Academic literature on the topic 'Autoimmune Metaplastic Atrophic Gastritis'

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.

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.

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.”

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.

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.

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.

INTRODUCTION: Gastric cancer is the third leading cause of cancer mortality worldwide and the fifth for incidence. Atrophic gastritis and intestinal metaplasia are considered precancerous conditions on which dysplasia and gastric cancer could be developed. This transformation from normal gastric mucosa to gastric cancer is known as Correa’s cascade. Autoimmune gastritis is a chronic disease occurring in up to 8% of the general population. This condition is characterized by loss of the oxyntic glands with consequent hypochlorhydria, lack of intrinsic factor production, and, in a later stage, pernicious anemia. Cumulative evidence suggests that electronic chromoendoscopy with narrow band imaging (NBI) is highly accurate for the diagnosis of precancerous conditions. A new type of endoscopic classification has been proposed: the Endoscopic Grading of Gastric Intestinal Metaplasia (EGGIM) may be used to assess the risk of patients by the endoscopic assessment of IM in the antrum, in the incisura and in the corpus with the use of high resolution NBI scopes. AIMS: The aims of this project are: 1. To investigate the occurrence of and risk factors for gastric neoplastic lesions in patients with AIG and EAG 2. To investigate the role of electronic chromoendoscopy at follow-up in EAG and AIG in optimizing gastric preneoplastic and neoplastic lesions detection: comparison of the diagnostic yield with the use of NBI scopes of target oriented biopsies versus the updated Sydney system protocol with traditional white light (WL) scopes 3. To investigate specific endoscopic features at electronic chromoendoscopy of visible gastric polypoid lesions using HR-NBI compared to traditional WL gastroscopy in newly diagnosed and followed-up EAG and AIG patients. 4. To assess the cost-effectiveness of surveillance strategies based on independent risk factors in a low risk area to maximize the exploitation of the endoscopic resources in a longitudinal cohort study performed on patients with AIG and EAG. RESULTS: 1. MAG may be found in about one of three patients undergoing endoscopy for upper gastrointestinal symptoms. Clinical predictors are age older than 55 years, current smoking, active H. pylori infection, and postprandial fullness, especially for corpus-involving and corpus-restricted MAG. 2. More than half of AG patients complained of GI symptoms, in particular, dyspepsia, alone in 70% or associated to GERD in 17.7% of symptomatic patients, confirming the significant occurrence of symptoms in this population. In autoimmune gastritis patients, the demonstrated association between early satiety and postprandial fullness with younger age, no smoker and not anemic status should be kept in mind in the work-up of these patients. 3. GERD is not infrequent in atrophic body gastritis (ABG) being symptoms present in a quarter of patients, suggesting that ABG not exclude per se arising of oesophageal complaints. In ABG we found that microscopic esophagitis is a common finding but its clinical relevance remains to be investigated with further studies. 4. EGGIM classification showed a high diagnostic performance compared to OLGIM. This approach could be used to simplify the surveillance of these patients by avoiding biopsies. A possible confounding factor leading to overestimation of presence of intestinal metaplasia might be the presence of foveolar hyperplasia that should be taken into account before final staging is communicated to the patient. This endoscopic diagnostic tool could become a promising instrument for surveillance for gastric cancer. 5. When HR-endoscopy with NBI does not show suspicious areas of GIM, antrum and body biopsies can be sent in the same vial (when H. Pylori status is necessary) or do without biopsies when the purpose is only to detect patients with premalignant conditions deserving surveillance. 6. NBI analysis of the mucosal pattern seems to be effective to endoscopically discriminate between adenomas and HP, while the main characteristic of T1-GC seems to be the presence of a central erosion, sometimes with a clear demarcation line. The endoscopic NBI characterization of GPL may contribute to optimize the management of these lesions. 7. Our study provided a cost estimate of a 4-year endoscopic surveillance in Italy, and it showed how the restriction of an eventual program to subgroups of AG patients with pernicious anaemia may lead to a nearly 50% cost reduction still detecting 74% of gastric neoplastic lesions. CONCLUSIONS: Based on the studies conducted during this PhD project, the occurrence and risk factors for gastric neoplastic lesions in patients with AIG and EAG has been assessed; the role of electronic chromoendoscopy at follow-up in EAG and AIG in order to stage the presence of intestinal metaplasia and to distinguish between gastric polypoid lesions was demonstrated and the cost-effectiveness of surveillance strategies based on independent risk factors in a low risk area on patients with AIG and EAG was provided. In 2012 the first European guidelines on precancerous conditions (MAPS) where published and these studies were considered for the development of the update of this guideline in 2019 showing the importance of these evidences in the management of gastric precancerous conditions.

Autoimmune atrophic gastritis (AAG) is a slowly progressive organ-specific, immune-mediated condition, characterized by atrophy of the oxyntic mucosa with subsequent hypochlorhydria and hypergastrinemia. When this pathological process occurs, the subsequent reduced mass of specialized parietal cells can lead to impaired gastric acid and intrinsic factor secretion, eventually resulting in malabsorption of iron and vitamin B12 with consequent iron deficiency and/or pernicious anemia as well as an impairment of gastric microbiota composition and an increased risk of gastric tumours. The prevalence of AAG in the general population is estimated to be as high as 2-5%. Patients affected by AAG are likely to develop several neoplasms, in particular type-1 neuroendocrine tumors in percentage variable from 0.4% to 7% and gastric cancer (GC) with an incidence ranging between 0% and 1.8% per year. In AAG, the development towards GC depends on several factors such as conditions leading to an increased intragastric pH and oxidative stress, gastric microbiota composition, host factors such as the immune pathway, rather than environmental risk factors like smoke, alcohol, body mass index and diet. The increased GC risk associated to AAG emphasizes the importance of diagnosing and monitoring these patients, as recommended by the last European guidelines on diagnosis and management of precancerous gastric conditions (MAPS II). Many questions regarding the natural history of AAG and the risk factors for the development of GC in patients affected by AAG are still opened. On the basis of this scenario, several monocentric and multicentric studies were conducted within this PhD project with the aim to in-depth assess several clinical, biochemical, histological and immunological aspects, not previously investigated, that may contribute to better understand the natural history of AAG as well as the risk factors involved in gastric carcinogenesis and the best management of this gastric precancerous condition. Considering the studies performed on gastric microbiota and immunological pathways in AAG, we can consider them as the first pieces of evidence, and they certainly cannot be interpreted as a point of arrival but should rather be viewed as a starting point for future research in this very complex and intriguing field in which much work is yet to be done.

This chapter addresses the diagnosis, investigation, and management of anaemia due to a deficiency in iron, vitamin B12, or folate. Erythropoiesis requires an adequate supply of iron for haem formation, as well as vitamin B12 and folic acid (folate) to support high levels of DNA synthesis, and a lack of any of these will result in anaemia. Iron-deficient anaemias are typically microcytic, while a deficiency in vitamin B12 or folate results in megaloblastic haemopoiesis and a macrocytic anaemia. Iron deficiency results from poor dietary iron intake, poor absorption, increased demands, blood loss, or combinations of these. The usual cause of severe vitamin B12 deficiency in Western countries is an autoimmune atrophic gastritis, in which there is a loss of gastric parietal cell numbers and an absence of intrinsic factor production, which effectively prevents vitamin B12 absorption. This is the classical pernicious anaemia, and it is often seen in association with other autoimmune disorders. Folate deficiency may result from poor diet, malabsorption, or when demand for folate is increased, for example, during pregnancy, or with increased haemopoiesis in haemolytic anaemias or myeloproliferative disorders.