Here, we ascertained the clinical characteristics of Chinese patients with autoimmune gastritis (AIG) and determined the correlation of dietary and lifestyle factors with AIG occurrence and development to establish a noninvasive predictive model for AIG.

In this case-control study, we enrolled 479 patients from seven independent centers nationwide in China; of them, 279 had AIG, 112 had chronic atrophic gastritis mostly in the antrum, and 88 had chronic nonatrophic gastritis. Their clinical and lifestyle data were systematically collected and analyzed. Finally, a multivariate logistic regression disease prediction model was then established and validated.

Most of the 279 patients with AIG were middle-aged, older, and female. In the predictive model of AIG, the larger amount of cooking oil used per meal and comorbid autoimmune thyroid disease was considered risk factors, and a diet rich in vitamin B12 was considered a protective factor. We plotted a receiver operating characteristic (ROC) curve of the model in the discovery and validation cohorts, and the areas under the ROC curves were 0.72 and 0.74, respectively. In addition, dietary structure, eating habits, sleep quality, and smoking status were noted to be correlated with the occurrence of gastrointestinal symptoms and complications, as well as histopathological grades of AIG.

Dietary and lifestyle factors may predict AIG risk in Chinese populations and were related to AIG prognosis.

Immune checkpoint inhibitors (ICIs) are crucial in cancer treatment, and the associated immune-related adverse events (irAEs) have garnered significant attention, yet reports on associated immune related gastritis are limited. The diagnosis of immune related gastritis remains predominantly exclusionary, meanwhile its management diverges significantly from that of conventional gastritis. Current guidelines lack standardized grading criteria, and substantial data from large-scale, tertiary clinical studies are absent, therefore we conducted a systematic review of Medline, Web of Science, and Embase databases, identifying 31 articles from 2017 to December 31, 2023, involving 258 patients. Clinical manifestations included epigastric pain (53.1%), mucosal erythema (56.1%), and lymphocyte infiltration (48.6%). Corticosteroid therapy was common (94.7%), with 86.7% experiencing post-treatment improvement. 80% of patients can be diagnosed through endoscopy and pathology, while the remaining 20% may require PET-CT. Hormonal therapy is favored but diverges from standard management. Accurate diagnosis is crucial in managing immune related gastritis effectively.

Architectural distortion and basal plasmacytosis are the most widely recognized histologic features of chronic ileal inflammation. However, these features might be difficult to assess in small, poorly oriented, or superficial biopsies. Additional features of chronic mucosal damage, including pseudopyloric or pseudofoveolar metaplasia and Paneth cell hyperplasia, have been less commonly reported, and their broader appreciation could facilitate the diagnosis of chronic ileal inflammatory conditions. The prevalence of gastric-like (pseudopyloric and pseudofoveolar) metaplasia and Paneth cell hyperplasia was evaluated in 102 ileal biopsies obtained from patients with Crohn's disease (n = 47), ulcerative colitis with endoscopically normal ileum (n = 20) or with backwash ileitis (n = 20), and nonsteroidal anti-inflammatory drugs- (NSAIDs-) induced ileitis (n = 15). Gastric-like metaplasia was identified in 23% of CD and 13% of NSAID-induced ileitis cases, whereas it was absent among all ulcerative colitis cases. Pseudopyloric metaplasia, pseudofoveolar metaplasia, or a combination of both was documented in 13%, 2%, and 9% of Crohn's disease cases, respectively. NSAID-associated cases showed only pseudopyloric metaplasia. Paneth cell hyperplasia was detected in 43% of Crohn's disease cases, 13% of NSAID-induced ileitis cases, and 5% of backwash ileitis cases. Accordingly, pseudofoveolar metaplasia, pseudopyloric metaplasia, and Paneth cell hyperplasia are not uncommon in conditions causing chronic ileal inflammation. They are most frequently detected in Crohn's disease, but may also be present in NSAID-induced ileitis, whereas they are significantly less common in backwash ileitis and absent in normal ileum. Given the surface localization of pseudofoveolar metaplasia, its identification can be particularly helpful when dealing with poorly oriented or superficial samples.

At the end of the last century, a far-sighted 'working party' held in Sydney, Australia addressed the clinicopathological issues related to gastric inflammatory diseases. A few years later, an international conference held in Houston, Texas, USA critically updated the seminal Sydney classification. In line with these initiatives, Kyoto Global Consensus Report, flanked by the Maastricht-Florence conferences, added new clinical evidence to the gastritis clinicopathological puzzle.The most relevant topics related to the gastric inflammatory diseases have been addressed by the Real-world Gastritis Initiative (RE.GA.IN.), from disease definitions to the clinical diagnosis and prognosis. This paper reports the conclusions of the RE.GA.IN. consensus process, which culminated in Venice in November 2022 after more than 8 months of intense global scientific deliberations. A forum of gastritis scholars from five continents participated in the multidisciplinary RE.GA.IN. consensus. After lively debates on the most controversial aspects of the gastritis spectrum, the RE.GA.IN. Faculty amalgamated complementary knowledge to distil patient-centred, evidence-based statements to assist health professionals in their real-world clinical practice. The sections of this report focus on: the epidemiology of gastritis; Helicobacter pylori as dominant aetiology of environmental gastritis and as the most important determinant of the gastric oncogenetic field; the evolving knowledge on gastric autoimmunity; the clinicopathological relevance of gastric microbiota; the new diagnostic horizons of endoscopy; and the clinical priority of histologically reporting gastritis in terms of staging. The ultimate goal of RE.GA.IN. was and remains the promotion of further improvement in the clinical management of patients with gastritis.

In the setting of pronounced inflammation, changes in the epithelium may overlap with neoplasia, often rendering it impossible to establish a diagnosis with certainty in daily clinical practice. Here, we discuss the underlying molecular mechanisms driving tissue response during persistent inflammatory signaling along with the potential association with cancer in the gastrointestinal tract, pancreas, extrahepatic bile ducts, and liver. We highlight the histopathological challenges encountered in the diagnosis of chronic inflammation in routine practice and pinpoint tissue-based biomarkers that could complement morphology to differentiate reactive from dysplastic or cancerous lesions. We refer to the advantages and limitations of existing biomarkers employing immunohistochemistry and point to promising new markers, including the generation of novel antibodies targeting mutant proteins, miRNAs, and array assays. Advancements in experimental models, including mouse and 3D models, have improved our understanding of tissue response. The integration of digital pathology along with artificial intelligence may also complement routine visual inspections. Navigating through tissue responses in various chronic inflammatory contexts will help us develop novel and reliable biomarkers that will improve diagnostic decisions and ultimately patient treatment.

Vitamin D (VD) deficiency can result from insufficiency of either light exposure or VD intake. We investigated the biological effects of VD deficiency for 7 months on the mouse gastric glands. Varying degrees of VD deficiency were induced in C57BL/6 mice by keeping them on standard diet with constant-dark conditions (SDD) or VD deficient diet with constant-dark conditions (VDD). Samples of serum, glandular stomach, and gastric contents were collected for LCMS/MS, RT-PCR, immunohistochemistry, and acid content measurements. Both SDD and VDD mice had a significant decline in 25OHVD metabolite, gastric epithelial cell proliferation, and mucin 6 gene expression. These effects were enhanced with the severity of VD deficiency from SDD to VDD. Besides and compared to the control group, SDD mice only displayed a significant increase in the number of zymogenic cells (p ≤ 0.0001) and high expression of the adiponectin (p ≤ 0.05), gastrin (p ≤ 0.0001), mucin 5AC (*** p ≤ 0.001) and the Cyclin-dependent kinase inhibitor 1A (**** p ≤ 0.0001). These phenotypes were unique to SDD gastric samples and not seen in the VDD or control groups. This study suggests that the body reacts differently to diverse VD deficiency sources, light or diet.

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.

We report a case of autoimmune gastritis (AIG) in which gastric mucosal atrophy improved with Helicobacter pylori eradication. Based on endoscopic findings (advanced gastric atrophy with vascular visibility and diffuse redness in remnant oxyntic mucosa), a woman in her 40s was suspected of having AIG coexisting with an active H. pylori infection. This was confirmed by a positive anti-parietal cell antibody (PCA, 1:160), an elevated serum gastrin level (638 pg/mL), and positive anti-H. pylori antibody (Hp Ab, 15.5 U/mL) and H. pylori stool antigen tests. Seven months after eradication, reduced vascular visibility and disappearance of diffuse redness on endoscopy and reduced PCA (1:40) and Hp Ab (5.1 U/mL) titers were observed, although histopathological findings (basal-predominant lymphocytic infiltration, destruction of parietal and chief cells, pseudopyloric metaplasia, and enterochromaffin-like cell hyperplasia) were consistent with AIG. Endoscopy 26 months after eradication showed further improvement in atrophic findings in the gastric corpus and histopathological recovery of parietal and chief cells in fundic glands. Serum gastrin levels returned to normal (64 pg/mL), and the PCA titer fell further (1:20).

This study is aimed toward investigating the evolution of each Correa's step after Helicobacter pylori eradication in a long-term follow-up and exploring the factors correlated with a high-risk of gastric cancer.

A total of 1824 H. pylori-infected subjects were enrolled to receive screening endoscopy. Among them, 491 received surveillance endoscopy. The patients were divided into Correa's steps I to VI, from normal to gastric cancer. A group-based trajectory model was used to classify patients as persistent high-risk status or not.

The prevalence rates of positive corpus-predominant gastritis index (CGI) were 20%-40% in all age groups and Correa's steps IV-V increased >35% after 50 years based on screening endoscopy. Successful eradication of H. pylori regressed CGI after the 1st year-and-thereafter (P < 0.05) and decreased Correa's step progression (Relative risk 0.66 [95% CI 0.49-0.89], P = 0.01); however, it did not regress OLGA and OLGIM. Not only in steps IV-V, but also in step III, the patients had a risk of developing gastric cancer (11.13-76.41 and 4.61 per 1000 person-years). Age (Hazard ratio 1.012 [1.003-1.020], P = 0.01), OLGA stages ≥ I (2.127 [1.558-2.903], P < 0.001), and OLGIM stages ≥ I (1.409 [1.119-1.774], P = 0.004) were correlated independently with a persistent high-risk status.

The patients in Correa's steps III-V, but not I-II, were at risk of gastric cancer after H. pylori eradication. Age, OLGA stages ≥ I, and OLGIM stages ≥ I were independent factors correlated to a persistent high-risk of gastric cancer. The data may be useful when scheduling surveillance endoscopy for subjects in each Correa's step (NCT04527055).

This report describes a patient with early-stage autoimmune gastritis (AIG) presenting with a normal endoscopic appearance. A 66-year-old man with autoimmune thyroiditis was suspected of having AIG because of a previous history of vitamin B12 deficiency when receiving steroid therapy for interstitial pneumonia 5 years earlier. At presentation, he tested positive for anti-parietal cell antibody (1:320) and anti-intrinsic factor antibody, but not for vitamin B12 deficiency. His gastrin level was elevated (338 pg/mL), but his pepsinogen (PG) I level (56.1 ng/mL) and PGI/PGII ratio (7.6) were normal. Endoscopically, neither atrophic nor inflammatory changes were observed. Histopathologic examination, however, showed mild atrophic changes with dense lymphocytic infiltration in the deep lamina propria and focal destruction of parietal cells in the greater curvature of the corpus. PGI-positive/MUC6-positive pseudo-pyloric metaplasia was observed in the area from which H+/K+-ATPase-positive parietal cells had disappeared. Chromogranin A immunostaining showed linear hyperplasia of enterochromaffin-like cells. By contrast, atrophic changes were not evident in the lesser curvature of the corpus, except for mild lymphocytic infiltration around and into the fundic glands. These serological and histopathological findings suggested that the patient had early-stage AIG with a normal endoscopic appearance.

A 60-year-old woman presented with a protruding tumor at the anterior wall of the middle gastric body, and she was positive for anti-parietal cells antibodies with elevated serum gastrin level. Final diagnosis was a mixed neuroendocrine-non-neuroendocrine neoplasm consisting of adenocarcinoma (tub1) and neuroendocrine tumor G2 with autoimmune gastritis.

The most common histological type of gastric cancer (GC) is gastric adenocarcinoma arising from the gastric epithelium. Less common variants include mesenchymal, lymphoproliferative and neuroendocrine neoplasms. The Lauren scheme classifies GC into intestinal type, diffuse type and mixed type. The WHO classification includes papillary, tubular, mucinous, poorly cohesive and mixed GC. Chronic atrophic gastritis (CAG) and intestinal metaplasia are recommended as common precancerous conditions. No definite precancerous condition of diffuse/poorly/undifferentiated type is recommended. Chronic superficial inflammation and hyperplasia of foveolar cells may be the focus. Presently, the management of early GC and precancerous conditions mainly relies on endoscopy including diagnosis, treatment and surveillance. Management of precancerous conditions promotes the early detection and treatment of early GC, and even prevent the occurrence of GC. In the review, precancerous conditions including CAG, metaplasia, foveolar hyperplasia and gastric hyperplastic polyps derived from the gastric epithelium have been concluded, based on the overview of gastric epithelial histological organization and its renewal.

This article summarizes and systematizes the available data from the literature on chronic autoimmune gastritis (CAG) in order to increase the awareness of specialists about the modern possibilities for diagnosing the disease, including its early stages. The clinical manifestation of the disease includes possible variants such as gastrointestinal, hematological (first of all, the formation of iron deficiency and B12-deficiency anemia), and neurological variants. Patients with chronic autoimmune gastritis are characterized by comorbidity with other autoimmune diseases. In this paper, data on the most informative serological markers for the diagnosis of CAG, as well as laboratory tests to detect micronutrient deficiencies, information on the characteristic changes in the gastric mucosa, and the prognosis of the disease, are presented. The diagnosis of CAG should be based on a multidisciplinary approach that combines a thorough analysis of a patient's complaints with a mandatory assessment of nutritional status, as well as the results of serological, endoscopic, and histological research methods.