A perspective on risk factors for esophageal adenocarcinoma: emphasis on Helicobacter pylori infection.

Kountouras, Jannis; Doulberis, Michael; Papaefthymiou, Apostolis; Polyzos, Stergios A; Vardaka, Elizabeth; Tzivras, Dimitri; Dardiotis, Efthimios; Deretzi, Georgia; Giartza-Taxidou, Evaggelia; Grigoriadis, Savas; Katsinelos, Panagiotis (2019). A perspective on risk factors for esophageal adenocarcinoma: emphasis on Helicobacter pylori infection. Annals of the New York Academy of Sciences, 1452(1), pp. 12-17. New York Academy of Sciences 10.1111/nyas.14168

Text Kountouras_et_al-2019-Annals_of_the_New_York_Academy_of_Sciences (1).pdf - Published Version Restricted to registered users only Available under License Publisher holds Copyright. Download (176kB) | Request a copy

Gastroesophageal reflux disease (GERD) and the increasing rate of its associated complications, including esophageal adenocarcinoma (EAC), has stimulated a plethora of studies attempting to evaluate provocative and protective factors. Helicobacter pylori (Hp) infection (Hp-I) was initially considered as a beneficial condition in GERD management based on rather limited data. Large-scale regional studies revealed an alternative approach, by suggesting a positive relationship between Hp-I and EAC development. Regarding pathophysiology, Hp-I induces gastric microbiota disturbances through hypochlorhydria and chronic inflammation, with a subsequent possible effect on the GERD-Barrett's esophagus (BE)-EAC cascade. Additionally, both direct effects on esophageal mucosa and indirect effects on known mechanisms of GERD, such as acid pocket and transient lower esophageal sphincter relaxation, remain to be elucidated. Hp contribution to carcinogenesis is related to oncogenic gastrin, cyclooxygenase-2, and prostaglandins; Ki-67 is also expressed and represents an index of BE-related malignancy. Moreover, Hp-I is vigorously suggested as a risk factor for metabolic syndrome, which may be the link between Hp-I and EAC. Although further studies are necessary to establish a pathophysiologic risk between Hp-I and the GERD-BE-EAC sequence, the theory of Hp protection against GERD seems outdated.

Interest & Impact

Downloads

2 since deposited on 26 Aug 2019
0 in the past 12 months

Citations

5 Citations in Web of Science ®
6 Citations in Scopus

Search

in Google Scholar™

Services

Actions (login required)

Edit item

Actions (login required)

Edit item