Assessment of the content of neuroendocrine cells in the gastric mucosa in patients with autoimmune gastritis
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Abstract:
The aim of the study was to evaluate the content of neuroendocrine cells in immunohistochemically stained preparations and determine differences in the number of neuroendocrine cells (NEC) in the body of the stomach in autoimmune gastritis (AIG) and other forms of gastritis. Material and methods. The study included 27 cases of AIG and 9 cases of chronic atrophic gastritis not associated with autoimmune mechanisms of disease. The age of the patients ranged from 36 to 77 years and averaged 54.9 years. Biopsies were taken according to accepted protocols: 2–3 biopsies from the antrum and 2 biopsies from the body of the stomach. An immunohistochemical reaction was carried out with an antibody to chromogranin A on an automatic Bond Max immunostainer (Leica, Germany). The slides were digitized on an Aperio AT2 scanner (Leica, Germany), and QuPath v.0.3.0 software for viewing and analyzing digital images of slides was used for morphometric analysis of digital images and counting. The results were processed in the Jamovi program, Version 1.6 ( https://www.jamovi.org ). Results. According to the results of counting in the group of patients with AIG, there was an increase in the quantity of NEC. Ranges of hyperplasia of neuroendocrine cells were revealed: 648–1736 cells per 1 mm2 square were detected for AIG, 416–605 cells per 1 mm2 for other forms of gastritis. In the AIG group median is 925 cells per 1 mm2, the 1st quartil is 877 cells per 1 mm2, 3rd quartil is 1172 cells per 1 mm2, interquartile range is 295 cells per 1 mm2 (asymmetrical distribution). In the group with other forms of gastritis arithmetic mean is 522±23 cells per millimeter square (normal distribution). Conclusion. The obtained results allowed to confirm NEC hyperplasia in patients with AIG. A statistically significant difference was found in the number of NEC in the body of the stomach in the group of AIG and other gastritis (p≤0,01), which can be proposed as an additional morphological criteria for diagnosing AIG.Keywords:
Autoimmune Gastritis
Atrophic gastritis
Chromogranin A
Chromogranin A is an important tool in the diagnosis of neuroendocrine tumors. Autoimmune gastritis is an autoimmune disorder marked by hypergastrinemia, which stimulates enterochromaffin-like cell proliferation. Chromogranin A is also elevated in autoimmune gastritis patients with a different level of increase in each patient. The goal of this study is to explore constituents that influence serum chromogranin A levels in autoimmune gastritis patients.One hundred and eighty-eight autoimmune gastritis patients and 20 patients with type I gastric carcinoid tumors were analyzed retrospectively and compared to 110 functional dyspepsia patients in terms of factors that might affect serum chromogranin A levels.The mean serum chromogranin A level was 171.17±67.3 ng/mL in autoimmune gastritis patients (n=62) without enterochromaffin-like cell hyperplasia, and 303.3±102.82 ng/mL in patients (n=126) with enterochromaffin-like cell hyperplasia (p<0.001). The presence of corpus atrophy (p=0.026, OR: 5.03, CI 95%: 1.21-20.88, β=1.61) and presence of enterochromaffin-like cell hyperplasia (p=0.017, OR: 6.59, CI 95%: 1.4-31.08, β=1.88) were found as risk factors associated with serum chromogranin A level.Factors influencing raised serum chromogranin A levels in autoimmune gastritis were the presence of ECL cell hyperplasia and serum gastrin levels. Serum chromogranin A levels maybe helpful in distinguishing autoimmune gastritis patients and gastric carcinoid type I from the control group, but not useful in the differentiation of individuals with autoimmune gastritis from patients with gastric carcinoids.
Chromogranin A
Autoimmune Gastritis
Atrophic gastritis
Enterochromaffin-like cell
Enterochromaffin cell
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To assess characteristics of oxyntic gastric atrophy (OGA) in autoimmune gastritis (AIG) compared with OGA as a consequence of Helicobacter pylori infection.Patients undergoing oesophagogastroduodenoscopy from July 2011 to October 2014 were prospectively included (N=452). Gastric biopsies were obtained for histology and H. pylori testing. Serum gastrin-17 (G17), pepsinogen (PG) I, PGII and antibodies against H. pylori and cytotoxin-associated gene A protein were determined in all patients. Antibodies against parietal cells and intrinsic factor were determined in patients with advanced (moderate to severe) OGA. Areas under the receiver operating characteristic curves (AUCs) were calculated for serum biomarkers and compared with histology.Overall, 34 patients (8.9%) had advanced OGA by histology (22 women, age 61±15 years). Current or past H. pylori infection and AIG were present in 14/34 and 22/34 patients, respectively. H. pylori-negative AIG patients (N=18) were more likely to have another autoimmune disease (OR 6.3; 95% CI 1.3 to 29.8), severe corpus atrophy (OR 10.1; 95% CI 1.9 to 54.1) and corpus intestinal metaplasia (OR 26.9; 95% CI 5.3 to 136.5) compared with H. pylori-positive patients with advanced OGA. Antrum atrophy was present in 39% of H. pylori-negative AIG patients. The diagnostic performance of G17, PG I and PGI/II was excellent for AIG patients (AUC=0.83, 0.95 and 0.97, respectively), but limited for H. pylori-positive patients with advanced OGA (AUC=0.62, 0.75 and 0.67, respectively).H. pylori-negative AIG has a distinct clinical, morphological and serological phenotype compared with advanced OGA in H. pylori gastritis.
Autoimmune Gastritis
Intestinal metaplasia
Histology
Atrophic gastritis
Spirillaceae
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Background: Helicobacter pylori infection is often diagnosed with non-endoscopic methods, such as serology or breath or antigen stool tests. These tests provide information on the presence or absence of the H. pylori gastritis only. We investigated whether atrophic gastritis can be diagnosed and typed nonendoscopically if the serum levels of pepsinogen I (S-PGI) and gastrin-17 (S-G-17) are assayed in connection with H. pylori testing. Methods: The present investigation is an observational case-control study comprising 100 selected dyspeptic outpatients with (cases) or without (controls) advanced (moderate or severe) atrophic gastritis. Before the blood tests, all patients underwent a diagnostic gastroscopy with multiple biopsies. The series of cases includes 56 patients. Eight had an advanced antrum limited atrophic gastritis, 13 had resected antrum (in two of whom the corpus mucosa in the stump was atrophic), and 30 had corpus-limited atrophic gastritis. Four patients had an advanced atrophic gastritis in both the antrum and corpus (multifocal atrophic gastritis), and the whole stomach was removed in one patient. Twenty of the 44 controls had a non-atrophic H. pylori gastritis. Both the antrum and corpus were normal and healthy in 24 patients. The S-PGI and S-G-17 were determined with EIA methods using monoclonal antibodies to PGI and amidated G-17. Postprandial S-G-17 (S-G-17prand) was measured 20 min after a protein-rich drink. The H. pylori antibodies were assayed with a polyclonal EIA method. Results: A low S-PGI (<25 μg/l; an empirical cut-off with best discrimination) was found in 31 of 37 patients (84%) with and in 3 of 63 patients (5%) without corpus atrophy in the biopsy specimens. A low S-G-17prand (<5 pmol/l) was found in all 8 patients with H. pylori -associated antral atrophy and in 11 of 14 patients (79%) with resected antrum but in 3 of 20 control patients (15%) with H. pylori -related non-atrophic gastritis. Median and mean values of both S-G-17prand and S-PGI decreased with increasing grade of antral and corpus atrophy, respectively. Among all patients with atrophic gastritis (multifocal atrophic gastritis, or atrophic gastritis limited to antrum or corpus) or resected stomach, 50 of 56 patients (89%; CI 95%: 81%-97%) had a low SPGI and/or a low S-G-17prand with positive H. pylori serology. Such low values were found in 3 of the 44 control patients (7%; CI 95%: 0%-14%). Conclusions: Low serum levels of G-17prand and PGI are conceivable biomarkers of atrophic antral and corpus gastritis, respectively. A low S-G-17prand is a sign of the multifocal or antrum-limited atrophic gastritis in patients infected with H. pylori .
Atrophic gastritis
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SUMMARYChronic (atrophic) gastritis (AG)iscommoninactive duodenal (DU)andgastric ulcer (GU)disease. Inthis casecontrol study inconsecutive prospective outpatients (571cases and1074 controls) whohadundergone diagnostic uppergastrointestinal endoscopy androutine biopsies from bothantral andbodymucosa, wecalculated therisk ofcoexisting active DUand/or GU indifferent gastritis oftheantrumorbodyandaccording tograde (superficial gastritis, mild, moderate orsevere atrophic gastritis). Therisk ofcoexisting active gastroduodenal ulcer (ulcer induodenumand/or stomach), aswell astherisk ofDUorGU,wasdependent uponthepresence andgrade ofgastritis in antrumandbodymucosa. Therisk ofcoexisting ulcer, asexpressed asanageadjusted relative risk (RR)andcalculated asoddsratio ofgastritis incases andcontrols, wassignificantly increased inthe presence ofsuperficial antral andbodygastritis (RR=8.5 (7'0-20 0)inmen;RR=5.8(33-10.2) in women), ascompared withtherisk ofulcer insubjects withhistologically normal mucosa(RR=1). Therisk ofulcer, andtherisk ofGU inparticular, increased further withincreasing severity of antral gastritis. Insuchpatients withmoderate orsevere atrophic antral gastritis theRR of coexisting ulcer evenexceeded 20inmenand10inwomen(RR=25.6 (9'0-72.7) inmen;RR=11.7 (5.9-23.0) inwomen). Ontheother hand, theRRofulcer, andtheRRofDUinparticular, wasbelow 1inthepresence ofatrophic gastritis inthegastric body,irrespective ofthegradeofgastritis inthe antrum. We conclude thatthetypeandgradeofgastritis strongly predicts therisk ofcoexisting peptic ulcer, andthat therisk ofcoexisting DUorGUincreases withanincrease ingrade ofAG of theantrumbutdecreases withanincrease ingrade ofAGofthegastric body.
Atrophic gastritis
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Atrophic gastritis, whether caused by Helicobacter pylori infection or as a result of an autoimmune process, is associated with corpus atrophy. However, whereas atrophic gastritis caused by H. pylori involves the antrum, the antrum is spared in autoimmune gastritis. Here, we report the use of magnifying endoscopy to identify and distinguish atrophic gastritis caused by H. pylori from 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 to H. pylori infection. 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 in H. pylori infection 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.
Autoimmune Gastritis
Atrophic gastritis
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Atrophic gastritis
Chronic gastritis
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Atrophic gastritis
Pepsin
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A series of 143 subjects representing an Estonian urban population was examined for the occurrence and extent (absent, mild, moderate, severe) of Helicobacter pylori colonization in antral and body biopsy specimens (Giemsa staining). These data were correlated with the presence and grade of chronic gastritis (normal, mild, moderate, or severe superficial chronic gastritis; mild, moderate, or severe atrophic gastritis) in the antrum and the body. Gastritis of any grade was found in the antrum and/or the body in 140 (98%) subjects. The overall extent of H. pylori colonization in the whole series did not differ between the antrum and the body. Of 93 subjects with superficial gastritis, H. pylori was found in the antrum and/or the body in 87 (94%) cases. Of 47 subjects with atrophic gastritis in the antrum and/or the body, H. pylori was not found in 12 (25%). In subjects with gastritis the absence of H. pylori either in the antrum or in the body was relatively common (in 30 of 143 subjects). The grade of superficial gastritis showed a highly significantly positive correlation with the extent of H. pylori colonization in the antrum but not in the body, Correspondingly, the grade of atrophic gastritis in the antrum correlated negatively to the grade of colonization. The total absence of H. pylori was particularly associated with the absence of gastritis in the antrum. Conversely, severe body H. pylori colonization was found in subjects who had atrophic antral gastritis, and severe antral colonization in subjects who had at least moderate superficial antral gastritis and who showed a coexistent normal or slight superficial gastritis in the body. We concluded that the presence and extent of H. pylori colonization are strongly linked to specific profiles of antrofundal gastritis.
Atrophic gastritis
Chronic gastritis
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The serum gastrin response to a standard protein meal has been determined in achlorhydric patients with atrophic gastritis and contrasted with the response in normal subjects whose gastric contents were kept continuously neutral by intragastric bicarbonate instillation. Five normal subjects showed a significant increase in serum gastrin from a mean (± SEM) of 17 ± 3 pg/ml to 119 ± 10 pg/ml but their response did not approach that of four patients with atrophic gastritis and antral sparing (605 ± 133 pg/ml to 1418 ± 186 pg/ml). By contrast, in four patients with antral gastritis, there was no significant change in gastrin levels (24 ± 13 pg/ml to 55 ± 19 pg/ml). These studies indicate that the gastrin-secreting cell mass is increased in atrophic gastritis with antral sparing and decreased in atrophic gastritis with antral involvement, as compared to the normal state. They provide further evidence for the existence in man of two distinct forms of atrophic gastritis.
Atrophic gastritis
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Atrophic gastritis is a precancerous condition that is commonly caused by chronic Helicobacter pylori (H. pylori) infection. This blinded, controlled study was designed to determine if serum gastrin and pepsinogens were reliable markers of atrophy in asymptomatic patients.One hundred and forty-seven asymptomatic patients underwent endoscopy with multiple gastric biopsies obtained for histology, culture, and rapid urease test. Fasting serum gastrin (total and G-17) and serum pepsinogens (I-II) were determined by standard immunoassays. Gastric atrophy was histologically assessed in accordance with internationally accepted criteria; three main patterns of gastritis were distinguished: (a) nonatrophic gastritis, (b) atrophic antrum-restricted and antrum-predominant gastritis, and (c) corpus-restricted gastritis. Receiving operating characteristic (ROC) analysis was used to determine the best cut-off for each serum test in nonatrophic gastritis versus antrum-restricted/antrum-predominant atrophic gastritis.No significant differences in serum gastrin and pepsinogens I-II were detected in nonatrophic gastritis versus patients with antrum-restricted/antrum-predominant atrophic gastritis. The positive likelihood ratios for an abnormal serum test to detect antrum-restricted/antrum-predominant atrophy in the gastric body were total serum gastrin 2.13 (95% CI 0.99, 4.6), gastrin-17: 1.55 (95% CI 0.75, 36.17), pepsinogen I: 2.74 (1.4, 5.4), pepsinogen II: 1.74 (1.27, 2.39), and the ratio of pepsinogen I and II: 1.8 (1.2-2.8). Negative likelihood ratios ranged from 0.20 to 0.65.In an asymptomatic population, serum gastrin (total and G-17) and pepsinogens I-II (and their ratio) do not discriminate nonatrophic versus antrum-restricted/predominant atrophic gastritis.
Atrophic gastritis
Rapid urease test
Pepsin
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