This protocol addresses autoimmune metaplastic atrophic gastritis (AMAG) in patients with concurrent Helicobacter pylori infection — a recognised trigger of the autoimmune process affecting the gastric lining.
H. pylori infection has been shown to induce an autoimmune process in the gastric lining, including the oxyntic mucosa. Addressing the bacterial infection is therefore a key consideration in the management of early-stage AMAG in this setting.
The primary clinical objective is reduction of the autoimmune antibody burden associated with AMAG. Achieving bacterial eradication has been linked to a measurable decrease in these antibody levels.
DOI: 10.14309/ajg.0000000000002968
Several studies have been confirmed that H. pylori infection can induce autoimmune process in the gastric lining including oxyntic mucosa, eradication of H. pylori can decrease the levels of antibodies associated with AMAG and has been proven effective to cure early stages of autoimmune gastritis.
View source ↗