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Autoimmune gastritis (AIG) is an autoimmune disorder characterized by the destruction of gastric parietal cells and atrophy of the oxyntic mucosa which induces intrinsic factor deficiency and hypo-achlorhydria. AIG predominantly affects the antral mucosa with AIG patients experiencing increased inflammation and a predisposition toward the development of gastric adenocarcinoma and type I neuroendocrine tumors. The exact pathogenesis of this autoimmune disorder is incompletely understood although dysregulated immunological mechanisms appear to major contributors. This review of autoimmune gastritis, an unmet medical need, summarizes current knowledge on pro- and anti-inflammatory cytokines and strategies for the discovery of novel biomarkers and potential pharmacological targets.

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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.

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PURPOSE: Calcitonin (Ct) is currently the most sensitive biochemical marker of C-cell disease (medullary thyroid cancer [MTC] and C-cell hyperplasia), but its specificity is relatively low. Our aim was to examine whether autoimmune atrophic gastritis (AAG) and chronic hypergastrinemia, with or without chronic autoimmune thyroiditis (AT), are conditions associated with increased Ct levels. METHODS: Three groups of patients were consecutively enrolled in this  multicentric study: group A consisted of patients with histologically-proven AAG (n = 13; 2 males, 11 females); group B fulfilled the criteria for group A but also had AT (n = 92; 15 males, 77 females); and group C included patients with AT and without AAG (n = 37; 6 males, 31 females). RESULTS: Median Ct levels did not differ between the three groups. Ct levels were undetectable in: 8/13 cases (61.5%) in group A, 70/92 (76.1%) in group B, and 27/37 (73.0%) in group C. They were detectable but ≤ 10 ng/L in 4/13 (30.8%), 20/92 (21.7%) and 7/37 (18.9%) cases, respectively; and they were > 10 ng/L in 1/13 (7.7%), 2/92 (2.2%) and 3/37 (8.1%) cases, respectively (P = 0.5). Only three patients had high Ct levels (> 10 ng/L) and high gastrin levels and had an MTC. There was no correlation between Ct and gastrin levels (P = 0.353, r = 0.0785). CONCLUSIONS: High gastrin levels in patients with AAG do not explain any hypercalcitoninemia, regardless of whether patients have AT or not. This makes it mandatory to complete the diagnostic process to rule out MTC in patients with high Ct levels and AAG.

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BACKGROUND: Autoimmune gastritis (AIG) is a progressive, chronic, immune-mediated inflammatory disease characterized by the destruction of gastric parietal cells leading to hypo/anacidity and loss of intrinsic factor. Gastrointestinal symptoms such as dyspepsia and early satiety are very common, being second in terms of frequency only to anemia, which is the most typical feature of AIG. AIM: To address both well-established and more innovative information and knowledge about this challenging disorder. METHODS: An extensive bibliographical search was performed in PubMed to identify guidelines and primary literature (retrospective and prospective studies, systematic reviews, case series) published in the last 10 years. RESULTS: A total of 125 records were reviewed and 80 were defined as fulfilling the criteria. CONCLUSION: AIG can cause a range of clinical manifestations, including dyspepsia. The pathophysiology of dyspepsia in AIG is complex and involves changes in acid secretion, gastric motility, hormone signaling, and gut microbiota, among other factors. Managing dyspeptic symptoms of AIG is challenging and there are no specific therapies targeting dyspepsia in AIG. While proton pump inhibitors are commonly used to treat dyspepsia and gastroesophageal reflux disease, they may not be appropriate for AIG. Prokinetic agents, antidepressant drugs, and non-pharmacological treatments may be of help, even if not adequately evidence-based supported. A multidisciplinary approach for the management of dyspepsia in AIG is recommended, and further research is needed to develop and validate more effective therapies for dyspepsia.

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OBJECTIVES: To explore the prevalence, characteristics, age distribution and etiology changes of chronic atrophic gastritis (CAG) in South China. METHODS: This study included all patients who underwent endoscopy examinations from 2011 to 2020 in our hospital. Patients were divided into groups 1 (2011-2015) and 2 (2016-2020). The prevalence, characteristics, age distribution and etiology changes of CAG were compared between groups. RESULTS: Overall CAG prevalence was 20.92% (24,084/115,110) from 2011 to 2020; prevalence significantly differed between groups (18.78%, 8468/45,087, in group 1 and 22.30%, 15,616/70,023, in group 2). Patients with CAG had significantly younger age (under 45) and more corpus atrophy and more autoimmune atrophic gastritis (AAG) in group 2 than in group 1. AAG prevalence in group 2 was 30.11% (4702/15,616) significantly higher than 13.57% (1149/8468) in group 1. 82 patients with AAG later exhibited gastric cancer without obvious clinical features over the decade. CONCLUSIONS: CAG is increasing and seems starting earlier among people during the study period. We need to focus on diagnosis and treatment of corpus related atrophy and AAG, especially for the young. Laboratory examination, endoscopic biopsy and surveillance are important for CAG.

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BACKGROUND: Incomplete intestinal metaplasia (IM) is reportedly associated with higher gastric cancer (GC) risk than its complete variant. AGA Guidelines recommend including IM subtyping in routine pathology reports. This study assesses the prevalence of complete versus incomplete IM in gastric conditions with different GC risks. METHODS: IM subtyping (complete vs. incomplete) and grading (IM extension: G1: ≤30%; G2: >30%) were assessed in 386 patients with IM + ve gastric biopsy sets that included both antral and oxyntic samples. Cases were categorized as: (a) IM foci in otherwise normal mucosa (n = 59); (b) Helicobacter pylori gastritis (n = 138); (c) reactive gastropathy (141); and (d) autoimmune atrophic gastritis (AIG, n = 48). Odds ratios (OR) and their 95% CI were used in comparing the prevalence of incomplete IM and the correlation between subtype and IM extension. RESULTS: Incomplete IM was present in 37.7% of patients with H. pylori gastritis, 8.3% of those with AIG 5.0% of those with reactive gastropathy, and none of those with otherwise normal mucosa. Incomplete IM was strongly associated with more extensive (G2-IM) mucosal intestinalization (OR = 6.69; 95% CI = 2.77-9.40). CONCLUSION: Incomplete IM is significantly more prevalent in conditions (H. pylori gastritis) known to carry a higher risk of GC and is strongly associated with its extension. The low prevalence of incomplete IM in AIG (8.3%) and reactive gastropathy (5.2%) is in keeping with the low GC risk associated with these conditions.

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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.

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The prevalence of autoimmune atrophic gastritis (AAG) in vitiligo patients was estimated at about 15%. In both conditions, a release of specific antibodies and an autoimmune destruction of target cells (melanocytes in vitiligo, parietal cells (PC) in AAG) mediated by CD8-T lymphocytes was demonstrated to perform a comparative histological study of vitiligo skin and AAG mucosa. In two patients with concomitant vitiligo and AAG, biopsies from the vitiligo lesions and gastric mucosa from corpus fundus were performed. Sections were immunostained with E-cadherin, Coll IV, CD8, CD20, CD4 antibodies. The skin sections also were stained with HES, HMB45, MITF. Common histological findings were found in both diseases. Adhesivity impairment with down expression of E-cadherin and Coll IV was objectivated. The protruding MITF+melanocytes and the detached PC were surrounded by an infiltrate including CD8 and CD4. CD8 was infiltrating the epidermis in close contact with the remaining melanocytes and the gastric glands around the remaining PC. In both diseases, the autoimmune process could be preceded by a detachment of either melanocytes in vitiligo or PC in AAG possibly in relation to an initial adhesivity impairment of these cells. Common autoimmune mechanisms could be suggested for both diseases.

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Introduction: Proton pump inhibitors (PPIs) have been widely prescribed as a primary treatment for acid-related disorders. A large body of literature reported several adverse outcomes due to PPI therapy, including an increased risk of gastric cancer (GC). Autoimmune atrophic gastritis (AAG) is a chronic inflammatory disorder affecting the oxyntic mucosa, leading to mucosal atrophy, intestinal metaplasia, and reduced gastric acid secretion, up to the possible development of dysplasia and intestinal-type GC. Whether PPI use may increase the GC risk in AAG patients has not yet been investigated. We conducted a case-control study in AAG patients to assess the association between the PPI use before AAG diagnosis and the development of GC at follow-up (FU). Materials and Methods: Patients were included from a prospective cohort of AAG patients (diagnosed 1992-2021) in a referral center for gastric autoimmunity; all patients adhered to an endoscopic-histological FU program according to Management of precancerous conditions and lesions in the stomach (MAPS) I/II (management of epithelial precancerous conditions) guidelines. At diagnosis, clinical/biochemical data and PPI use before AAG diagnosis (withdrawn at the time of diagnosis), for at least 12 months, were evaluated. Patients who developed gastric neoplastic lesions (GNLs) at FU were considered as cases; patients without a diagnosis of GNLs at FU were considered as controls. At a total FU of 2.3 years (1-13), 35 cases were identified, and controls were matched 2:1 by age ( ± 3 years), gender, and years of FU (n=70); therefore, a total of n=105 patients were included in the study. Results: The proportion of PPI users before AAG diagnosis was significantly higher in cases than in controls (54.3% vs. 18.6%, p<0.001). At logistic regression, considering as a dependent variable the development of GNLs at FU, a positive association was shown for PPI use before AAG diagnosis (OR 9.6, 95%CI 2.3-40.3), while other independent variables as the use of antiplatelets/anticoagulants (OR 2.8, 95%CI 0.7-12.0), age ≥ 50 years (OR 2.0, 95%CI 0.2-18.1), 1st-degree family history for GC (OR 2.4, 95%CI 0.4-15.2), and smoking habit (OR 0.4, 95%CI 0.1-2.1) were not associated. Conclusions: PPI use before the diagnosis of AAG appears to considerably increase the risk of subsequent GNL development. Considering the common misuse of PPIs, physicians should regularly reevaluate the appropriateness of ongoing PPI therapy, in particular in patients with a clinical suspicion of or already diagnosed AAG.

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Gastric neuroendocrine neoplasms are uncommon tumors with variable differentiation and malignant potential. Three main subtypes are recognized: type 1, related to autoimmune atrophic gastritis; type 2, associated with Zollinger-Ellison and MEN1 syndrome; and type 3, sporadic. Although endoscopy alone is often sufficient for diagnosis and management of small, indolent, multifocal type 1 tumors, imaging is essential for evaluation of larger, high-grade, and type 2 and 3 neoplasms. Hypervascular intraluminal gastric masses are typically seen on CT/MRI, with associated perigastric lymphadenopathy and liver metastases in advanced cases. Somatostatin receptor nuclear imaging (such as Ga-68-DOTATATE PET/CT) may also be used for staging and assessing candidacy for peptide receptor radionuclide therapy. Radiotracer uptake is more likely in well-differentiated, lower-grade tumors, and less likely in poorly differentiated tumors, for which F-18-FDG-PET/CT may have additional value. Understanding disease pathophysiology and evolving histologic classifications is particularly useful for radiologists, as these influence tumor behavior, preferred imaging, therapy options, and patient prognosis.

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BACKGROUND: Autoimmune atrophic gastritis (AAG) is a type of chronic gastritis that mainly affects the gastric corpus. Due to the lack of standard diagnostic criteria and overlaps with the courses of Helicobacter pylori-related atrophic gastritis, reports on the diagnostic strategy of AAG at an early stage are limited. CASE SUMMARY: A 71-year-old woman with severe anemia was diagnosed with AAG. Endoscopic views and pathological findings showed the coexistence of normal mucosa in the gastric antrum and atrophic mucosa in the gastric fundus. Serological tests showed that anti-parietal cell antibodies and anti-intrinsic factor antibodies were both positive. Immunohistochemical results, which showed negative H+-K+ ATPase antibody staining and positive chromogranin A (CgA) staining, confirmed the mechanism of this disease. After vitamin B12 and folic acid supplementation, the patient recovered well. CONCLUSION: Successful diagnosis of AAG includes serological tests, endoscopic characteristics, and immunohistochemistry for H+-K+ ATPase and CgA antibodies.

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White globe appearance has recently been identified as a novel endoscopic marker useful in the diagnosis of early gastric cancer. Recently, this lesion has also been reported in the noncancerous stomach, including cases with autoimmune atrophic gastritis, although the clinical significance remains unclear. We present the details of a 68-year-old woman who began vonoprazan therapy for severe gastroesophageal reflux disease causing esophageal stricture. On follow-up endoscopy 1 year after beginning vonoprazan, multiple white globe appearance lesions developed in all sections of her stomach, except for the antrum. We also detected lesions during a yearly follow-up in the noncancerous stomach of a 70-year-old man who had received vonoprazan for 3 years. Lesions in both cases constituted cystic gland dilatations containing eosinophilic material. There was no evidence of accompanying autoimmune atrophic gastritis in either patient. This report is the first to our knowledge describing newly developed white globe appearance lesions in the noncancerous stomach during follow-up in two cases who received vonoprazan. Our findings suggest that these lesions in the noncancerous stomach might be associated with vonoprazan treatment. We investigated the two cases endoscopically and histologically, and we report our findings with a literature review.

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BACKGROUND: Autoimmune atrophic gastritis (AAG) diagnosis is based on specific histological findings and anti-parietal cell antibodies (PCA) considered the serological hallmark of AAG, although a subgroup of AAG patients may be seronegative. OBJECTIVES: To assess the occurrence and clinical features of seronegative compared to seropositive AAG. METHODS: This is a cross-sectional study including 516 consecutive adult patients (age 59.6 ±â€¯12.8 years, F:M = 2.2:1) with histologically proven AAG diagnosed in two Italian academic referral centers over the last 10 years. PCA were detected at AAG diagnosis. Variables related to the dependent variable of interest (i.e.PCA-negativity) were assessed by univariate/logistic regression analysis. RESULTS: 109/516 AAG patients were seronegative. The mean age of seronegative AAG patients was significantly higher compared to PCA-positive (65.9 ±â€¯14.1vs57.9 ±â€¯15.1 years; p<0.0001). The proportion of patients aged 70-79 and ≥80 years were, respectively, lower for PCA-positivity (5.1vs12.8%;21.3vs38.5%;p<0.005). Seronegativity was associated with age ≥50 years (OR2.4;95%CI 1.1-5.2), while for other variables (gender, comorbidities, anemia, atrophy severity) no association was found. In a sub-cohort of 101 AAG patients, PCA levels detected by ELISA were inversely correlated with age at AAG diagnosis (rho=-0.250;p = 0.0118). CONCLUSION: Roughly 20% of patients are seronegative at the time of AAG histological diagnosis and this is more common in elderly individuals.

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The association between autoimmune atrophic gastritis and thyroid disorders has been observed since the early 1960s and the expression "thyrogastric syndrome" was coined to indicate the presence of thyroid autoantibodies or autoimmune thyroid disease in patients with pernicious anemia, a late clinical stage of autoimmune atrophic gastritis. More recently, it was confirmed that autoimmune thyroid disorders, in particular Hashimoto's thyroiditis, may be frequently associated with other organ-specific, immune-mediated disorders, such as autoimmune atrophic gastritis or celiac disease. The association of Hashimoto's thyroiditis with autoimmune atrophic gastritis or celiac disease in adult patients is currently considered part of the polyglandular autoimmune syndromes which include several autoimmune disorders associated with an autoaggressive impairment of endocrine glands. From a clinical point of view, the thyro-entero-gastric autoimmunity may lead to potentially serious consequences like anemia, micronutrients deficiencies, and drugs malabsorption, as well as to an increased risk for malignancies. These alterations may frequently present in an underhand manner, with consequent diagnostic and treatment delays. Many aspects of the association between thyroid, gastric and intestinal autoimmune diseases still await clarification. The present review focuses on the embryological, genetic and pathophysiological aspects of thyro-entero-gastric autoimmunity. In particular, the current diagnostic criteria of autoimmune thyroid disease, autoimmune atrophic gastritis, and celiac disease are reviewed, along with the evidences for their association in poly-autoimmunity syndromes. The benefits of proactive screening of autoimmune thyroid disorders in patients with autoimmune gastritis or enteropathy and viceversa are also discussed.

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Defective spleen function increases susceptibility to bacterial infections which can be prevented by vaccine prophylaxis. Splenic hypofunction can be found in a number of autoimmune disorders; however, no data are available regarding autoimmune atrophic gastritis (AAG), autoimmune enteropathy (AIE) and autoimmune liver disease (AILD). Peripheral blood samples from patients with AAG (n = 40), AIE (n = 3) and AILD (n = 40) were collected. Patients affected by autoimmune disorders already known to be associated with splenic hypofunction, i.e. coeliac disease (CD) and ulcerative colitis (UC), were included as disease controls, while splenectomised patients and healthy subjects were evaluated as positive and negative controls, respectively. Counting of erythrocytes with membrane abnormalities, i.e. pitted red cells, was used as an indicator of spleen function (normal upper limit 4%). Defective splenic function was observed in 22 of the 40 patients with AAG (55.0%), in two of the three patients with AIE (66.6%) and in 35 of the 40 patients with AILD (87.5%). As expected, in untreated CD, refractory CD and UC there was a high prevalence of hyposplenism (43.7%, 88.2% and 54.4%, respectively). Due to the high prevalence of splenic hypofunction, patients with AAG, AILD and AIE should undergo pitted red cell evaluation and, if hyposplenic, they should be candidate to vaccine prophylaxis against encapsulated bacteria.

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BACKGROUND: Chronic autoimmune atrophic gastritis (CAAG) is an autoimmune disease characterized by hypo/achlorhydria. A role of CAAG in the pathogenesis of nutritional deficiencies has been reported, therefore we hypothesized a possible association between CAAG and 25-OH-Vitamin D [25(OH)D] deficiency. Aim of the present study is to evaluate the prevalence of 25(OH)D deficiency in CAAG patients. METHODS: 87 CAAG patients (71 females; mean age 63.5 ± 12.8 years) followed at our Centre from January 2012 to July 2015 were consecutively evaluated. 25(OH)D, vitamin B12, parathormone, and calcium were measured in all the CAAG patients. The results were compared with a control group of 1232 healthy subjects. RESULTS: In the CAAG group the mean 25(OH)D levels were significantly lower than in the control group (18.8 vs. 27.0 ng/ml, p < 0.0001). 25(OH)D levels < 20 ng/ml was observed in 57 patients, while levels < 12.5 ng/ml in 27 patients. A significant correlation between vitamin B12 values at diagnosis and 25(OH)D levels was observed (rs = 0.25, p = 0.01). Interestingly, the CAAG patients with moderate/severe gastric atrophy had lower 25(OH)D values as compared to those with mild atrophy (11.8 vs. 20 ng/ml; p = 0.0047). Moreover, the 25(OH)D levels were significantly lower in CAAG patients with gastric carcinoid as compared to those without gastric carcinoid (11.8 vs. 19.8 ng/ml; p = 0,0041). CONCLUSION: Data from the present study showed a significant reduction of 25(OH)D levels in CAAG patients and a possible impairment of vitamin D absorption in CAAG may be postulated. Any implication to the genesis of gastric carcinoids remains to be elucidated.

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Rosai-Dorfman disease (RDD), or sinus histiocytosis with massive lymphadenopathy, has been described involving both lymph nodes and extranodal sites, but extranodal RDD rarely involves the gastrointestinal tract. Although the etiology is unclear, several risk factors have been shown to be highly associated with this disease process, including viral infection and immune alterations. In this article, we present a case of a 79-year-old male with a history of autoimmune atrophic gastritis and multiple carcinoid tumors of the stomach presenting with a new stomach mass. An additional large sigmoid colon mass and adjacent enlarged lymph node was identified through imaging, prior to surgery. Through extensive pathologic analysis, we identified the first case of predominant extranodal RDD involving gastric mucosa and submucosa in a background of atrophic gastritis, with additional involvement of the sigmoid colon. Based on this case and literature review, we further discuss possible risk factors and pathogenesis of this disease process.

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The progressively growing knowledge of the pathophysiology of a number of immune-mediated gastrointestinal and liver disorders, including autoimmune atrophic gastritis, coeliac disease, autoimmune enteropathy, inflammatory bowel disease, autoimmune hepatitis, primary sclerosing cholangitis, primary biliary cholangitis and autoimmune pancreatitis, together with the improvement of their detection methods have increased the diagnostic power of serum antibodies. In some cases - coeliac disease and autoimmune atrophic gastritis - they have radically changed gastroenterologists' diagnostic ability, while in others - autoimmune hepatitis, inflammatory bowel disease and autoimmune pancreatitis - their diagnostic performance is still inadequate. Of note, serum antibody misuse in clinical practice has raised a number of controversies, which may generate confusion in the diagnostic management of the aforementioned disorders. In this review, we critically re-evaluate the usefulness of serum antibodies as biomarkers of immune-mediated gastrointestinal and liver disorders, and discuss their pitfalls and merits.

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