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A perspective on risk factors for esophageal adenocarcinoma: emphasis on Helicobacter pylori infection
Author(s) -
Kountouras Jannis,
Doulberis Michael,
Papaefthymiou Apostolis,
Polyzos Stergios A.,
Vardaka Elizabeth,
Tzivras Dimitri,
Dardiotis Efthimios,
Deretzi Georgia,
GiartzaTaxidou Evaggelia,
Grigoriadis Savas,
Katsinelos Panagiotis
Publication year - 2019
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/nyas.14168
Subject(s) - gerd , gastroenterology , medicine , helicobacter pylori , atrophic gastritis , barrett's esophagus , malignancy , pathophysiology , esophagus , gastrin , risk factor , disease , adenocarcinoma , gastritis , reflux , cancer , secretion
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a pathophysiologic risk between Hp‐ I and the GERD−BE−EAC sequence, the theory of Hp protection against GERD seems outdated.