[Relations between endoscopic and histological aspects of superficial gastritis, atrophic gastritis and gastric atrophy in aged patients].
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Aged↗
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Results for “Gastritis, Atrophic”
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The interaction between vitamin K nutriture and warfarin administration in patients with bacterial overgrowth due to atrophic gastritis.
Atrophic gastritis patients have intestinal bacterial overgrowth which could produce menaquinones. The aim of this study was to evaluate the interaction between a diet low in phylloquinone and minidoses of warfarin in subjects with and without bacterial overgrowth. Subjects with atrophic gastritis (indicated by serum pepsinogen ratio) and healthy volunteers were studied while fed a restrictive phylloquinone diet and while receiving a minidose of warfarin. Coagulation times, serum osteocalcin, serum undercarboxylated osteocalcin, plasma phylloquinone, plasma K-epoxide, plasma undercarboxylated prothrombin (PIVKA)-II and urinary gamma-carboxyglutamic acid (Gla) were measured. At baseline, there were no differences between groups for any variable measured. Comparisons between baseline and post intervention in both groups, showed significant increases in circulating levels of K-epoxide, PIVKA II and undercarboxylated osteocalcin. However, no differences were observed when comparisons were made between groups. Our data do not support the hypothesis that bacterial synthesis of menaquinones in patients with bacterial overgrowth due to atrophic gastritis confers considerable resistance to the effect of warfarin.
Aged↗
Increased gastric absorption of polyethylene glycols in atrophic gastritis.
Atrophic gastritis increases the risk of developing gastro-intestinal tumours. An impaired barrier function of the gastric mucosa could contribute to this risk. The absorption of polyethylene glycols (molecular weights 414-766), expressed as recovery in 6-hour urine, was studied both after oral and duodenal loads in patients with atrophic gastritis (n = 18) and compared with controls without gastritis (n = 9). The patients had a higher absorption after oral than after duodenal load for molecular weights 502-546. The differences in absorption after oral and duodenal loads were correlated with the severity of the atrophy in the antrum. No differences were found in the controls. Absorption after the duodenal load did not differ between the study groups. The increased gastric absorption of polyethylene glycols in patients with atrophic gastritis may be caused by a permeability disturbance of the gastric mucosa.
Administration, Oral↗
[Problem of diverse pathogenesis of simple atrophic gastritis compared with atrophic gastritis in pernicious anemia].
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Anemia, Pernicious↗
Helicobacter pylori and the risk and management of associated diseases: gastritis, ulcer disease, atrophic gastritis and gastric cancer.
This review addresses the role of H. pylori and the effect of H. pylori eradication on gastritis, peptic ulcer disease, atrophic gastritis and gastric cancer. Specific emphasis is given to various factors that influence the clinical course of this infection. H. pylori induces chronic gastritis in virtually all infected subjects. This inflammation can lead to peptic ulceration and atrophic gastritis in a considerable number of infected subjects. A minority eventually develops gastric cancer. The risk of such complications depends upon the severity of gastritis, which is determined by various host- and bacteria-related factors. Among bacterial factors, most of the evidence addresses the cagA pathogenicity island, the presence of which has been associated with more severe gastritis, peptic ulceration, atrophic gastritis and gastric cancer. Among host factors, most of the evidence focuses on acid production in response to H. pylori infection. An increase in acid secretion limits H. pylori gastritis to the antrum at the risk of duodenal ulcer disease; a reduction allows more proximal inflammation at the risk of atrophic gastritis, gastric ulcer disease, and gastric cancer. Gastritis and atrophy negatively influence acid secretion. H. pylori eradication is required in peptic ulcer disease and may be advocated in patients on profound acid suppressive therapy; it has been shown to cure gastritis and prevent ulcer recurrence. Further study is required to determine the efficacy of H. pylori eradication in the primary and secondary prevention of atrophic gastritis and gastric cancer.
Chronic Disease↗
Role of Helicobacter pylori in the pathogenesis of atrophic gastritis.
BACKGROUND: Atrophic gastritis is defined as a loss of the glandular structures and a collapse of the reticulin skeleton of the stomach mucosa. It is often accompanied by intestinal metaplasia. Both conditions result from long-term persistent chronic active gastritis and significantly increase the risk for gastric cancer. METHODS: Review of the role of Helicobacter pylori in the pathogenesis of atrophic gastritis. Specific attention is given to the classifications and histologic features of atrophic gastritis, the frequency with which atrophic gastritis occurs in H. pylori-infected subjects, the factors that influence the process of development of atrophic gastritis in the presence of infection, and the various mechanisms by which this bacterial infection may induce atrophic gastritis. In addition, the possible role of H. pylori in the etiology of auto-immune atrophic gastritis and pernicious anemia is discussed. CONCLUSIONS: H. pylori infection eventually causes atrophic gastritis in a considerable number of infected subjects. In different populations, the prevalence of atrophic gastritis increases by 1 to 3% per annum. Factors that may increase the risk for atrophy are infection at an early age, cytotoxin production by the infecting strain, and lowering of acid output. The association between H. pylori infection and the development of atrophic gastritis significantly supports the role of this infection in gastric carcinogenesis.
Gastritis, Atrophic↗
Expression of bcl-2 in autoimmune and Helicobacter pylori-associated atrophic gastritis.
Chronic atrophic gastritis can be induced either by H. pylori or by an autoimmune process. The protein product of bcl-2, which is a protooncogene, blocks apoptosis. Aberrant bcl-2 expression has been found in 68% of atrophic gastritis patients. The aim of this study was to compare bcl-2 expression in 20 autoimmune atrophic gastritis patients to that in 20 H. pylori-associated atrophic gastritis patients. Twenty patients with H. pylori antral gastritis but without atrophy served as controls. The bcl-2 expression was assessed by immunohistochemical staining of gastric biopsies, using mouse anti-human bcl-2 monoclonal antibodies. Autoimmune atrophic gastritis patients were younger, mainly females, with a significantly higher serum gastrin level than the H. pylori-associated atrophic gastritis group (P < 0.001). The bcl-2 was expressed in 10/20 (50%) of autoimmune atrophic gastritis patients, in 9/20 (45%) of H. pylori-associated atrophic gastritis patients (P = 0.73), and in 2/20 (10%) of controls. There was no correlation between bcl-2 expression and the presence of intestinal metaplasia (P = 0.35). Our findings confirm that H. pylori-associated atrophic gastritis and autoimmune atrophic gastritis are two different conditions, but with equal expression of bcl-2. Excessive expression of bcl-2 is found only in atrophic gastritis, but not in H. pylori antral gastritis without atrophy.
Adult↗
[Endoscopic and biopsy studies on chronic gastritis. 1. Atrophic gastritis].
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Adult↗
Role of anti-parietal cell antibody in Helicobacter pylori-associated atrophic gastritis: evaluation in a country of high prevalence of atrophic gastritis.
BACKGROUND: Helicobacter pylori plays an important part in the progression of atrophic gastritis; however, markers for predicting the progression of atrophic gastritis remain unidentified. We investigated the relation between the degree of atrophic gastritis and the amount of anti-parietal cell antibodies (APCAs) present. METHODS: In 219 Japanese patients, APCA was investigated by enzyme-linked immunosorbent assay (ELISA) and by Western blotting. The grade of corpus atrophy was estimated by histology and serum pepsinogen levels. Serum levels of pepsinogen were evaluated by radioimmunoassay. RESULTS: Helicobacter pylori infection did not affect the APCA levels determined by ELISA. Long-term administration of proton-pump inhibitors and H. pylori eradication did not influence the levels of APCAs. However, in H. pylori-positive patients, the levels of APCA determined by ELISA were statistically higher in patients with severe atrophy than in those with mild atrophy as determined histologically (0.67+/-0.48 versus 0.45+/-0.40; A492, mean+/-s, P=0.01) and serologically by pepsinogen levels (0.66+/-0.51 versus 0.44+/-0.40. P=0.002). The levels of pepsinogen I/II ratio were correlated with APCA levels only in the H. pylori-positive group. Western blotting showed that major antigen was identical with the beta-subunit of H+,K+-ATPase. CONCLUSION: APCA plays an important part in the progression of corpus atrophy after H. pylori infection.
Adolescent↗
Interactions between gastric epithelial stem cells and Helicobacter pylori in the setting of chronic atrophic gastritis.
Chronic atrophic gastritis (ChAG), a Helicobacter pylori-associated risk factor for the development of gastric cancer, involves loss of acid-producing parietal cells. Recent studies in gnotobiotic mouse models of ChAG have shown that parietal cell loss results in amplification of multi- and oligo-potential gastric stem cells that express sialylated glycan receptors recognized by H. pylori adhesins. Moreover, H. pylori resides within a subset of these stem cells. Studies of the transcriptomes of gastric stem cells, harvested directly from the stomachs of uninfected mice, using laser capture microdissection, suggest that they have the ability to complement some of the metabolic needs of H. pylori. These findings indicate that proliferating and non-proliferating gastric stem cells provide a habitat that could support H. pylori persistence in a gastric ecosystem that has lost its acid barrier to colonization by environmental, oral and intestinal microbes. One consequence to the host might be an increased risk of tumorigenesis.
Animals↗
Helicobacter pylori eradication therapy improves atrophic gastritis and intestinal metaplasia: a 5-year prospective study of patients with atrophic gastritis.
AIM: : To investigate the effect of the eradication of Helicobacter pylori on histological gastritis. METHODS: : Twenty-six patients with moderate to severe atrophy received successful eradication therapy of H.pylori. Four patients dropped out and 22 were followed up prospectively for 5 years. The grades of gastritis were estimated from gastric biopsy specimens. The grade of intestinal metaplasia was also evaluated by dye-endoscopy using methylene blue (methylthioninium chloride). The serum levels of pepsinogen, gastrin and anti-parietal cell antibody were also determined. RESULTS: : The grades of atrophy decreased in patients with successful eradication therapy in the gastric corpus (before vs. 5 years after eradication, 2.09 +/- 0.15 vs. 0.91 +/- 0.17; P < 0.01) and in the antrum (2.14 +/- 0.17 vs. 1.36 +/- 0.17; P < 0.01). The levels of intestinal metaplasia were also decreased in the corpus (0.91 +/- 0.24 vs. 0.50 +/- 0.16; P < 0.05) and in the antrum (1.41 +/- 0.20 vs. 1.00 +/- 0.16; P < 0.05), which was also demonstrated by the methylene blue (methylthioninium chloride) staining method (33.4 +/- 8.2% vs. 23.0 +/- 6.5%; P < 0.05). The improvement of corpus atrophy correlated well with the high serum level of pepsinogen I (P = 0.005), but showed no correlation with the levels of anti-parietal cell antibody. CONCLUSIONS: : These results suggest that gastric atrophy and intestinal metaplasia are reversible events in some patients.
Adult↗
[Chronic atrophic gastritis and the risk of cancer].
Chronic gastritis, which is frequent in subjects over 50 years old, is caused by the concurrence of predisposing and congenital conditions and exogenous harmful factors, in particular foods. In etiopathogenetic terms it is worth considering autoimmune diseases and duodenogastric back-flow separately. Lesions develop progressively from superficial gastritis to atrophic gastritis and finally to gastric atrophy; they are frequently found together with intestinal metaplasia, formed by areas of the epithelium with the morphological and histochemical characteristics of intestinal mucosa, which are the expression of a modified regeneration of the gastric wall. It is acknowledged that chronic atrophic gastritis is a precancerous phenomenon which is the majority of cases leads to the onset of intestinal cancer, passing through the stages of chronic gastritis, metaplasia and dysplasia. Identification of this lesion may therefore help to prevent cancer: diagnosis is essentially performed using endoscopy (together with histocytological tests and bioptic staining) and laboratory tests (enzyme and CEA assays in the gastric juices). Rather than prescribing generic medical therapy or surgical treatment, which is only possible in selected cases of alkaline gastritis, attention is focused on curing unhealthy habits and on an endoscopic follow-up (every 2 years in cases of gastritis, and more frequently in cases of metaplasia or dysplasia).
Gastritis, Atrophic↗
Significance of endoscopically visible blood vessels as an index of atrophic gastritis.
The endoscopic criteria for atrophic gastritis are. 1. pale mucosa; 2. shiny surface and 3. prominent submucosal vessels. To evaluate the diagnostic accuracy of circumscribed atrophic gastritis based on these findings, we studied 184 consecutive upper gastrointestinal endoscopies. The endoscopic diagnosis of atrophic gastritis was made only if two endoscopists both agreed on the findings and interpretation. The location of the atrophic pattern and whether it was circumscribed or diffuse were recorded. Two biopsy specimens were than obtained. Histologic material was interpreted by a pathologist who had no prior knowledge of the endoscopic findings. Twenty-five patients (13%) had atrophic gastritis endoscopically; in four it was diffuse and in 21 it was circumscribed. Utilizing the criteria of Whitehead, et al, atrophic gastritis was diagnosed histologically in three of four patients with diffuse gastritis but in one of those considered to have circumscribed atrophic gastritis. It is concluded from these preliminary data that a circumscribed atrophic mucosal pattern is a frequent endoscopic finding that does not necessarily represent atrophic gastritis histologically.
Adult↗
Progressive increase in the functional G cell mass with age in atrophic gastritis.
Patients with atrophic gastritis but normal antral mucosa and achlorhydria were divided into three groups according to age-under 40, 40 to 70, and over 70 years. Serum gastrin, both basal and following a standard protein meal, was estimated in all patients by radioimmunoassay. There was a significant correlation between the magnitude of the gastrin response and age, the older the patient the greater the response. These results suggest that with increasing duration of gastritis and continued stimulation of a normal antrum in the absence of inhibition by acid, the functional G (gastrin) cell mass increases. However the possibility exists that each cell may secrete more gastrin in response to the same stimulus with age. This may be resolved by counting the number of G cells in the stomachs of subjects with atrophic gastritis and different ages.
Achlorhydria↗
Intestinal metaplasia, atrophic gastritis and stomach cancer: trends over time.
BACKGROUND: The pathogenetic association of chronic atrophic gastritis and intestinal metaplasia with gastric cancer implies that the trends seen in these disorders over time should be similar. Both should similarly decrease in incidence with time, and a time-related relationship should occur between the incidence of gastric cancer and the rate of development of atrophic gastritis in the stomach of Helicobacter pylori-infected subjects. AIMS AND METHODS: We reviewed some recent studies from Finland on the time trends seen in chronic gastritis, atrophic gastritis (and intestinal metaplasia) and gastric cancer over a period of 15 years (1977-1992). In addition, using results from earlier studies from Japan and Finland, we formed hypotheses on how the time-dependent evolution and extension of atrophic gastritis may accord with the occurrence of gastric cancer in the stomach. RESULTS: Our investigations showed that the incidence of gastric cancer and the prevalence of H. pylori-associated gastritis, atrophic gastritis and intestinal metaplasia have decreased similarly in outpatient series during the last 15 years. Correspondingly, gastric cancer, atrophic gastritis and intestinal metaplasia are cohort phenomena in the population, and the prevalence rate of atrophic gastritis is correlated with the cohort-specific incidence of gastric cancer; both are high in cohorts born near the beginning of the century but are quite low in those born in recent decades. Since antral and angular areas of the stomach are primary sites for gastric cancer tumours, the earlier investigations indicate that the time-dependent progression of gastritis in grade (development of atrophic gastritis and intestinal metaplasia) and extent (spreading of gastritis by pylorocardial extension) is well correlated with the rate and predisposition of gastric cancer tumours in the distal and angular stomach. CONCLUSIONS: We conclude that atrophic gastritis (or intestinal metaplasia) and gastric cancer are very much alike in time trends and in course. This parallelism favours suggestions that H. pylori-associated gastritis with atrophic and metaplastic sequelae (atrophic gastritis) contribute to the pathogenesis of gastric cancer.
Finland↗
Biomarkers in various types of atrophic gastritis and their diagnostic usefulness.
Atrophic gastritis has been shown to involve either the oxyntic gland area, resulting in hypergastrinemia and hypopepsinogenemia I, the antral gland area, causing hypogastrinemia without change in serum pepsinogen I (diffuse antral gastritis; DAG), or the entire gastric mucosa (multifocal atrophic gastritis; MAG), resulting in both hypogastrinemia and hypopepsinogenemia I; and rare atrophic gastritis limited to the oxyntic gland area, with antibodies against oxyntic cells and/or intrinsic factor (autoimmune metaplastic atrophic gastritis; AMAG). This study was performed on 126 patients with various forms of gastritis and on 126 age- and gender-matched controls, who were subjected to endoscopy with biopsy, H. pylori testing (13C-UBT, serology), assays for serum gastrin and pepsinogen I, and testing for basal and pentagastrin-induced gastric acid secretion. The following groups of patients were examined: group I (N = 22), with AMAG; group II (N = 53), with DAG; group III (N = 51), with MAG; and group IV (N = 126), age- and gender-matched controls without gastritis. The following changes were found. In group I very high serum gastrin and very low pepsinogen I were observed, and all patients were achlorhydric and H. pylori negative. In group II, with low serum gastrin and normal pepsinogenemia and gastric chlorhydria, all patients were H. pylori positive. In group III, with lower serum gastrin and lower pepsinogen I levels and reduced chlorhydria, all patients were also H. pylori positive. And all group IV controls, with normal serum gastrin and pepsinogen I and normal gastric acid secretion without antral or fundic gastritis, were H. pylori negative. We conclude that measurements of serum gastrin and pepsinogen I and gastric acid secretion as well as testing for H. pylori infection may be useful in noninvasive diagnosis of various types of atrophic gastritis and in identification of patients with premalignant gastritis and a high risk of gastric cancerogenesis.
Adult↗
[Focal atrophy with stellate scars in children with chronic gastritis associated to Helicobacter pylori. Is this early atrophic gastritis?].
BACKGROUND: Atrophic gastritis has not been described in children in the setting of Helicobacter Pylori infection. METHODS: Gastric biopsies of six children (7 to 11 years old) with history of HpCG and recent therapeutic eradication of H. Pylori, were reviewed. In the 6 H. Pylori was documented with histology, culture, direct visualization and/or serology before treatment. Cases were compared with five biopsies of age-matched patients showing none of the above-mentioned clinical data. All the biopsies were formalin-fixed, paraffin embedded and stained with hematoxilin-eosin, Masson trichrome and reticulin stain. RESULTS: The biopsies of the six treated patients showed variable-in-size stellate-shaped spots of glandular loss replaced by dense connective tissue with few inflammatory cells. The fibrous tissue showed a central area of scarring and radially oriented spikes extending to adjacent interglandular tissue, more evident with the Masson trichrome stain. Density of inflammatory cells in the lamina propria was variable. H. Pylori organisms were consistently absent. On the reticulin stain the atrophic areas showed coarser and compacted reticulin. Stellate scars were not present in the five controls. CONCLUSIONS: Small foci with fibrous scars may be found in children with long standing HpCG, perhaps as an early sequel of it. We hypothesize that if the chronic gastritis-gastric atrophy process is a continuum, these stellate scars may be representing the very beginning of the multifocal atrophic gastritis usually seen in adult patients.
Atrophy↗
Serum levels of amidated gastrin-17 and pepsinogen I in atrophic gastritis: an observational case-control study.
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 non-endoscopically 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 microg/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%; Cl 95%: 81%-97%) had a low S-PGI and/or a low S-G-17prand with positive H. pylori serology. Such low values werc 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.
Antibodies, Bacterial↗