Published online Jun 14, 2018. doi: 10.3748/wjg.v24.i22.2373
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
Helicobacter pylori (Hp) is a major human pathogen causing chronic, progressive gastric mucosal damage and is linked to gastric atrophy and cancer. Hp-positive individuals constitute the major reservoir for transmission of infection. There is no ideal treatment for Hp. Hp infection is not cured by a single antibiotic, and sometimes, a combined treatment with three or more antibiotics is ineffective. Atrophic gastritis (AG) is a chronic disease whose main features are atrophy and/or intestinal metaplasia of the gastric glands, which arise from long-standing Hp infection. AG is reportedly linked to an increased risk for gastric cancer, particularly when extensive intestinal metaplasia is present. Active or past Hp infection may be detected by conventional methods in about two-thirds of AG patients. By immunoblotting of sera against Hp whole-cell protein lysates, a previous exposure to Hp infection is detected in all AG patients. According to guidelines, AG patients with Hp positivity should receive eradication treatment. The goals of treatment are as follows: (1) Cure of infection, resolution of inflammation and normalization of gastric functions; (2) possible reversal of atrophic and metaplastic changes of the gastric mucosa; and (3) prevention of gastric cancer. An ideal antibiotic regimen for Hp should achieve eradication rates of approximately 90%, and complex multidrug regimens are required to reach this goal. Amongst the factors associated with treatment failure are high bacterial load, high gastric acidity, Hp strain, smoking, low compliance, overweight, and increasing antibiotic resistance. AG, when involving the corporal mucosa, is linked to reduced gastric acid secretion. At a non-acidic intra-gastric pH, the efficacy of the common treatment regimens combining proton pump inhibitors with one or more antibiotics may not be the same as that observed in patients with Hp gastritis in an acid-producing stomach. Although the efficacy of these therapeutic regimens has been thoroughly tested in subjects with Hp infection, there is a paucity of evidence in the subgroup of patients with AG. Bismuth-based therapy may be an attractive treatment in the specific setting of AG, and specific studies on the efficacy of bismuth-based therapies are needed in patients with AG.
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.