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

Jannis Kountouras, Christos Zavos, Stergios A. Polyzos, Panagiotis Katsinelos

Aristotle University of Thessaloniki, Ippokration Hospital, Thessaloniki, Macedonia, Greece

Department of Medicine, Second Medical Clinic, Aristotle University of Thessaloniki, Ippokration Hospital, Thessaloniki, Macedonia, Greece
Correspondence to: Jannis Kountouras, MD, PhD, Professor of Medicine, 8 Fanariou St, Byzantio, 551 33, Thessaloniki, Macedonia, Greece, Tel.: +30 2310 892238, Fax: +30 2310 992794, e-mail: jannis@auth.gr
Received 11 September 2014; accepted 22 September 2014

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].


1.  Zullo A, Hassan C, De Francesco V, Manta R, Romiti A, Gatta L. Helicobacter pylori infection and gastroesophageal cancer:unveiling a Hamletic dilemma. Ann Gastroenterol 2014;27:291-293.

2.  Kountouras J, Chatzopoulos D, Zavos C, et al. Helicobacter pylori infection might contribute to esophageal adenocarcinoma progress in subpopulations with gastroesophageal reflux disease and Barrett's esophagus. Helicobacter 2012;17: 402-403.

3.  Kountouras J, Stergiopoulos C, Zavos C. Obstructive sleep apnea and environmental contributors for Barrett's Esophagus. Clin Gastroenterol Hepatol 2014;12: 1055-1056.

4.  Kountouras J, Zavos C, Chatzopoulos D, Katsinelos P. Helicobacter pylori and gastro-oesophageal reflux disease.Lancet 2006;368:986.

5.  Kountouras J, Chatzopoulos D, Zavos C%. Eradication of Helicobacter pylori% might halt the progress to oesophageal adenocarcinoma in patients with gastro-oesophageal reflux disease and Barrett's oesophagus. Med Hypotheses 2007;68: 1174-1175.

6.  Kyrgidis A, Kountouras J, Zavos C, Chatzopoulos D. New molecular concepts of Barrett's esophagus:clinical implications and biomarkers. J Surg Res 2005;125: 189-212.

7.  Kountouras J, Zavos C, Chatzopoulos D, Katsinelos P. New aspects of Helicobacter pylori infection involvement in gastric oncogenesis. J Surg Res 2008;146: 149-158.

8.  Kountouras J, Zavos C, Chatzopoulos D, et al. Letter:is Helicobacter pylori behind Barrett's oesophagus and colorectal neoplasms? Aliment Pharmacol Ther 2013;37:837.

9.  Kapetanakis N, Kountouras J, Zavos C, et al. Association of Helicobacter pylori infection with colorectal cancer. Immunogastroenterology 2013;2: 47-56.

10.  Kountouras J, Kapetanakis N, Zavos C, Polyzos SA, Romiopoulos I. Active Helicobacter pylori infection on colorectal mucosa-adenomatous polyp-adenocarcinoma sequence. Eur J Gastroenterol Hepatol 2014;26: 243-244.


Conflict of Interest: None