Helicobacter pylori infection and gastroesophageal reflux disease - Barrett’s esophagus sequence “dilemma”

Regarding Zullo et al’s Hamletic dilemma [1], the authors claimed that the reasons why Helicobacter pylori (Hp) does not prevent gastroesophageal reflux disease (GERD) symptoms, though appears to prevent Barrett’s esophagus (BE), remain unclear.

Concerning this conflicting scenario, upper gastrointestinal microbiota appear to be involved in GERD and BE pathophysiology; the occurrence of nitrate-reducing Campylobacter species in the esophagus of BE patients compared with controls without BE, may imply that there is a link with BE initiation, maintenance, or exacerbation [2,3]. Hp infection (Hp-I) may also be involved in GERD pathogenesis, at least in some ethnic populations, thereby predisposing for BE development, a long-standing GERD complication and well-recognized premalignant condition involved in gastroesophageal junction cancer, also mentioned by the authors [1], and esophageal adenocarcinoma development [2]. In this respect, contrary to expectations, ethnic Malays who have a long history of low Hp-I prevalence, GERD, BE and distal esophageal cancers are all of low incidence, suggesting that Hp-I is not protective against the aforementioned diseases; its absence is more likely to be beneficial [3]. Our data show that Hp-I is frequent in Greek GERD patients and its eradication leads to better control of GERD symptoms [4,5]; consistent associations are also reported by others [4]. The interplay between Hp and host factors holds an important role in GERD and BE pathogenesis; Hp could contribute to GERD and BE pathogenesis via several mechanisms including induction of several mediators, oncogenes and metabolic parameters (i.e., obesity, insulin resistance) mentioned previously [2-4]; for instance, Hp-induced gastrin is an oncogenic growth factor contributing to esophageal, gastric, and colon carcinogenesis [6,7]. Recent data indicate that both Hp-I and BE are associated with an increased risk of colorectal adenoma (CRA) and colorectal cancer (CRC) development, reflecting real relationship [8-10]; Hp-I seems to be involved in GERD-BE-EA and CRA-CRC sequences, at least in some subpopulations, and its eradication might inhibit these oncogenic properties [8-10].