Ulcers and gastritis

Association of autoimmune type atrophic corpus gastritis with Helicobacter pylori infection (Veijola et al., World J Gastroenterol 2010 [1])

It is increasingly recognized that parietal cell antibodies (PCA), previously assumed to be exclusive to autoimmune gastritis, are associated with Helicobacter pylori infection. Veijola et al. reported association of autoimmune-type atrophic corpus gastritis with H. pylori infection [1]. In the study they investigated the signs of previous H. pylori infection in patients with different grades of atrophic gastritis in order to assess the proportion of gastric atrophy not associated with H. pylori infection. In total, 23 patients with different grades of atrophic gastritis were analyzed using enzyme immunoassay-based serology, immunoblot-based serology, and histology to reveal a past or a present H. pylori infection. In addition, serum markers for gastric atrophy (pepsinogen I, pepsinogen I/II, and gastrin) and autoimmunity (PCA and intrinsic factor, antibodies) were determined. Of the 14 patients with severe gastric atrophy, as demonstrated by histology and serum markers, and no evidence for an ongoing H. pylori infection, eight showed H. pylori antibodies by immunoblotting. All eight had elevated PCA, four of whom also had intrinsic factor antibodies. Of the six immunoblot-negative patients with severe corpus atrophy, PCA and intrinsic factor antibodies were detected in four patients. Among the patients with low-to-moderate grade atrophic gastritis (all except one with an ongoing H. pylori infection), serum markers for gastric atrophy and autoimmunity were seldom detected. However, only one H. pylori-negative patient with mild atrophic gastritis had PCA and intrinsic factor antibodies suggestive of a pre-atrophic autoimmune gastritis. They concluded that atrophic corpus gastritis, including autoimmune-type severe atrophy with vitamin B₁₂-malabsorption, is associated with a long-standing H. pylori infection in most cases.

Interestingly, vitamin B₁₂ deficiency, previously associated with autoimmune gastritis, is increasingly described in the elderly, irrespective of H. pylori status. It is difficult to evaluate the role played by genetics, increased use of proton pump inhibitors (PPIs), and H. pylori infection, as current patient work-up does not regularly include screening for PCA and intrinsic factor antibodies. Long-standing H. pylori infection probably plays a role in many patients with pernicious anemia, in whom the active infectious process has been gradually replaced by an autoimmune disease that terminates in a burned-out infection and the irreversible destruction of the gastric body mucosa. In patients with H. pylori infection, superficial gastritis proceeds to atrophic gastritis in about half of the patients. In some patients, antral intestinal metaplasia disappears and PCA appears; thus, the disease resembles classic autoimmune gastritis [2]. Gastric H+/K+-ATPase is also the major autoantigen in chronic H. pylori-induced atrophic gastritis in corpus mucosa [3]. If the classic autoimmune type gastric atrophy is an end-stage of H. pylori-induced gastric autoimmunity with atrophic gastritis, the prevalence of pernicious anemia should decrease with declining prevalence of H. pylori infection. It still remains to be shown whether H. pylori infection is crucial for the development of autoimmune-type atrophic gastritis.

References

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