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Journal articles on the topic 'Autoimmune Metaplastic Atrophic Gastritis'

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Author: Grafiati

Published: 11 March 2023

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1

Pittman, Meredith E., Lysandra Voltaggio, Feriyl Bhaijee, Scott A. Robertson, and Elizabeth A. Montgomery. "Autoimmune Metaplastic Atrophic Gastritis." American Journal of Surgical Pathology 39, no. 12 (December 2015): 1611–20. http://dx.doi.org/10.1097/pas.0000000000000481.

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2

Park, Jason Y., Dora Lam-Himlin, and Roopa Vemulapalli. "Review of autoimmune metaplastic atrophic gastritis." Gastrointestinal Endoscopy 77, no. 2 (February 2013): 284–92. http://dx.doi.org/10.1016/j.gie.2012.09.033.

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3

Philip, Shawn, Luz Sullivan, and Nour Parsa. "A Rare Case of Autoimmune Metaplastic Atrophic Gastritis." American Journal of Medical Case Reports 9, no. 10 (June 25, 2021): 516–18. http://dx.doi.org/10.12691/ajmcr-9-10-10.

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4

Hall, Sara N., and Henry D. Appelman. "Autoimmune Gastritis." Archives of Pathology & Laboratory Medicine 143, no. 11 (November 1, 2019): 1327–31. http://dx.doi.org/10.5858/arpa.2019-0345-ra.

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Context.— Autoimmune gastritis (AG) is a corpus-restricted chronic atrophic gastritis associated with intrinsic factor deficiency, either with or without pernicious anemia. Autoimmune gastritis is a microscopic disease because patients present with no or vague symptoms, and clinicians rarely find endoscopic changes. Autoimmune gastritis only becomes a clinical disease when pathologists diagnose it in gastric biopsies performed for a variety of clinical indications. Unfamiliarity with this disease can result in misdiagnosis of patients, and thus inadequate patient management. Objective.— To review the pathogenesis, clinical features, diagnostic criteria, differential diagnoses, sequelae, and surveillance recommendations for AG. Data Sources.— The sources of the study include a review of the pertinent literature for AG. Conclusions.— Autoimmune gastritis is an important disease characterized by a loss of oxyntic mucosa and presence of metaplastic epithelium and enterochromaffin-like cell hyperplasia. Awareness and proper diagnosis are critical to prevent mismanagement of patients.

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Jhala, Nirag C., Mario Montemor, Darshana Jhala, Lin Lu, Lynya Talley, Marian M. Haber, and Juan Lechago. "Pancreatic Acinar Cell Metaplasia in Autoimmune Gastritis." Archives of Pathology & Laboratory Medicine 127, no. 7 (July 1, 2003): 854–57. http://dx.doi.org/10.5858/2003-127-854-pacmia.

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Abstract Objective.—To determine the frequency and significance of pancreatic acinar cells in the gastric oxyntic mucosa. Design.—One hundred gastric oxyntic mucosal biopsy specimens from patients with chronic active gastritis (n = 30), multifocal atrophic gastritis (n = 15), autoimmune gastritis (n = 18), and normal gastric oxyntic mucosa (n = 37) were evaluated for the presence of pancreatic acinar cells. Formalin-fixed, paraffin-embedded tissues were stained with hematoxylin-eosin, and those positive for pancreatic acinar cells were immunostained with antibodies against trypsin and pancreatic amylase. Results.—Eleven (11%) of 100 oxyntic mucosal tissue samples contained pancreatic acinar cells. These samples came from 9 of the 18 (50%) specimens of autoimmune gastritis, 1 of the 15 (6.6%) specimens of multifocal atrophic gastritis, and 1 of the 37 (2.7%) specimens of normal oxyntic mucosa. None of the samples with chronic active gastritis contained pancreatic acinar cells. Conclusions.—Pancreatic acinar cells were found in the oxyntic mucosa of patients with autoimmune gastritis significantly more frequently (P < .001) than in individuals with multifocal atrophic gastritis, normal oxyntic mucosa, or chronic active gastritis. Our study supports a metaplastic origin for pancreatic acinar cells in the oxyntic mucosa. Furthermore, detection of pancreatic acinar cells in the oxyntic mucosa of patients with gastritis strongly suggests an autoimmune pathogenesis.

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Dirschmid, Klaus, and Manfred Stolte. "Gastric Lesions in Patients With Autoimmune Metaplastic Atrophic Gastritis." American Journal of Surgical Pathology 35, no. 8 (August 2011): 1244. http://dx.doi.org/10.1097/pas.0b013e31821e8976.

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7

Antico, Antonio, Marilina Tampoia, Danilo Villalta, Elio Tonutti, Renato Tozzoli, and Nicola Bizzaro. "Clinical Usefulness of the Serological Gastric Biopsy for the Diagnosis of Chronic Autoimmune Gastritis." Clinical and Developmental Immunology 2012 (2012): 1–5. http://dx.doi.org/10.1155/2012/520970.

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Aim. To assess the predictive value for chronic autoimmune gastritis (AIG) of the combined assay of anti-parietal-cell antibodies (PCA), anti-intrinsic-factor antibodies (IFA), anti-Helicobacter pylori(Hp) antibodies, and measurement of blood gastrin.Methods. We studied 181 consecutive patients with anemia, due to iron deficiency resistant to oral replacement therapy or to vitamin B12 deficiency.Results. 83 patients (45.8%) tested positive for PCA and underwent gastroscopy with multiple gastric biopsies. On the basis of the histological diagnosis, PCA-positive patients were divided into 4 groups: (1) 30 patients with chronic atrophic gastritis; they had high concentrations of PCA and gastrin and no detectable IFA; (2) 14 subjects with metaplastic gastric atrophy; they had high PCA, IFA, and gastrin; (3) 18 patients with nonspecific lymphocytic inflammation with increased PCA, normal gastrin levels, and absence of IFA; (4) 21 patients with multifocal atrophic gastritis with “borderline” PCA, normal gastrin, absence of IFA and presence of anti-Hp in 100% of the cases.Conclusions. The assay of four serological markers proved particularly effective in the diagnostic classification of gastritis and highly correlated with the histological profile. As such, this laboratory diagnostic profile may be considered an authentic “serological biopsy.”

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Alakoski, Anna, Teea T. Salmi, Kaisa Hervonen, Hannu Kautiainen, Maarit Salo, Katri Kaukinen, Timo Reunala, and Pekka Collin. "Chronic Gastritis in Dermatitis Herpetiformis: A Controlled Study." Clinical and Developmental Immunology 2012 (2012): 1–5. http://dx.doi.org/10.1155/2012/640630.

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Background and Objective. Previous small studies suggest that chronic atrophic gastritis is common in dermatitis herpetiformis (DH). We here examined the frequency and topography of chronic gastritis in 93 untreated DH subjects and in 186 controls with dyspepsia.Methods. Specimens were drawn from the gastric corpus and antrum and examined for atrophy, intestinal metaplasia, andHelicobacter pylori. Duodenal biopsies were taken.Results. Atrophic corpus gastritis was more frequent in DH than in controls (16.0% and 2.7%, resp.,P<0.001); atrophy in the antrum was rare in both groups (3.2% and 1.1%,P=0.34). Intestinal metaplasia was present in 13 (14.0%) DH and 12 (6.5%) control patients (P=0.038) andH. pyloriin 17 (18.3%) and 17 (9.3%) (P=0.028), respectively. Small-bowel villous atrophy was seen in 76% of the DH patients, equally in patients with and without chronic gastritis. One DH patient with atrophic gastritis developed gastric cancer.Conclusion. In DH, chronic atrophic gastritis was common in the corpus, but not in the antrum.H. pyloriwill partly explain this, but corpus atrophy is suggestive of an autoimmune etiology. Atrophic gastritis may increase the risk of gastric cancer. We advocate performing upper endoscopy with sufficient histologic samples in DH.

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9

Livzan, M. A., O. V. Gaus, and S. I. Mozgovoi. "Chronic atrophic gastritis: patient manage." Russian Medical Inquiry 5, no. 6 (2021): 427–32. http://dx.doi.org/10.32364/2587-6821-2021-5-6-427-432.

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Patient management in chronic atrophic gastritis (CAG) in real clinical practice is a difficult task for a clinician. It is mainly due to the lack of reliable clinical stigmas that allow suspecting the presence of gastric mucosal atrophy. The diagnosis of chronic atrophic gastritis is valid only after a morphological assessment of gastrobiopaths taken during an endoscopy. According to a contemporary view, regardless of the inflammatory process etiology, CAG can progress to stomach cancer. At the same time, the point of no-return (at which the risk of inflammatory changes progression in the gastric mucosa and carcinogenesis preserves) is the CAG formation with the presence of intestinal metaplasia, even after the etiological factor is eliminated. Patients of this group, depending on the severity of inflammatory changes and atrophy, require constant dynamic follow-up and timely implementation of necessary measures for cancer prevention. To inhibit the progression of gastric mucosal precancerous changes, it is necessary to include the regimen using gastroprotective drugs for patients with CAG. Patients with autoimmune gastritis (in addition to the gastroprotective drugs) need to conduct regimens of cyanocobalamin therapy to prevent hematological and neurological disease manifestations. KEYWORDS: chronic atrophic gastritis, intestinal metaplasia, gastric cancer, Helicobacter pylori, autoimmune gastritis, gastroprotection, carcinoprevention, eradication therapy, rebamipide. FOR CITATION: Livzan M.A., Gaus O.V., Mozgovoi S.I. Chronic atrophic gastritis: patient management. Russian Medical Inquiry. 2021;5(6):427–432 (in Russ.). DOI: 10.32364/2587-6821-2021-5-6-427-432.

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Tryapitsyn, Aleksandr V., Vladimir A. Malkov, Emil M. Gasanov, and Ilya Belyakov. "Chronic gastritis and precancerous diseases of the stomach: Is there a chance of a correct diagnosis?" HERALD of North-Western State Medical University named after I.I. Mechnikov 13, no. 1 (June 8, 2021): 85–102. http://dx.doi.org/10.17816/mechnikov60431.

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AIM: The purpose of the study is to investigate the occurrence of the main forms of chronic gastritis, metaplastic and dysplastic changes in the gastric mucosa, the degree of their severity, and to assess their potential risk for the development of gastric cancer. MATERIALS AND METHODS: The study involved 2982 patients who underwent esophagogastroduodenoscopy with a standard biopsy of the gastric mucosa for morphological assessment and bacterioscopy. If autoimmune gastritis was suspected, an additional serological diagnosis was performed. When detecting intestinal metaplasia of the gastric mucosa as well as neoplastic changes according to the histological report, the description of this report was analyzed in order to identify possible equivalents in the macroscopic description of the mucous membrane. RESULTS: Out of 2982 histological studies of gastric mucosa biopsies, 1273 cases (42.7%) were found to contain H. pylori contamination. In 726 cases (24.3%), intestinal metaplasia. 66 biopsies (2.21%) showed the presence of low-grade intraepithelial neoplasia of the mucosa, 2 biopsies showed indeterminate neoplasia and 4 biopsies showed high-grade neoplasia. In 3 out of the total number of the samples, intravascular gastric adenocarcinoma was detected. In 168 cases (5.6%), gastritis was detected with predominant inflammation of the fundal region characteristic of autoimmune gastritis. In 286 biopsies (10.6%), inflammatory and/or atrophic changes and/or metaplastic changes were preserved, which, as a rule, did not have high activity and pronounced inflammation. In the remaining 1279 cases (42.9%), there was no significant inflammation or atrophic changes. The analysis of endoscopic findings showed that the detectability of intestinal metaplasia of the gastric mucosa without a biopsy study was 13.3%. DISCUSSION OF THE RESULTS: According to the results of the conducted research and analysis, it can be stated that at present, the correct diagnosis of chronic gastritis with the establishment of the etiological factor, prognosis and risks of stomach cancer development is practically not feasible within the modern health care system. This not only deprives a doctor of the opportunity to make a correct diagnosis and prescribe adequate treatment to a patient, but also makes almost all cascades of carcinogenesis, including early cancer, invisible.

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Kato, Minoru, Noriya Uedo, Ervin Toth, Satoki Shichijo, Akira Maekawa, Takashi Kanesaka, Yoji Takeuchi, et al. "Differences in image-enhanced endoscopic findings between Helicobacter pylori-associated and autoimmune gastritis." Endoscopy International Open 09, no. 01 (January 2021): E22—E30. http://dx.doi.org/10.1055/a-1287-9767.

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Abstract Background and study aims The aim of this study was to elucidate the differences in image-enhanced endoscopy (IEE) findings between Helicobacter-pylori-associated and autoimmune gastritis. Patients and methods Seven H. pylori-naïve, 21 patients with H. pylori-associated gastritis and seven with autoimmune gastritis were enrolled. Mucosal atrophy in the corpus was evaluated using autofluorescence imaging and classified into small, medium and large. In a 2 × 2-cm area of the lesser curvature of the lower corpus, micromucosal pattern was evaluated by magnifying narrow band imaging and proportion of foveola (FV)- and groove (GR)-type mucosa was classified into FV > 80 %, FV 50 % to 80 %, GR 50 % to 80 %, and GR > 80 %, then a biopsy specimen was taken. Results Fifteen of 21 (71 %) H. pylori-associated gastritis patients exhibited medium-to-large atrophic mucosa at the corpus lesser curvature. All autoimmune gastritis patients had large atrophic mucosa throughout the corpus (P < 0.001). All H. pylori-naïve patients had the FV > 80 % micromucosal pattern. Nineteen of 21 (90 %) H. pylori-associated gastritis patients had varying proportions of GR- and FV-type mucosae and five of seven (71 %) autoimmune gastritis patients showed FV > 80 % mucosa (P < 0.001). Compared with patients who were H. pylori-naïve, patients with H. pylori-associated and autoimmune gastritis exhibited a higher grade of atrophy (P < 0.001), but only patients with H. pylori-associated gastritis showed a higher grade of intestinal metaplasia (P = 0.022). Large mucosal atrophy with FV > 80 % micromucosal pattern had sensitivity of 71 % (95 % CI: 29 %–96 %) and specificity of 100 % (95 % CI: 88 % to 100 %) for diagnosis of autoimmune gastritis. Conclusions IEE findings of the gastric corpus differed between H. pylori-associated and autoimmune gastritis, suggesting different pathogenesis of the two diseases.

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Mohsin, Luma, Faiza Jamil, Muhammad Uzair Lodhi, Natasha Ahmed, Michael Richins, and Ahmed Mahmood. "S3176 Autoimmune Metaplastic Atrophic Gastritis in a Patient of South American Descent." American Journal of Gastroenterology 116, no. 1 (October 2021): S1308. http://dx.doi.org/10.14309/01.ajg.0000786236.28322.bd.

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Nehme, Fredy, Kyle Rowe, William Palko, Nathan Tofteland, and William Salyers. "Autoimmune metaplastic atrophic gastritis and association with neuroendocrine tumors of the stomach." Clinical Journal of Gastroenterology 13, no. 3 (November 28, 2019): 299–307. http://dx.doi.org/10.1007/s12328-019-01074-7.

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14

Jeong, Sangho, Eunyoung Choi, Christine P. Petersen, Joseph T. Roland, Alessandro Federico, Rossana Ippolito, Francesco P. D'Armiento, et al. "Distinct metaplastic and inflammatory phenotypes in autoimmune and adenocarcinoma‐associated chronic atrophic gastritis." United European Gastroenterology Journal 5, no. 1 (February 2017): 37–44. http://dx.doi.org/10.1177/2050640616644142.

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15

Dunn, Andrew L. J., Michael G. Drage, Christa L. Whitney-Miller, Loralee A. McMahon, and Raul S. Gonzalez. "Gastrin Staining in Inflamed Stomach Biopsies Labeled as “Antral” Rarely Detects Atrophic Gastritis." American Journal of Clinical Pathology 154, no. 6 (July 7, 2020): 761–66. http://dx.doi.org/10.1093/ajcp/aqaa098.

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Abstract Objectives Autoimmune metaplastic atrophic gastritis (AMAG) is an underrecognized entity, especially in its early stage. This study assessed whether the use of gastrin immunohistochemistry would increase sensitivity for diagnosing early AMAG. Methods Three-hundred gastric biopsies were prospectively stained for gastrin by immunohistochemistry. Inclusion criteria included well-oriented gastric mucosa with mucus glands and minimal plasma cell infiltrate not suspected to represent pyloric metaplasia. Patient age, sex, designated location of biopsy, presence or absence of intestinal metaplasia, and clinical information were not criteria. Any case with absence of gastrin-positive endocrine cells reflexed to chromogranin immunohistochemistry. Maloriented biopsies or cases with current Helicobacter infection were excluded. Results The 298-patient study cohort comprised 222 females (mean age, 47 years; range, 16-80 years) and 76 males (mean age, 49 years; range, 7-80 years). Biopsies were designated as “antral/antral nodules” (61%), and the rest were labeled “gastric/random stomach” (39%). Nine cases (3%) exhibited absence of gastrin-positive endocrine cells; one of those showed endocrine cell hyperplasia by chromogranin staining. Conclusions Pathologists should be aware of the histologic features of early AMAG and meticulously analyze tissue regardless of specimen labeling. Gastrin immunostain is a supplemental diagnostic tool when encountering inflamed antral-appearing specimens.

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Rustgi, Sheila D., Priyesha Bijlani, and Shailja C. Shah. "Autoimmune gastritis, with or without pernicious anemia: epidemiology, risk factors, and clinical management." Therapeutic Advances in Gastroenterology 14 (January 2021): 175628482110387. http://dx.doi.org/10.1177/17562848211038771.

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Autoimmune gastritis (AIG) is a chronic immune-mediated, inflammatory condition that involves the destruction of the gastric oxyntic mucosa through the autoimmune-mediated loss of parietal cells, with replacement by atrophic and metaplastic tissue. Diagnosing AIG is important, given the need for ongoing clinical management and vigilance with respect to downstream complications, the most serious of which is gastric adenocarcinoma. Other clinical consequences include gastric neuroendocrine tumors, consequences related to decreased gastric acid and decreased intrinsic factor due to parietal cell destruction and antibodies against intrinsic factor (e.g. micronutrient deficiencies), as well as concomitant autoimmune disorders. Considering the prevalence of AIG and the potential for severe clinical outcomes, it is important to engage in efforts to reduce practice pattern variability related to diagnosis and management. Accordingly, herein, we review of the epidemiology, pathogenesis, clinical presentation of AIG, including both gastric and extragastric manifestations, and provide an overview of clinical management.

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Mihály, Emese, Tamás Micsik, Márk Juhász, László Herszényi, and Zsolt Tulassay. "Gastritis and gastropathy." Orvosi Hetilap 155, no. 2 (January 2014): 43–61. http://dx.doi.org/10.1556/oh.2014.29807.

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Alterations of the stomach mucosa in response to different adverse effects result in various morphological and clinical symptoms. Gastric mucosa alterations can be classified on the bases of diverse viewpoints. It makes this overview difficult, that identical toxic effects may cause different mucosal changes and different toxic agents may produce similar mucosal appearance. The more accurate understanding of the pathological processes which develop in the stomach mucosa needs reconsideration. The authors make an attempt to define gastritis and gastropathy in order to classify and present their features. Gastritis is a histological definition indicating mucosal inflammation. Acute gastritis is caused by infections. The two most important forms of chronic gastritis are metaplastic atrophic gastritis with an autoimmune origin and Helicobacter pylori inflammation. Gastropathy is the name of different structural alterations of the mucosa. Its most important feature is the paucity of inflammatory signs. Gastropathies can be divided into 4 categories based on the nature of the underlying pathological effect, on its morphological appearance and the way of the development. Differential diagnosis is an important pathological and clinical task because different treatment methods and prognosis. Orv. Hetil., 2014, 155(2), 43–61.

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Zhang, Hejun, Xueqiong Nie, Zhiqiang Song, Rongli Cui, and Zhu Jin. "Hyperplastic polyps arising in autoimmune metaplastic atrophic gastritis patients: is this a distinct clinicopathological entity?" Scandinavian Journal of Gastroenterology 53, no. 10-11 (October 24, 2018): 1186–93. http://dx.doi.org/10.1080/00365521.2018.1514420.

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Nehme, Fredy, Michael Green, William Salyers, and Nathan Tofteland. "Case Series of Autoimmune Metaplastic Atrophic Gastritis and Association with Neuroendocrine Tumors of the Stomach." American Journal of Gastroenterology 111 (October 2016): S1149. http://dx.doi.org/10.14309/00000434-201610001-02359.

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Bloomquist, Maria S., and Shilpa Jain. "Su1255 – Autoimmune Metaplastic Atrophic Gastritis (AMAG) – Better Precise Than Random: A Retrospective Single Institution Review." Gastroenterology 156, no. 6 (May 2019): S—521—S—522. http://dx.doi.org/10.1016/s0016-5085(19)38181-8.

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Akhtar, D., M. A. Donaldson, N. H. Akhtar, H. Yang, and F. Donnellan. "A136 A RARE CAUSE OF AUTOIMMUNE ATROPHIC PANGASTRITIS COMPLICATED WITH GASTRIC OUTLET OBSTRUCTION." Journal of the Canadian Association of Gastroenterology 5, Supplement_1 (February 21, 2022): 7–8. http://dx.doi.org/10.1093/jcag/gwab049.135.

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Abstract Background Chronic gastritis comes in two well recognized forms: environmental, which is most commonly antral or multifocal in distribution and is typically caused by Helicobacter Pylori (HP) infection, and autoimmune gastritis(AIG), which affects the corpus and fundus. Presented here is a case of autoimmune atrophic pangastritis(AIAP). Aims To increase awareness of a rare condition with limited data on available treatment modalities. Methods Case Report Results A 68-year old female with autoimmune hypothyroidism, presented with weight loss and elevated anti-TTG serology. Index esophagogastroduodenoscopy (EGD) biopsies demonstrated chronic non-specific gastritis limited to the antrum. Strict gluten free diet adherence was initiated. Testing for HLA revealed HLADq2 and HLADq8 negativity but HLADq2.5 positivity. Subsequent EGD showed a markedly atrophic appearing gastric body. The corresponding biopsies demonstrated persistent moderately chronic active gastritis with severe atrophy now involving the body, fundus and antrum. The biopsies were negative for HP. Notably, there was a lack of ECL-cell hyperplasia and the number of antral G cells appeared decreased. Anti-parietal cell antibody serology was positive with a titre of 1:80. Despite combination therapy with budesonide and mesalamine and treatment for HP given persistent symptoms, the patient’s course was further complicated by gastric-outlet obstruction (GOO). Urgent EGD biopsies showed pyloric stenosis requiring dilation. Endoscopic Ultrasound (EUS) guided biopsies were negative for malignancy. The patient was started on corticosteroids and azathioprine(AZA). Most recently, an EGD on AZA, continued to demonstrate severe chronic active pangastritis now with intestinal metaplasia involving the body. Corticosteroid therapy was reinitiated with a plan to start mycophenolate mofetil (MMF). Conclusions AIAP is a rarely described entity, not well documented in the literature. An eight patient case series reported a distinctive form of atrophic gastritis that was independent of HP infection with the absence of neuroendocrine hyperplasia that involved the body and antrum. Thyroid disease, specifically Hashimoto thyroiditis is present in about 40% of patients with AIG. Additionally, AIG progression to atrophic gastritis with intestinal metaplasia confers an increased risk for gastric adenocarcinoma in more than 10% of patients. Limited literature exists regarding the management of AIAP. Pediatric data suggests the use of prednisone and/or azathioprine for AIAP. Furthermore, a recent case report of AIAP demonstrated clinical and endoscopic remission with MMF. Currently, no guidelines exist for the treatment, screening and monitoring of patients with AIAP. This case report presents a rare case of AIAP refractory to AZA complicated with GOO and adds to the little literature that exists. Funding Agencies None

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Woodford, Amanda M., Rabhea Chaudhry, Gabriella A. Conte, Varsha Gupta, and Madhurima Anne. "Chronic Atrophic Gastritis Presenting as Hemolytic Anemia due to Severe Vitamin B12 Deficiency." Case Reports in Hematology 2021 (July 31, 2021): 1–5. http://dx.doi.org/10.1155/2021/9571072.

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Vitamin B12 is an essential nutrient which plays an important role in neurological function, hematopoiesis, and DNA synthesis. Low levels usually stem from either poor intake or a malabsorptive process. Presently, the most common cause of vitamin B12 deficiency is food-bound cobalamin malabsorption, which occurs when there is impaired release of vitamin B12 from ingested food due to an outstanding factor preventing the release of the nutrient from its transport protein. Such causes include achlorhydria, gastritis, gastrectomy, or the use of PPIs or antacids. A rarer cause is autoimmune chronic atrophic gastritis, resulting in pernicious anemia. In this disease process, there is destruction of parietal cells and thus a reduction in intrinsic factor, which is essential to the absorption of vitamin B12. Deficiency will result in a variety of abnormalities including but not limited to pancytopenia, paresthesias, and neuropsychiatric symptoms. A rare manifestation of vitamin B12 deficiency is hemolytic anemia, which occurs due to intramedullary and extramedullary dysfunction. This case describes a 46-year-old male with no past medical history who presented with chest pain, fatigue, and progressive weakness, found to have hemolytic anemia, ultimately attributed to vitamin B12 deficiency. Antiparietal cell antibodies and intrinsic factor antibodies (IFA) were both negative. Still, the patient underwent an endoscopy with biopsies of the stomach; pathology was consistent with chronic metaplastic atrophic gastritis. The patient improved with intramuscular vitamin B12 supplementation. This case highlights both a rare cause and presentation of vitamin B12 deficiency. Patients with autoimmune chronic atrophic gastritis should have antiparietal cell or intrinsic factor antibodies. Still, seronegative patients have been reported, like this patient. Additionally, hemolytic anemia secondary to vitamin B12 deficiency is uncommon. The presentation will usually mirror that of a thrombotic microangiopathy (TMA), including hemolytic anemia with schistocytes on peripheral blood smear and thrombocytopenia, as it did in this patient. This clinical entity is described as pseudothrombotic microangiopathy and is crucial to identify in order to prevent the initiation of invasive treatment strategies such as plasmapheresis.

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Chen, Chuyan, Yi Yang, Peng Li, and Haiyi Hu. "Incidence of Gastric Neoplasms Arising from Autoimmune Metaplastic Atrophic Gastritis: A Systematic Review and Case Reports." Journal of Clinical Medicine 12, no. 3 (January 30, 2023): 1062. http://dx.doi.org/10.3390/jcm12031062.

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Autoimmune metaplastic atrophic gastritis (AMAG) is associated with an increased risk of gastric neoplasms. This study aimed to systematically analyze the incidence rate of gastric cancer (GC), low-grade dysplasia (LGD) and type-1 gastric neuroendocrine tumor (gNETs) development in AMAG adults. Studies on AMAG patients reporting the incidence of gastric neoplasms was identified through a systematic search in PUBMED and EMBASE. Study quality was assessed using the Joanna Briggs Institute quality assessment tool. Incidence rates of GC, LGD and type-1 gNETs were examined by meta-analysis. Thirteen studies met eligibility criteria. Incidence rate of gastric cancer calculated from the pooled data was 0.14% per person-year in both single-center studies and national registration studies. Meta-analysis showed a relative risk of 11.05 (95% CI: 6.39–19.11) for gastric cancer development in AMAG patients. The calculated pooled gastric LGD and type-1 gNETs incidence rates were 0.52% and 0.83% per person-year, respectively. As for experience from our center, we presented three distinctive cases of gastric neoplasm arising from the background of AMAG. This study underscores the potential for malignant transformation of precancerous lesions and reiterates the importance of careful esophagogastroduodenoscopy screening.

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Zhang, Hejun, Zhu Jin, Rongli Cui, Shigang Ding, Yonghui Huang, and Liya Zhou. "Autoimmune metaplastic atrophic gastritis in chinese: a study of 320 patients at a large tertiary medical center." Scandinavian Journal of Gastroenterology 52, no. 2 (September 27, 2016): 150–56. http://dx.doi.org/10.1080/00365521.2016.1236397.

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Zhang, Hejun, Zhu Jin, Rongli Cui, Xueqiong Nie, and Shigang Ding. "Su1233 - Gastric Hyperplastic Polyps in Patients with Autoimmune Metaplastic Atrophic Gastritis at a Large Tertiary Medical Center." Gastroenterology 154, no. 6 (May 2018): S—512. http://dx.doi.org/10.1016/s0016-5085(18)31933-4.

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Rana, Zaid, Linoj Panicker, Jamie L. Skrove, Juan Sarol, Lizette Duckworth, and Javier Sobrado. "Can You See the Carcinoid Tumor? A Case of Autoimmune Metaplastic Atrophic Gastritis (AMAG) and Carcinoid Tumor." American Journal of Gastroenterology 113, Supplement (October 2018): S1687. http://dx.doi.org/10.14309/00000434-201810001-03086.

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Zecchini, R., F. Azzolini, P. Cecinato, V. Iori, L. De Marco, M. Zanelli, F. Parmeggiani, et al. "P.05.4 A RARE CASE OF MIXED ADENO-NEUROENDOCRINE GASTRIC CARCINOMA (MANEC) ASSOCIATED TO AUTOIMMUNE METAPLASTIC ATROPHIC GASTRITIS (AMAG)." Digestive and Liver Disease 48 (February 2016): e148. http://dx.doi.org/10.1016/s1590-8658(16)30195-5.

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Stashek, Kristen M., Rashmi Tondon, Stuti G. Shroff, Robert Roses, Emma E. Furth, and David C. Metz. "Tu1298 Neoplasia in Patients With Atrophic Metaplastic Autoimmune Gastritis (AMAG): Screening and Surveillance Endoscopy Should Become Standard of Care." Gastroenterology 150, no. 4 (April 2016): S868. http://dx.doi.org/10.1016/s0016-5085(16)32924-9.

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Mahmud, Nadim, Kristen M. Stashek, Bryson W. Katona, Rashmi Tondon, Stuti G. Shroff, Robert E. Roses, Emma E. Furth, and David C. Metz. "Tu1320 - The Prevalence and Incidence of Neoplasia in Patients with Autoimmune Metaplastic Atrophic Gastritis: A Renewed Case for Surveillance Endoscopy." Gastroenterology 154, no. 6 (May 2018): S—933. http://dx.doi.org/10.1016/s0016-5085(18)33146-9.

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Badamas, Jemilat, Mark Lazarev, Sameer Dhalla, and Elizabeth Montgomery. "Prevalence of Anemia, Vitamin B12 Deficiency and Gastric Neoplastic Lesions are Similar in African Americans and Caucasians with Autoimmune Metaplastic Atrophic Gastritis." American Journal of Gastroenterology 106 (October 2011): S49. http://dx.doi.org/10.14309/00000434-201110002-00121.

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Lopez-Diaz, Lymari, Karen L. Hinkle, Renu N. Jain, Yana Zavros, Cynthia S. Brunkan, Theresa Keeley, Kathryn A. Eaton, Juanita L. Merchant, Catherine S. Chew, and Linda C. Samuelson. "Parietal cell hyperstimulation and autoimmune gastritis in cholera toxin transgenic mice." American Journal of Physiology-Gastrointestinal and Liver Physiology 290, no. 5 (May 2006): G970—G979. http://dx.doi.org/10.1152/ajpgi.00461.2005.

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The stimulation of gastric acid secretion from parietal cells involves both intracellular calcium and cAMP signaling. To understand the effect of increased cAMP on parietal cell function, we engineered transgenic mice expressing cholera toxin (Ctox), an irreversible stimulator of adenylate cyclase. The parietal cell-specific H+,K+-ATPase β-subunit promoter was used to drive expression of the cholera toxin A1 subunit (CtoxA1). Transgenic lines were established and tested for Ctox expression, acid content, plasma gastrin, tissue morphology, and cellular composition of the gastric mucosa. Four lines were generated, with Ctox-7 expressing ∼50-fold higher Ctox than the other lines. Enhanced cAMP signaling in parietal cells was confirmed by observation of hyperphosphorylation of the protein kinase A-regulated proteins LASP-1 and CREB. Basal acid content was elevated and circulating gastrin was reduced in Ctox transgenic lines. Analysis of gastric morphology revealed a progressive cellular transformation in Ctox-7. Expanded patches of mucous neck cells were observed as early as 3 mo of age, and by 15 mo, extensive mucous cell metaplasia was observed in parallel with almost complete loss of parietal and chief cells. Detection of anti-parietal cell antibodies, inflammatory cell infiltrates, and increased expression of the Th1 cytokine IFN-γ in Ctox-7 mice suggested that autoimmune destruction of the tissue caused atrophic gastritis. Thus constitutively high parietal cell cAMP results in high acid secretion and a compensatory reduction in circulating gastrin. High Ctox in parietal cells can also induce progressive changes in the cellular architecture of the gastric glands, corresponding to the development of anti-parietal cell antibodies and autoimmune gastritis.

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Petersson, F., K. Borch, and L. E. Franzén. "Prevalence of Subtypes of Intestinal Metaplasia in the General Population and in Patients with Autoimmune Chronic Atrophic Gastritis." Scandinavian Journal of Gastroenterology 37, no. 3 (January 2002): 262–66. http://dx.doi.org/10.1080/003655202317284156.

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Dilaghi, Emanuele, Gianluca Esposito, Giulia Pivetta, Gloria Galli, Emanuela Pilozzi, Bruno Annibale, and Edith Lahner. "Endoscopic diagnosis of gastric intestinal metaplasia in patients with autoimmune gastritis using narrow-band imaging: does pseudopyloric metaplasia muddy the waters?" Endoscopy International Open 10, no. 04 (April 2022): E434—E440. http://dx.doi.org/10.1055/a-1776-7628.

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Abstract Background and study aims In autoimmune atrophic gastritis (AAG), associated with intestinal (IM) and/or pseudopyloric metaplasia (PPM), endoscopic surveillance is recommended for gastric cancer risk mainly linked to IM. Endoscopic Grading of Gastric Intestinal Metaplasia (EGGIM) reliably identifies IM, but has not been assessed in AAG. We aimed to assess the performance of EGGIM (index test) versus histology (reference test) of corpus IM in AAG. Patients and methods This was a cross-sectional study of 210 AAG patients undergoing surveillance gastroscopy with narrow-band imaging (NBI): corpus IM scored according to EGGIM, histology according to updated Sydney system, and morphological criteria. Results NBI identified corpus IM in 88.6 % of AAG patients: EGGIM were 0, 1, 2, 3, 4 in 11.4 %, 0.5 %, 33.3 %, 1.9 %, and 52.9 %, respectively. Histology identified corpus IM in 78.1 % and PPM in 79.5 % of patients. PPM was present with IM in 57.6 % and without IM in 21.9 % patients, 20.5 % had IM without PPM. EGGIM, compared to histology, correctly classified 76.2 % of patients, showing high sensitivity (91.5 %, 95 %CI 86.1–95.3). EGGIM correctly classified 93 % of patients with IM without PPM, 90.9 % with both metaplasias, and 21.7 % with PPM without IM yielding low specificity (21.7 %, 95 %CI 10.9–36.4). Conclusions In AAG, EGGIM showed high accuracy and sensitivity identifying > 90 % of patients with histological corpus IM. EGGIM overestimated IM when PPM without IM was present, yielding low specificity. These findings raise the question of whether in AAG, PPM and IM may display similar endoscopic features on NBI.

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Jeong, Sangho, Eunyoung Choi, Christine Petersen, Joseph T. Roland, Alessandro Federico, Francesco P. D, Marco Romano, and James R. Goldenring. "270 Autoimmune Atrophic Gastritis in Humans Is Associated With SPEM and Intestinal Metaplasia but Shows Low Proliferation and Reduced Macrophage and Neutrophil Infiltrates." Gastroenterology 146, no. 5 (May 2014): S—65. http://dx.doi.org/10.1016/s0016-5085(14)60229-8.

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Park, Do Youn. "Histopathologic Diagnosis of Atrophic Gastritis and Intestinal Metaplasia." Korean Journal of Helicobacter and Upper Gastrointestinal Research 20, no. 2 (June 10, 2020): 96–100. http://dx.doi.org/10.7704/kjhugr.2020.0011.

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Atrophic gastritis and intestinal metaplasia are well-known to be reliable indicators of gastric cancer risk. They are clinically important in deciding whether to recommend endoscopic surveillance. Herein I review the histopathologic diagnosis of atrophic gastritis and IM. Gastric atrophy is divided into metaplastic atrophy and non-metaplastic atrophy. IM is categorized as complete (type I) and incomplete (type II, III). Systematic interpretation of gastric atrophy and IM using the updated Sydney system or operative link on gastritis assessment is recommended. Furthermore, I suggest using the consensus definition of gastric atrophy and incomplete IM in the gastric biopsy pathology report to support the surveillance of high-risk gastric cancer group.

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Minalyan, Artem, Jihane N. Benhammou, Aida Artashesyan, Michael Lewis, and Joseph R. Pisegna. "Autoimmune atrophic gastritis: current perspectives." Clinical and Experimental Gastroenterology Volume 10 (February 2017): 19–27. http://dx.doi.org/10.2147/ceg.s109123.

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Yagi, Kazuyoshi, Atsuo Nakamura, Atsuo Sekine, and David Graham. "Features of the Atrophic Corpus Mucosa in Three Cases of Autoimmune Gastritis Revealed by Magnifying Endoscopy." Case Reports in Medicine 2012 (2012): 1–4. http://dx.doi.org/10.1155/2012/368160.

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Atrophic gastritis, whether caused byHelicobacter pyloriinfection or as a result of an autoimmune process, is associated with corpus atrophy. However, whereas atrophic gastritis caused byH. pyloriinvolves the antrum, the antrum is spared in autoimmune gastritis. Here, we report the use of magnifying endoscopy to identify and distinguish atrophic gastritis caused byH. pylorifrom autoimmune gastritis. The mucosal pattern in autoimmune gastritis is that of closely arranged small round and oval pits, thus differing from the pattern seen in atrophic mucosa due toH. pyloriinfection. We speculate that this reflects differences in inflammation between the two types of gastritis. In autoimmune gastritis the inflammation is directed primarily against gastric glands, whereas inH. pyloriinfection the inflammation is directed against the bacteria on or near the surface and the damage initially affects the surface epithelium. During repair, the normal regular round pits are destroyed, whereas they remain largely intact in mucosa with autoimmune-associated atrophy. Confirmation of the features of autoimmune gastritis revealed by magnifying endoscopy would not only make the endoscopic diagnosis of autoimmune gastritis more accurate, but also help to elucidate changes in the surface epithelial structure of gastritis due to various causes.

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Kim, Young Jung, Sun-Young Lee, Hojun Yang, Jeong Hwan Kim, In-Kyung Sung, and Hyung Seok Park. "Nodular Gastritis as a Precursor Lesion of Atrophic and Metaplastic Gastritis." Korean Journal of Gastroenterology 73, no. 6 (2019): 332. http://dx.doi.org/10.4166/kjg.2019.73.6.332.

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Mahadik, J., K. Patel, and N. Cortes-Santiago. "Epstein-Barr Virus associated gastric carcinoma in a patient with germline STAT3 gain-of-function mutation." American Journal of Clinical Pathology 156, Supplement_1 (October 1, 2021): S65. http://dx.doi.org/10.1093/ajcp/aqab191.134.

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Abstract Introduction/Objective Signal transducer and activator of transcription 3 (STAT3) is a transcription factor involved in inflammation, proliferation, differentiation and survival. STAT3 gain-of-function (GoF) disorders are characterized by immune dysregulation and present with polyendocrinopathy, enteropathy, X-linked syndrome (IPEX)- or autoimmune lymphoproliferative syndrome (ALPS)-like features. While patients with STAT-3 GoF are known to have an increased risk for hematologic malignancies, neither solid tumors nor an increased risk for EBV-associated disorders have been described. We report the first case of an EBV-associated solid organ tumor in a patient with STAT-3 GoF. Methods/Case Report A 21-year-old male with germline mutation in STAT3 (variant p. M329K) presented with early satiety, abdominal pain and worsening of chronic anemia. Serology showed high EBV DNA PCR levels. Endoscopy showed multiple nodular lesions in the stomach, which were biopsied to reveal EBV-associated high-grade dysplasia and intramucosal adenocarcinoma. Initiation of chemotherapy with a poor response led to a total gastrectomy. Gross examination of the specimen showed a 7.9 x 6.5 x 1.8 cm tan-brown, exophytic mass in the posterior wall of the body and antrum, involving the greater curvature. Histology revealed an adenocarcinoma with tubulovillous morphology extending into the lamina propria, without invasion into the muscularis mucosa or submucosa. EBER in-situ hybridization was diffusely positive in the tumor cells. The background mucosa showed severe chronic active and atrophic gastritis with intestinal metaplasia and low-grade dysplasia. All the seventy examined lymph nodes were negative for metastasis. Helicobacter-like organisms were not seen. Results (if a Case Study enter NA) NA Conclusion This is the first report of a solid tumor in a patient with STAT3 GoF mutation. The role of the patient’s underlying immune dysregulation disorder in the development of EBV-associated gastric adenocarcinoma is unclear and warrants further investigation. The case also highlights the importance of a close clinical follow-up in this patient population, as unexpected malignancies can develop at younger ages.

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Avasthi, Deepti, Jean Thomas, Leela Krishna Vamsee Miriyala, and Salil Avasthi. "Autoimmune atrophic gastritis in systemic sclerosis." BMJ Case Reports 14, no. 8 (August 2021): e242851. http://dx.doi.org/10.1136/bcr-2021-242851.

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Systemic sclerosis (SSc) is a rare connective tissue disorder with a complex pathogenesis involving vascular dysfunction, small vessel proliferation as well as alterations of innate and adaptive immunity. Gastrointestinal (GI) involvement in SSc is almost universal and affects nearly 90% of the patients. Of all the GI manifestations, 30%–75% are oesophageal abnormalities, including gastro-oesophageal reflux disease, reflux oesophagitis and Barret’s oesophagus. The incidence of gastric manifestations is about 22% with a common presentation of gastric antral vascular ectasia (GAVE). However, autoimmune atrophic gastritis (AIG) is not a known manifestation of SSc. Our case has a unique presentation of the coexistence of GAVE and AIG. We have conducted a thorough literature review to study a possible association of AIG and SSc and understand the pathology of SSc.

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Lenti, M. V., D. Padula, A. Dequarti, E. Miceli, C. Alvisi, O. Luinetti, A. Di Sabatino, M. Di Stefano, and G. R. Corazza. "OC.07.9 POTENTIAL AUTOIMMUNE ATROPHIC GASTRITIS." Digestive and Liver Disease 48 (February 2016): e98. http://dx.doi.org/10.1016/s1590-8658(16)30076-7.

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Lee, Sean. "Stomach This: A Novel Type of Gastritis." Gastroenterology Pancreatology and Hepatobilary Disorders 5, no. 6 (October 1, 2021): 01–04. http://dx.doi.org/10.31579/2641-5194/032.

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Atrophic gastritis can be environmental in origin and involve the antrum or autoimmune in origin and involve the body and fundus. We present a rare case of autoimmune atrophic pangastritis (AIAP), a distinct type of autoimmune gastritis (AIG) affecting the entire stomach, which should be considered in patients with other autoimmune disorders.

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Conti, Laura, Bruno Annibale, and Edith Lahner. "Autoimmune Gastritis and Gastric Microbiota." Microorganisms 8, no. 11 (November 19, 2020): 1827. http://dx.doi.org/10.3390/microorganisms8111827.

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Autoimmune atrophic gastritis is an organ-specific immune-mediated condition characterized by atrophy of the oxyntic mucosa. Autoimmune atrophic gastritis (AIG) is characterized by a progressive loss of acid-secreting parietal cells leading to hypo-achlorhydria. Due to this peculiar intra-gastric environment, gastric microbiota composition in individuals with autoimmune atrophic gastritis was first supposed and then recently reported to be different from subjects with a normal acidic healthy stomach. Recent data confirm the prominent role of Helicobacter pylori as the main bacterium responsible for gastric disease and long-term complications. However, other bacteria than Helicobacter pylori, for example, Streptococci, were found in subjects who developed gastric cancer and in subjects at risk of this fearful complication, as well as those with autoimmune gastritis. Gastric microbiota composition is challenging to study due to the acidic gastric environment, the difficulty of obtaining representative samples of the entire gastric microbiota, and the possible contamination by oral or throat microorganisms, which can potentially lead to the distortion of the original gastric microbial composition, but innovative molecular approaches based on the analysis of the hyper-variable region of the 16S rRNA gene have been developed, permitting us to obtain an overall microbial composition view of the RNA gene that is present only in prokaryotic cells.

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Rugge, Massimo, Matteo Fassan, Fabio Farinati, and Robert M. Genta. "The war of the worlds: metaplastic versus nonmetaplastic atrophic gastritis." Gastrointestinal Endoscopy 73, no. 2 (February 2011): 411–12. http://dx.doi.org/10.1016/j.gie.2010.06.030.

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Turner, Kevin, and Robert M. Genta. "Sa1252 Barrett's Esophagus: The Inverse Association With Non-atrophic Helicobacter Gastritis Is Stronger Than With Atrophic Metaplastic Gastritis." Gastroenterology 150, no. 4 (April 2016): S257—S258. http://dx.doi.org/10.1016/s0016-5085(16)30923-4.

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Lenti, Marco Vincenzo, Emanuela Miceli, Donatella Padula, Antonio Di Sabatino, and Gino Roberto Corazza. "The challenging diagnosis of autoimmune atrophic gastritis." Scandinavian Journal of Gastroenterology 52, no. 4 (December 31, 2016): 471–72. http://dx.doi.org/10.1080/00365521.2016.1275771.

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Neumann, William L., Elizabeth Coss, Massimo Rugge, and Robert M. Genta. "Autoimmune atrophic gastritis—pathogenesis, pathology and management." Nature Reviews Gastroenterology & Hepatology 10, no. 9 (June 18, 2013): 529–41. http://dx.doi.org/10.1038/nrgastro.2013.101.

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Zauli, Daniela, Antonella Tosti, G. Biasco, F. Miserocchi, Annalisa Patrizi, Daniela Azzaroni, G. Andriani, G. Di Febo, and Carla Callegari. "Prevalence of Autoimmune Atrophic Gastritis in Vitiligo." Digestion 34, no. 3 (1986): 169–72. http://dx.doi.org/10.1159/000199325.

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M. Yu. Zak, S. V. Muzyka, and M. O. Klymenko. "Autoimmune gastritis: problems of diagnosis and therapy." Modern Gastroenterology, no. 4 (September 30, 2019): 59–66. http://dx.doi.org/10.30978/mg-2019-4-59.

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Chronic gastritis (CG) is one of the most widespread internal diseases, which affects up to 20 % of the adult population. The modern CG paradigm considers disease as a launchpad for the formation of stomach cancer, as well as erosive and ulcerative lesions, including those induced by anti-inflammatory drugs’ intake. The widespread symptoms of gastric dyspepsia often lead to the CG overdiagnosis, while verification of the diagnosis should be based on clinical endoscopic and pathomorphological criteria. In recent years, a large body of scientific data has been presented on the role of different types of microorganisms, including H. Pylori bacteria, of the duodenogastric reflux, medications’ intake in the CG development and progression. However, the autoimmune form of this disease is poorly understood. It is well known that autoimmune gastritis (AIG) is the most important factor in the development of pernicious anemia, and hypochlorhydria leads to iron deficiency anemia. At the same time, the role of AIG in the formation of gastric atrophy and metaplasia is not well understood. A question of gastro-carcinogenic potential of AIG remains open. Diagnosis of AIG requires the determination of not only clinical endoscopic, histopathological parameters, but also a comprehensive analysis of serological data. From the standpoint of modern classifications: Kyoto consensus and the OLGA/OLGIM CG system, it is of interest to correlate between serological and pathological markers in patients with AIG. The treatment of AIG is not specific and does not fundamentally differ from the treatment of other forms of CG. However, given the pathogenetic features of AIG, the development of methods for the correction of immunopathological processes that characterize this disease is promising. AIG treatment is aimed of the infection eradication, restoration of the motor-evacuation function of the gastroduodenal zone, neutralizing the damaging effects of bile acids, but gastroprotection is a strategic direction in the treatment of the disease. In particular, the use of drugs based on bismuth salts promotes restoration of the structural and functional state of the gastric mucosa, inhibits the progression of AIG, as well as promotes regression of atrophy and intestinal metaplasia.

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Krolevets, T. S., M. A. Livzan, and S. I. Mozgovoy. "Hyperplasia of enterochromaffin-like (ECL) cells as a precursor of neuroendocrine gastric tumors in autoimmune gastritis." Experimental and Clinical Gastroenterology, no. 9 (October 7, 2022): 147–52. http://dx.doi.org/10.31146/1682-8658-ecg-205-9-147-152.

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The purpose of this publication is to update knowledge about chronic autoimmune gastritis and about cases of hyperplasia of enterochromaffin-like (ECL) cells as precursors of the development of neuroendocrine gastric tumor type 1 due to clinical example’s demonstration. Discussion: the types and main characteristics of neuroendocrine tumors of the stomach were discussed, in particular tumors type 1 associated with autoimmune gastritis. The mechanisms of formation of neuroendocrine tumors in the stomach against the background of an autoimmune process were presented, two clinical examples presenting the algorithm of diagnosis of autoimmune gastritis and associated neuroendocrine tumors were presented. Both clinical examples demonstrated the presence of subepithelial formations of the stomach body according to FGDS, which have not been morphologically identified. Timely repeated FGDS with sampling of biopsies according to the OLGA standard made it possible to verify the formations, and the serological markers helped in clarifying the diagnosis and morphological nature of tumors. Conclusion: analysis of clinical data, anamnesis and esophagoduodenoscopy with morphological evaluation of the gastric mucosa biopsy may help to find out the cause and nature of chronic inflammation in the gastric mucosa. Atrophy of the glands in the stomach body, pseudopiloric metaplasia, hyperplasia of enterochromaffin (ECL) cells are sufficient morphological criteria for autoimmune gastritis. The study of the level of chromogranin A in blood serum can be considered as a marker of the development of type 1 neuroendocrine gastric tumor in patients with autoimmune gastritis and the presence of polyps in the stomach body.

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