Update in Molecular Aspects and Diagnosis of Autoimmune Gastritis

Abstract

Recent studies have advanced our understanding of the pathophysiology of autoimmune gastritis, particularly its molecular aspects. The most noteworthy recent advancement lies in the identification of several candidate genes implicated in the pathogenesis of pernicious anemia through genome-wide association studies. These genes include PTPN22, PNPT1, HLA-DQB1, and IL2RA. Recent studies have also directed attention towards other genes such as ATP4A, ATP4B, AIRE, SLC26A7, SLC26A9, and BACH2 polymorphism. In-depth investigations have been conducted on lymphocytes and cytokines, including T helper 17 cells, interleukin (IL)-17A, IL-17E, IL-17F, IL-21, IL-19, tumor necrosis factor-α, IL-15, transforming growth factor-β1, IL-13, and diminished levels of IL-27. Animal studies have explored the involvement of roseolovirus and H. pylori in relation to the onset of the disease and the process of carcinogenesis, respectively. Recent studies have comprehensively examined the involvement of autoantibodies, serum pepsinogen, and esophagogastroduodenoscopy in the diagnosis of autoimmune gastritis. The current focus lies on individuals demonstrating atypical presentations of the disease, including those diagnosed in childhood, those yielding negative results for autoantibodies, and those lacking the typical endoscopic characteristics of mucosal atrophy. Here, we discuss the recent developments in this field, focusing on genetic predisposition, epigenetic modifications, lymphocytes, cytokines, oxidative stress, infectious agents, proteins, microRNAs, autoantibodies, serum pepsinogen, gastrin, esophagogastroduodenoscopy and microscopic findings, and the risk of gastric neoplasm.

Autoimmune Atrophic Gastritis: A Clinical Review

“…H. pylori-positive patients with corpus atrophic gastritis seem to have high levels of anti-parietal cell antibodies, which decrease significantly after H. pylori eradication. The destruction of parietal cells by H. pylori-related inflammation may lead to the exposure of molecular patterns of the ATPase pump H+/K+ and consequently the production of anti-parietal cell antibodies as a consequence of a cross reaction between molecular antigens of the bacterium and molecular patterns of the ATPase pump H+/K+; this is more likely to occur in genetically predisposed subjects with specific MHC class II haplotypes [16] (Table 1). Two recent case reports showed that H. pylori-related gastritis ultimately transitioned into AAG; furthermore, they showed that the progression of AAG caused a spontaneous disappearance of H. pylori infection as a consequence of the worsening of the gastric atrophy [17].…”

“…Iwamuro M, Curr Issues Mol Biol 2023 [16] Helicobacter pylori may play a role in the induction/exacerbation of AAG.…”

Differential Diagnoses and Management Approaches for Gastric Polyposis

“…Autoimmune gastritis is a persistent inflammation of the stomach arising from the autoimmune system's erroneous targeting and subsequent destruction of gastric parietal cells, resulting in reduced gastric acid secretion and vitamin B12 deficiency [54][55][56]. Reduced gastric acid production leads to elevated levels of gastrin.…”

A Comprehensive Review of Upper Gastrointestinal Symptom Management in Autoimmune Gastritis: Current Insights and Future Directions

“…This immune-mediated process is driven by the production of autoantibodies against the H+/K+-ATPase (proton pump) and intrinsic factor, leading to the malabsorption of vitamin B12 and causing pernicious anemia. Over time, the progressive loss of gastric acid-producing cells results in a hypo-or achlorhydric environment within the stomach [1][2][3].…”