Minireviews
Copyright ©The Author(s) 2018. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jun 14, 2018; 24(22): 2373-2380
Published online Jun 14, 2018. doi: 10.3748/wjg.v24.i22.2373
Treatment of Helicobacter pylori infection in atrophic gastritis
Edith Lahner, Marilia Carabotti, Bruno Annibale
Edith Lahner, Marilia Carabotti, Bruno Annibale, Medical-Surgical Department of Clinical Sciences and Translational Medicine, Sant’Andrea Hospital, University Sapienza, Rome 00189, Italy
Author contributions: Lahner E designed the review and wrote the paper; Carabotti M performed the literature search and revised the paper; Annibale B supervised and approved the final version of the review.
Conflict-of-interest statement: The authors declare no potential conflicts of interest.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Bruno Annibale, MD, PhD, Full Professor, Medical-Surgical Department of Clinical Sciences and Translational Medicine, Sapienza University of Rome, Via Grottarossa 1035, Rome 00189, Italy.bruno.annibale@uniroma1.it
Telephone: +39-6-33775289 Fax: +39-6-33776006
Received: April 12, 2018
Peer-review started: April 13, 2018
First decision: April 27, 2018
Revised: May 16, 2018
Accepted: May 26, 2018
Article in press: May 28, 2018
Published online: June 14, 2018
Processing time: 59 Days and 16.8 Hours
Core Tip

Core tip: Atrophic gastritis (AG) may arise from long-standing Helicobacter pylori (Hp) infection and is linked to increased gastric cancer risk. According to guidelines, Hp-positive AG patients should receive eradication treatment. The goals of treatment are as follows: (1) Cure of infection, (2) possible reversal of atrophic/metaplastic changes, and (3) prevention of gastric cancer. When involving the corporal mucosa, AG is linked to reduced acid secretion. At a non-acidic intra-gastric pH, the efficacy of common treatment regimens may not be the same as those observed in an acid-producing stomach. There is a paucity of evidence of efficacy of eradication regimens in AG patients. Bismuth-based therapies may be promising.