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Vitamin D possesses a crucial role in preserving bone health, modulating the immune system responses, and supporting various physiological functions throughout the body. Chronic atrophic autoimmune gastritis (CAAG) constitutes an autoimmune condition marked by inflammation and damage to the stomach cells, often resulting in a decreased ability to absorb certain nutrients, including vitamin B12 and iron. Although, vitamin D is not directly affected by this condition, the sufficiency of this micronutrient seems to have important implications for overall health and management of the disease. The aim of the current review was to assess the incidence and related features of vitamin D deficiency in patients with CAAG and to elucidate the complex regulatory role of this nutrient, in an effort to improve patient outcomes. Vitamin D greatly contributes to the regulation of the immune system. In patients with CAAG, the immune system attacks the stomach lining; thus, the maintenance of a healthy and balanced immune response is important. In autoimmune conditions such as CAAG, where inflammation plays a decisive role in disease progression, vitamin D could potentially exert a role in managing and controlling the associated symptoms. Adequate vitamin D levels may help in regulating the immune response and reducing inflammation. In addition, patients with CAAG are at risk of nutrient deficiencies, including vitamin B12 and iron, which can lead to anemia and bone health issues. As vitamin D is critical for calcium absorption and bone health, assurance of sufficient levels of this micronutrient can be beneficial in preventing or mitigating bone-related complications. In conclusion, regular monitoring of vitamin D levels, among other nutrients, and appropriate supplementation, when necessary, can help improve overall health and well-being in these patients.

There is limited research evaluating the diagnosis and treatment of patients with autoimmune gastritis (AIG) and pernicious anemia (PA). We used a 2-phase data collection process to examine the literature and individual patient accounts. Phase one comprised a systematically conducted literature review focusing on diagnosis and treatment, relationships with healthcare practitioners and health-related quality of life (HRQOL). Phase two involved analysis of individual accounts via posts in online patient forums. We identified 6 main themes: the diagnosis journey, seeking treatment, patient-provider relationships, HRQOL, patient disempowerment, and the “expert patient.” Our findings confirm significant knowledge gaps concerning AIG/PA across the healthcare community. These have a cascading effect starting with delays in diagnosis and poor treatment protocols and often lead to complete withdrawal from care seeking. The establishment of standard consensus guidelines and improved clinical awareness should be urgently addressed. Interventions that better help patients understand their illness are also needed to improve psychological health. Without these changes disengagement from health systems, and poor health outcomes, will continue for this population group.

The Japanese diagnostic criteria for autoimmune gastritis (AIG) were established by the “Study Group on the establishment of diagnostic criteria for type A gastritis,” which is related to a workshop associated with the Japan Gastroenterological Endoscopy Society (JGES) and the Committee of AIG Research Group (CARP). The criteria were set as follows: the cases of confirmed diagnosis are patients in whom either the endoscopic or histological findings, or both, meet the requirements for AIG and who are confirmed to be positive for gastric autoantibodies (either anti-parietal cell or anti-intrinsic factor antibodies, or both). The presentation of endoscopic findings of early-stage AIG in the diagnostic criteria was withheld owing to the need for further accumulation and characterization of endoscopic clinical data. Therefore, diagnosis of early-stage AIG only requires histological confirmation and gastric autoantibody positivity. Suspected cases are patients in whom either the endoscopic or histological findings, or both, meet only the requirements for AIG. Histological findings only meet the requirements for early stage. AIG has been underdiagnosed in the past, but our study group’s newly proposed diagnostic criteria will enable a more accurate and early diagnosis of AIG. The criteria can be used to stratify patients into various high-risk groups for gastric tumors and pernicious anemia. They would allow the establishment of an appropriate surveillance system in the coming years. Nevertheless, issues such as establishing the endoscopic findings of early-stage AIG and obtaining Japanese insurance coverage for gastric autoantibody tests require attention.

Helicobacter pylori (H. pylori) infection and autoimmune inflammation of the gastric mucosa are recognized as the leading etiological factors of chronic atrophic gastritis. The mechanisms of atrophy formation and progression with the risk of gastric cancer development are heterogeneous, which requires a deeper study of the molecular mechanisms of relationship, peculiarities of the course of autoimmune gastritis both in combination with H. pylori and after eradication, as well as without H. pylori infection (naïve AIG). This article presents the specific molecular and cellular patterns in the formation of these related conditions.

Corpus-restricted atrophic gastritis is a chronic inflammatory disorder leading to possible development of type 1 neuroendocrine tumors (T1gNET), intraepithelial neoplasia (IEN), and gastric cancer (GC). We aimed to assess occurrence and predictors of gastric neoplastic lesions in patients with corpus-restricted atrophic gastritis at long-term follow-up. A prospective single-center cohort of patients with corpus-restricted atrophic gastritis adhering to endoscopic-histological surveillance was considered. Follow-up gastroscopies were scheduled according to the management of epithelial precancerous conditions and lesions of the stomach guidelines. In case of new/worsening of known symptoms, gastroscopy was anticipated. Cox regression analyses and Kaplan-Meier survival curves were obtained. Two hundred seventy-five patients with corpus-restricted atrophic gastritis (72.0% female, median age 61 [23-84] years) were included. At a median follow-up of 5 (1-17) years, the annual incidence rate person-year was 0.5%, 0.6%, 2.8%, and 3.9% for GC/high-grade IEN, low-grade IEN, T1gNET, and all gastric neoplastic lesions, respectively. All patients showed at baseline operative link for gastritis assessment (OLGA)-2, except 2 low-grade (LG) IEN patients and 1 T1gNET patient with OLGA-1. Age older than 60 years (hazard ratio [HR] 4.7), intestinal metaplasia without pseudopyloric metaplasia (HR 4.3), and pernicious anemia (HR 4.3) were associated with higher risk for GC/HG-IEN or LG-IEN development and shorter mean survival time for progression (13.4, 13.2, and 11.1, respectively, vs 14.7 years, P = 0.01). Pernicious anemia was an independent risk factor for T1gNET (HR 2.2) and associated with a shorter mean survival time for progression (11.7 vs 13.6 years, P = 0.04) as well as severe corpus atrophy (12.8 vs 13.6 years, P = 0.03). Patients with corpus-restricted atrophic gastritis are at increased risk for GC and T1gNET despite low-risk OLGA scores, and those aged older than 60 years with corpus intestinal metaplasia or pernicious anemia seem to display a high-risk scenario.

INTRODUCTION:Autoimmune metaplastic atrophic gastritis (AMAG) is a precancerous condition that predisposes to gastric neuroendocrine tumors (gNETs). There exist no methods to stratify patients with AMAG for gNET risk.METHODS:We identified a cohort of patients with AMAG within a university health system using histopathologic and serologic criteria. We analyzed features predictive of prevalent gNET.RESULTS:We identified 181 patients with AMAG and 41 (22.7%) with prevalent gNET. Gastrin levels were elevated in gNET (1,859.8 vs 679.5 pg/mL, P < 0.001), and gastrin titers demonstrated good discrimination (c = 0.799, 95% CI 0.707–0.892) for gNET.DISCUSSION:Gastrin levels differ significantly between patients with AMAG with and without gNET.

With the development of research, the clinical characteristics of autoimmune gastritis (AIG) have become much clearer. However, due to its occult endoscopic appearance, it remains difficult to diagnose early, including ultra-early AIG. More cases and typical clinical characteristics should be proposed and concluded to guide clinicians. Hence, we selected two novel cases of early AIG and summarized their common endoscopic features in order to improve diagnostic ability. We found two interesting features for early AIG: 1) deep reticular blood vessels in the lower part of the cardia mucosa and 2) various manifestations of crypt opening shown on narrow-band imaging (NBI) magnification, such as dilation, pinhole-like, shrinkage, and disappearance. Future studies promise even more progress with the hope that these features can be found in more cases.

Autoimmune gastritis (AIG) and autoimmune liver diseases (AILDs)-including autoimmune hepatitis (AIH), primary biliary cholangitis (PBC), and primary sclerosing cholangitis (PSC)-are chronic organ-specific immune-mediated disorders. While both conditions frequently co-occur with other autoimmune diseases, the prevalence, clinical overlap, and immunological associations between AIG and AILDs remain underexplored. To investigate the prevalence of AIG in patients with AILD and characterize the clinical, serological, and histopathological features of this overlap, to improve early detection and guide integrated management strategies. We conducted a prospective study on 104 patients with a confirmed diagnosis of AILD. All participants were screened for anti-parietal cell antibodies (APCA); those testing positive underwent upper gastrointestinal endoscopy and gastric biopsies. Histological assessment was based on the updated Sydney System, with evaluation of mucosal inflammation, glandular atrophy, and intestinal metaplasia. APCA positivity was observed in 22.1% of AILD patients, with a female predominance (78.3%). The median age of AIG diagnosis in APCA-positive patients was 58 years. Among APCA-positive individuals, histological confirmation of AIG was achieved in 91.3%, with a high rate of intestinal metaplasia (95.7%) and variable OLGA stages of gastric atrophy. Comorbid autoimmune conditions were common, with 43.5% of APCA-positive patients also presenting with autoimmune thyroiditis. Notably, PBC was disproportionately represented in the APCA-positive subgroup (47.8%) compared to the overall cohort (39.0%). This study highlights a clinically significant association between AIG and AILDs, particularly in patients with PBC and concurrent autoimmune conditions. Given the elevated risk of gastric mucosal atrophy and potential neoplastic transformation, targeted screening for AIG in AILD patients-especially those with APCA positivity or thyroid autoimmunity-should be considered. These findings underscore the importance of cross-specialty surveillance and open new avenues for research into shared immunopathogenic mechanisms. This study found that a significant number of patients with autoimmune liver diseases, especially those with primary biliary cholangitis, also show signs of autoimmune gastritis. These results support the consideration of targeted screening for gastric involvement in selected patients to improve early detection and clinical management of associated complications.

We would like to provide an updated comprehensive perspective and identify the components linked to chronic spontaneous urticaria (CSU) without specific triggers in autoimmune atrophic gastritis (AAG). AAG is an organ-specific autoimmune disease that affects the corpus-fundus gastric mucosa. Although we lack a unified explanation of the underlying pathways, when considering all paediatric patients reported in the literature, alterations result in gastric neuroendocrine enterochromaffin-like (ECL) cell proliferation and paracrine release of histamine. Several mechanisms have been proposed for the pathogenesis of CSU, with much evidence pointing towards AAG and ECL cell responses, which may be implicated as potential factors contributing to CSU. The excessive production/release of histamine into the bloodstream could cause or trigger exacerbations of CSU in AAG, independent of Helicobacter pylori ; thus, the release of histamine from ECL cells may be the primary modulator. Conclusion : Considering the understanding of these interactions, recognising the respective roles of AAG in the pathogenesis of CSU may strongly impact the diagnostic workup and management of unexplained/refractory CSU and may inform future research and interventions in the paediatric population. What is Known: • Autoimmune atrophic gastritis is a chronic immune-mediated inflammatory disease characterised by the destruction of the oxyntic mucosa in the gastric body and fundus, mucosal atrophy, and metaplastic changes. • Autoimmune atrophic gastritis in paediatric patients is important because of the poor outcome and risk of malignancy and possibly underestimated entities primarily reported in single-case reports. What is New: • Upper gastrointestinal inflammatory disorders, independent of H. pylori, have been implicated as potential inducing factors in the development of chronic spontaneous urticaria. • If a paediatric patient presents with symptoms such as anaemia, reduced vitamin B12 levels, recurrent urticaria with no other detectable aetiology, positive anti-parietal cell antibodies, and elevated gastrin levels, autoimmune atrophic gastritis should be considered a possible cause of chronic urticaria.

Fundamental treatments for autoimmune gastritis (AIG) have not yet been established; thus, analyzing AIG pathogenesis in detail to obtain useful information for prognosis prediction and treatment is crucial. This study explored bacteria involved in AIG pathogenesis by focusing on the gastric microbiota composition. Gastric biopsy tissues were collected endoscopically from the gastric corpus and antrum of patients with AIG and chronic gastritis. Total DNA was extracted from gastric biopsy specimens and used for 16S rRNA gene amplicon sequencing analysis. Principal coordinate analysis of diversity using the weighted UniFrac distance revealed that following Helicobacter pylori eradication, the gastric bacterial composition of patients with AIG differed significantly from that of patients with chronic gastritis, exhibiting decreased Shannon index, Pielou’s evenness, and Simpson index of alpha diversity. The gastric microbiota of patients with AIG was characterized by an increased abundance of the genus Streptococcus and a reduced abundance of the genus Prevotella compared with that of patients with chronic gastritis.