, which has been considered as an advanced form of GERD, had a strong negative association with H. pylori.4 H. pylori seropositivity was inversely associated with Barrett's esophagus and reflux esophagitis with adjusted ORs (95% CIs) of 0.35 (0.22 to 0.56) and 0.42 (0.27 to 0.65), respectively.4
In conclusion, the study by Chung et al9 has contributed to a better understanding of a protective role of H. pylori against GERD by assessing the inverse relationship between H. pylori and severity of reflux esophagitis.
Footnotes
Financial support: None.
Conflicts of interest: None.
References
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