Autoimmune atrophic gastritis is an immune-mediated disease resulting in autoimmune destruction of the specialized acid-producing gastric parietal cells. As a consequence, in autoimmune atrophic gastritis, gastric acid secretion is irreversibly impaired, and the resulting hypochlorhydria leads to the main clinical manifestations and is linked, directly or indirectly, to the long-term neoplastic complications of this disease. In the last few years, autoimmune atrophic gastritis has gained growing interest leading to the acquisition of new knowledge on different aspects of this disorder. Although reliable serological biomarkers are available and gastrointestinal endoscopy techniques have substantially evolved, the diagnosis of autoimmune atrophic gastritis is still affected by a considerable delay and relies on histopathological assessment of gastric biopsies. One of the reasons for the diagnostic delay is that the clinical presentations of autoimmune atrophic gastritis giving rise to clinical suspicion are very different, ranging from hematological to neurological–psychiatric up to gastrointestinal and less commonly to gynecological–obstetric symptoms or signs. Therefore, patients with autoimmune atrophic gastritis often seek advice from physicians of other medical specialties than gastroenterologists, thus underlining the need for increased awareness of this disease in a broad medical and scientific community. 

Autoimmune Gastritis and Hypochlorhydria: Known Concepts from a New Perspective

Frequency of use of the revised Cochrane Risk of Bias tool (<scp>RoB</scp> 2) in Cochrane and non‐Cochrane systematic reviews published in 2023 and 2024

Overly complex methods may impair pragmatic use of core evidence-based medicine principles.

Autoimmune atrophic gastritis (AAG) is a non-self-limiting immune-mediated disorder exerting growing interest. The main autoantigen, the beta subunit of the proton pump (H+, K+-ATPase), is localised on the oxyntic mucosa parietal cells, limiting the autoimmune inflammatory damage to this stomach compartment. Clinical manifestations of AAG may occur late, once corpus-fundus atrophy occurs, and are characterised by loss of gastric acidity, impaired iron and/or cobalamin malabsorption, and increased risk of gastric type 1 neuroendocrine neoplasms and possibly gastric adenocarcinoma. Many topics regarding epidemiology, clinical features, pathogenesis, diagnosis, and management remain to be clarified. AAG patients are frequently misdiagnosed or diagnosed with delay. AAG still represents a clinical challenge and a great opportunity for advancing our knowledge on gastrointestinal autoimmune diseases and gastric precancerous conditions. The timely and correct diagnosis of AAG patients is clinically relevant to avoid potentially harmful consequences due to micronutrient deficiencies and related anaemia and neoplastic complications. The current position paper addresses AAG in adults and reflects the views of the Autoimmune gastRitis Italian netwOrk Study grOup (ARIOSO) on its epidemiology, clinical features, pathogenesis, diagnosis, and management. Improving the understanding of AAG would facilitate timely and accurate diagnosis, enhance clinical management and patients' quality of life, and reduce the economic and social burden of this underrecognized condition.

Autoimmune gastritis: Diagnosis, clinical management and natural history. A position paper by the Autoimmune gastRitis Italian netwOrk Study grOup (ARIOSO)

Autoimmune gastritis (AIG) is a chronic, organ-specific autoimmune disease characterized by progressive destruction of gastric parietal cells driven by autoreactive CD4+ T-cells, epithelial stress pathways, and microbial factors. Parietal cell loss results in achlorhydria, intrinsic factor deficiency, and vitamin B12 malabsorption, ultimately leading to pernicious anemia. Compensatory hypergastrinemia promotes enterochromaffin-like (ECL) cell hyperplasia and contributes to the development of type 1 gastric neuroendocrine neoplasms (gNENs). These clinical consequences are well recognized, yet the cellular and molecular mechanisms driving mucosal atrophy and neoplastic transformation remain incompletely defined. Recent advances highlight the role of endoplasmic reticulum stress, impaired autophagy, innate immune effectors, and dysbiosis in perpetuating inflammation and epithelial injury. The frequent coexistence of AIG with other autoimmune disorders further adds to its clinical complexity. Therapeutic options remain limited, spanning vitamin B12 replacement and endoscopic management to emerging targeted approaches. Netazepide, a gastrin/CCK2 receptor antagonist, is the only agent tested in clinical trials, whereas interventions targeting ER stress, autophagy, immune tolerance, or microbiome composition are still in the preclinical stage. Clarifying these mechanisms is crucial to improve biomarker development, optimize surveillance, and identify targeted therapies to prevent neoplastic transformation. 

The Autoimmune Gastritis Puzzle: Emerging Cellular Crosstalk and Molecular Pathways Driving Parietal Cell Loss and ECL Cell Hyperplasia

Autoimmune atrophic gastritis (AAG) is a chronic condition characterized by the presence of atrophy in the oxyntic mucosa due to anti-parietal cell antibodies. This review provides a comprehensive and up-to-date overview of autoimmune atrophic gastritis, reporting recent evidence on epidemiology, pathogenesis, diagnosis, clinical presentation, risk of malignancies, and management. The prevalence of AAG has been estimated at between 0.3% and 2.7% in the general population. The diagnosis of AAG is based on a combination of the serologic profile and the histological examination of gastric biopsies. Patients with AAG are often asymptomatic but can also have dyspeptic or reflux symptoms. The atrophy of the oxyntic mucosa leads to iron and vitamin B12 malabsorption, which may result in anemia and neurological affections. Autoimmune atrophic gastritis is associated with an increased risk of type I neuroendocrine tumors (NETs) and gastric cancer, with an incidence rate of 2.8% and 0.5% per person/year, respectively. Management is directed to reinstate vitamins and iron and to prevent malignancies with endoscopic surveillance. In conclusion, atrophic autoimmune gastritis is an infrequent condition, often asymptomatic and misdiagnosed, that requires an early diagnosis for appropriate vitamin supplementation and endoscopic follow-up for the early diagnosis of NETs and gastric cancer.

Autoimmune Atrophic Gastritis: A Clinical Review

Risk of bias (RoB) assessment is essential to the systematic review methodology. The new version of the Cochrane RoB tool for randomized trials (RoB 2) was published in 2019 to address limitations identified since the first version of the tool was published in 2008 and to increase the reliability of assessments. This study analyzed the frequency of usage of the RoB 2 and the adequacy of reporting the RoB 2 assessments in non-Cochrane reviews published in 2020. This meta-research study included non-Cochrane systematic reviews of interventions published in 2020. For the reviews that used the RoB 2 tool, we analyzed the reporting of the RoB 2 assessment. Among 3880 included reviews, the Cochrane RoB 1 tool was the most frequently used (N = 2228; 57.4%), followed by the Cochrane RoB 2 tool (N = 267; 6.9%). From 267 reviews that reported using the RoB 2 tool, 213 (79.8%) actually used it. In 26 (12.2%) reviews, erroneous statements were used to indicate the RoB 2 assessment. Only 20 (9.4%) reviews presented a complete RoB 2 assessment with a detailed table of answers to all signaling questions. The judgment of risk of bias by the RoB 2 tool was not justified by a comment in 158 (74.2%) reviews. Only in 33 (14.5%) of reviews the judgment in all domains was justified in the accompanying comment. In most reviews (81.7%), the RoB was inadequately assessed at the study level. In conclusion, the majority of non-Cochrane reviews published in 2020 still used the Cochrane RoB 1 tool. Many reviews used the RoB 2 tool inadequately. Further studies about the uptake and the use of the RoB 2 tool are needed.

Frequency of use and adequacy of Cochrane risk of bias tool 2 in non-Cochrane systematic reviews published in 2020: Meta-research study.

Simple Summary The management of patients with Barrett’s esophagus still poses several clinical issues to the clinician, from correctly defining diagnosis to choosing adequate treatment. This brief and evidence-based review is aimed at providing a practical guide for the adequate management of this condition. Abstract Barrett’s esophagus is the most important complication of gastro-esophageal reflux disease and the only known precursor of esophageal adenocarcinoma. The diagnosis and treatment of Barrett’s esophagus are clinically challenging as it requires a high level of knowledge and competence in upper gastrointestinal endoscopy. For instance, endoscopists should know when and how to perform biopsies when Barrett’s esophagus is suspected. Furthermore, the correct identification and treatment of dysplastic Barrett’s esophagus is crucial to prevent progression to cancer as well as it is the endoscopic surveillance of treated patients. Herein, we report practice-oriented answers to clinical questions that clinicians should be aware of when approaching patients with Barrett’s esophagus.

/pdf/management-of-barretts-esophagus-practice-oriented-answers-22ag4aer.pdf

Management of Barrett’s Esophagus: Practice-Oriented Answers to Clinical Questions

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Autoimmune Atrophic Gastritis: A Clinical Review

Frequency of use and adequacy of Cochrane risk of bias tool 2 in non-Cochrane systematic reviews published in 2020: Meta-research study.

Management of Barrett’s Esophagus: Practice-Oriented Answers to Clinical Questions