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PubMed1990

Peptic ulcer and chronic gastritis: their relation to age and sex, and to location of ulcer and gastritis.

The progression, age-behaviour and profiles of chronic gastritis were studied in 460 patients with active gastric or duodenal ulcer, and in 226 patients with ulcer scar. The results were compared with those obtained from a sample of subjects representing the general population. In patients with ulcer or ulcer scar, the progression of chronic gastritis was more rapid in antrum than in body mucosa, and was more rapid in patients with proximal ulcer in those with distal ulcer or in controls. In the body the progression of gastritis was significantly slower in patients with duodenal or juxtapyloric ulcer than in patients with proximal ulcer or in nonulcer controls: body gastritis tended to remain on the same level at all ages whereas it showed a steady progression with age in the nonulcer controls. The degree of gastritis showed a tendency to increase along the shift of ulcer to more proximal in the stomach; the prevalence of gastritis of pure B type (moderate or severe atrophy in antrum, but no atrophy in body mucosa) correspondingly increased along this shift. Severe antral atrophic gastritis was found in 7 per cent of proximal active gastric ulcers and in 20 per cent of proximal ulcer scars. The progression of antral and body gastritis was on the whole more rapid in males than in females irrespectively of the location of ulcer. We conclude that gastritis in different types of ulcers shows characteristic patterns of distribution, dynamics and progression with age. The high prevalence of severe grades of atrophic antral gastritis may also be of significance in regard to the pathogenesis of gastric cancer.

Aged↗
PubMed1989

The prevalence of Campylobacter pylori gastritis: a study of symptomatic nonulcer dyspepsia and bile gastritis.

We assessed the prevalence of Campylobacter pylori in various forms of endoscopic gastritis, including ulcer and nonulcer dyspepsia and bile gastritis and correlated it with histological evidence of inflammation. Multiple biopsy specimens were taken from 120 patients, including four normal controls, who underwent upper gastrointestinal endoscopy for evaluation of upper abdominal pain and discomfort, nausea, bilious vomiting, weight loss, and anemia. The patients included 58 men and 62 women, with a mean age of 53 years. Of these, 16 patients had gastric ulcers, 19 had duodenal ulcers, 26 had reflux gastritis (after either gastric surgery or cholecystectomy), one had a gastric polyp, one had Barrett's esophagus, and the remaining 53 had gastritis due to unspecified causes. Campylobacter-like organisms were demonstrated by light and electron microscopy in 50 of 69 patients of the nonbile gastritis group (72%) and in seven of 15 patients of the bile gastritis group (47%) (p0.05). The presence of bacteria in both groups correlated with histologically significant inflammation (particularly chronic active gastritis); similar histologic changes were noted in both major groups of nonbile gastritis and bile gastritis. Campylobacter pylori is common in all forms of gastritis in association with histologic inflammation.

Adult↗
PubMed1999

Gastritis associated with Crohn disease can be masked by Helicobacter pylori gastritis.

BACKGROUND: Crohn disease (CD) is typically associated with focal inflammatory infiltrations. It is, however, unclear to what extent this CD-associated gastritis is masked by Helicobacter pylori gastritis. METHODS: One hundred and three patients with CD underwent upper endoscopy. Antrum and corpus biopsy specimens were obtained and histologically evaluated for the presence of CD gastritis or H. pylori gastritis. In patients infected with H. pylori, eradication of the organism was initiated with repeated endoscopy/histology 7 days after termination of therapy. RESULTS: Thirty patients were infected by H. pylori. Definite diagnosis of CD gastritis was made in 4 patients, in contrast to 31 of the 73 patients with no H. pylori gastritis (P < 0.001). In 19 patients with either no (n = 13) or only suspected diagnosis of CD gastritis (n = 6), elimination of H. pylori enabled definite diagnosis of CD gastritis in 5 of 13 and 4 of 6 patients, respectively. CONCLUSION: Elimination of H. pylori facilitates the diagnosis of CD gastritis.

Adult↗
PubMed1992

Chemical gastritis and Helicobacter pylori related gastritis in patients receiving non-steroidal anti-inflammatory drugs: comparison and correlation with peptic ulceration.

AIMS: To evaluate the prevalence and significance of chemical gastritis, in comparison with gastritis related to Helicobacter pylori in patients receiving non-steroidal anti inflammatory drugs (NSAIDs). METHODS: Two hundred and eighteen patients were studied, 174 of whom were taking NSAIDs. Chemical gastritis was defined as the presence of foveolar hyperplasia, muscle fibres in the lamina propria, oedema and vasodilation, in the absence of a chronic inflammatory cell infiltrate. RESULTS: Chemical gastritis was found in 46 (26%) patients taking NSAIDs, and three (7%) in subjects not taking these drugs (p less than 0.01). H pylori was detected in 56 (32%) subjects taking NSAIDs compared with 22 (50%) not taking these agents (p less than 0.02). Ulcers were found in 16 out of 72 patients (22%) taking NSAIDs and without H pylori infection or chemical gastritis compared with 27 out of 56 (48%) with H pylori related gastritis (p less than 0.01), and 25 out of 46 (54%) with chemical gastritis (p less than 0.01). CONCLUSIONS: Peptic ulcers associated with the use of NSAIDs seem to occur more commonly in patients with chemical gastritis or H pylori infection. Patients taking NSAIDs also seem to have a greater prevalence of chemical gastritis but a lower prevalence of H pylori than those not taking these drugs.

Adult↗
PubMed1999

Does acid suppression by antacids and H2 receptor antagonists increase the incidence of atrophic gastritis in patients with or without H. pylori gastritis?

Currently there is controversial evidence that suggests that the accepted incidence of atrophic gastritis of 1.2 to 3.3% in patients with Helicobacter pylori gastritis may be increased by the long-term suppression of acid by a proton pump inhibitor (omeprazole). The purpose of this study is to show whether lesser forms of acid suppression by antacids or H2 receptor antagonists may have an influence on the development of atrophic gastritis. The authors recently reported a study in which a cohort of 36 patients with symptoms of dyspepsia were followed clinically for a period of 7 to 19 years. In that report all subjects underwent upper endoscopy with two biopsy specimens each from the antrum and fundus, on at least two occasions, 7 to 19 years apart. A diagnosis of atrophic gastritis was based on the interpretation of these biopsies by two gastrointestinal pathologists. The presence of H. pylori colonization was determined by tissue sampling and by a campylobacter-like organisms test of the antrum. Of the 36 patients in the authors' previous report, 33 had adequate baseline and follow-up data on medications consumed throughout the period of the study. In their current report they now present the findings of a retrospective review in which they correlate the presence of atrophic gastritis with the sole use of antacids and H2 receptor antagonists throughout the period of the study. In the cohort of 33 patients evaluated from the previous report, the authors found that atrophic gastritis had developed in all 28 patients positive for H. pylori, and in none of the 5 patients negative for H. pylori (p < 0.0001). A retrospective analysis of this previously studied cohort of 33 patients revealed that the use of antacids and H2 receptor antagonists did not predict the development of atrophic gastritis in either H. pylori-negative or -positive subjects. In a retrospective analysis of a cohort of 33 patients followed for an average of 11.7 years, atrophic gastritis developed in H. pylori-positive but not in H. pylori-negative subjects, irrespective of the use and duration of antacids or H2 receptor antagonists.

Aged↗
PubMed2006

Surface structure of antral gastric mucosa represents the status of histologic gastritis: fundamental evidence for the evaluation of antral gastritis by magnifying endoscopy.

BACKGROUND: Recent studies have demonstrated the diagnostic potential of magnifying endoscopy in cases of histologic gastritis. The aim of the present study was to clarify whether the mucosal surface structure reflects the degree of histologic gastritis below the surface. METHODS: Gastric biopsy specimens were obtained from 1018 Japanese patients and were stained with hematoxylin and eosin. In 863 sections examined, gastritis was graded by means of the updated Sydney system, and the surface structure was classified as one of four types: flat, irregular, papillary, or non-structured. In addition, 103 patients underwent gastric examination by magnifying gastroscopy. RESULTS: The surface structure of most biopsy sections with normal mucosa and no Helicobacter pylori infection was classified as the flat type. Grades of histological gastritis were statistically lower in flat-type sections than in other types. Histologic gastritis was found in 91% of sections with a non-flat surface structure. Helicobacter pylori infection was confirmed in 96% of these cases. Most biopsy sections in patients with abnormal magnifying endoscopy features were of the non-flat type and showed histologic gastritis. CONCLUSIONS: The surface structure of the gastric mucosa reflects the status of histologic gastritis. Magnifying gastroscopy could be a useful non-invasive method of diagnosing histologic gastritis.

Female↗
PubMed1990

Lymphocytic gastritis--prospective study of its relationship with varioliform gastritis.

Lymphocytic gastritis is a new histopathological entity characterised by a dense lymphocytic infiltration of surface and pit gastric epithelium. Previous retrospective work has suggested that lymphocytic gastritis is related to an endoscopic form of gastropathy comprising enlarged folds, nodules and erosions, commonly denoted as varioliform gastritis. In the present prospective study, the relationship is clearly shown; nearly 82% (54/66) of the varioliform gastritis observed in four different endoscopy units correspond histologically to lymphocytic gastritis. The correlation is even better if cases showing strictly antral localisation are excluded (53/55) - that is, more than 96%. The histological concept of lymphocytic gastritis seems, however, to extend beyond varioliform gastritis as of 67 cases of lymphocytic gastritis diagnosed during the period under study, one third had no particular endoscopic expression.

Adolescent↗
PubMed1999

The comparison of histologic gastritis in patients with duodenal ulcer, chronic gastritis, gastric ulcer and gastric cancer.

This study was designed to investigate the differences of histologic gastritis according to the endoscopic diagnosis, and between H. pylori positive and negative gastritis, using the Sydney system. A total of 122 patients (42 duodenal ulcer, 31 chronic gastritis, 35 gastric ulcer and 14 gastric cancer) underwent endoscopy with biopsies from the antrum and body. Among the 122 patients, 104 (85%) were H. pylori positive. H. pylori density of the antrum was significantly higher in duodenal ulcer than in chronic gastritis, gastric ulcer, and gastric cancer. The positivity of intestinal metaplasia was lowest in duodenal ulcer and highest in gastric cancer. H. pylori density as well as grade of activity, inflammation and atrophy were significantly higher in the antrum than in the body in duodenal ulcer, while in chronic gastritis, gastric ulcer and gastric cancer there was no difference of H. pylori density, activity, inflammation and atrophy between the antrum and body. The grade of activity and chronic inflammation were significantly higher in H. pylori positive patients than in H. pylori negative patients in both the antrum and body. In conclusion, the gastritis of duodenal ulcer was mainly localized to the antrum, while the gastritis of chronic gastritis, gastric ulcer or gastric cancer was rather uniform in the antrum and body. H. pylori seemed to be related to the development of chronic inflammation and activity.

Adult↗
PubMed2000

Helicobacter pylori gastritis of the gastric carcinoma phenotype: is histology capable of identifying high-risk gastritis?

Several studies have shown that Helicobacter pylori infection implies an increased risk for developing gastric carcinoma. However, it has to be considered that only a few among those infected with H. pylori develop gastric cancer. It is therefore desirable to identify risk indicators of H. pylori gastritis in the presence of which gastric carcinoma is most likely to occur. In our view, the risk indicators intestinal metaplasia and atrophy, frequently cited in the literature, are not suitable, as they are focal changes whose detection at the routine diagnostic workup may be confounded by sampling error and because early carcinoma (in particular of the diffuse type) is often not associated with intestinal metaplasia or atrophy. For this reason we investigated the diffuse gastritis parameters "grade of gastritis" and "activity of gastritis" for their suitability as risk indicators. We found that H. pylori gastritis, particularly in the corpus, is significantly more pronounced in gastric carcinoma patients or individuals with a family history of gastric cancer than in matched controls. Hence, a simple comparison of the grade of gastritis and activity of gastritis in the antrum and corpus might help identify patients with H. pylori gastritis with an increased cancer risk. Currently. we are testing this hypothesis in an ongoing gastric cancer prevention study in Germany, Austria, and Czechia.

Cell Transformation, Neoplastic↗
PubMedDate not supplied

Apoptosis in Helicobacter pylori gastritis and residual gastritis after distal gastrectomy.

BACKGROUND/AIMS: Active gastritis, accelerated cell turnover followed by apoptosis, DNA damage and hyperplasia are often seen in the anastomosis area after gastrectomy. Recently, it has been reported that H. pylori induces apoptosis on gastric cells. Until now, the surgical effect itself and H. pylori infection have not been well differentiated as causes of apoptosis associated with gastritis. Our aim is to clarify the relationship of residual gastritis after gastrectomy and H. pylori gastritis. METHODOLOGY: Residual gastritis model using the Mongolian gerbil has been established with microsurgical technique. Residual gastritis with and without H. pylori infection was studied by histopathological examination and quantitated by Rauws' score. Elevation of pH in gastric juice after surgery was confirmed. Stimulation of downstream events leading to apoptosis, cleavage of poly-ADP-ribose polymerase as a result of activation of caspase-3, was evaluated using Western blotting. RESULTS: Histopathologically, H. pylori infection led to deterioration after surgery. The postoperative Rauws' score with infection was higher than without infection. Cleavage of poly-ADP-ribose polymerase was increased after surgery in gerbils with and without H. pylori infection. Densitometric study showed a greater increase in the animals with H. pylori infection than those without infection that was enhanced after surgery (0.59 vs. 1.04, 0.73 vs. 1.17, respectively). CONCLUSIONS: Apoptosis is increased both in residual gastritis and H. pylori gastritis. Both enterogastric reflux and H. pylori infection may be linked to tumorigenesis in anastomosis sites followed by accelerated epithelial cell turnover followed by apoptosis.

Animals↗
PubMed1990

Helicobacter mustelae-associated gastritis in ferrets. An animal model of Helicobacter pylori gastritis in humans.

Gastric Helicobacter mustelae was present in 100% of 11 adult female ferrets (Mustela putorius furo). The high immunoglobulin G antibody levels to H. mustelae in all ferrets showed a significant immune response to the organism. Urease mapping of the ferret stomach indicated that the bacteria heavily colonized the proximal duodenum and antrum and, to a lesser extent, the corpus. The histological gastritis observed coincided with presence of H. mustelae. Superficial gastritis was noted in the oxyntic gastric mucosa, whereas in the distal antrum the chronic inflammatory response occupied the full thickness of the mucosa. In the proximal antrum and transitional mucosa, focal glandular atrophy and regeneration were observed. Seven control specific-pathogen-free ferrets were not colonized with the bacteria, did not have detectable levels of immunoglobulin G H. mustelae antibody, and did not have H. mustelae-associated gastritis. The ferret lacks the polymorphonuclear-cell response seen in active chronic gastritis typically described with Helicobacter pylori gastritis in humans. However, the lesion in ferrets does closely resemble the diffuse antral gastritis seen in a subset of adults with H. pylori gastritis as well as children infected with H. pylori. Like H. pylori, H. mustelae adheres tightly to gastric mucosa. The ferret infected with H. mustelae, in addition to specific-pathogen-free uninfected control ferrets, will make longitudinal studies possible, enabling dissection of multiple host and environmental variables that influence the effect of H. mustelae colonization on progression and severity of gastroduodenal disease.

Animals↗
PubMed1989

Mucosal mast cells in reflux gastritis and chronic (type B) gastritis.

The histological features that characterize alkaline reflux gastritis are typical of the histamine-mediated response to tissue injury. We have investigated this in nine patients with symptomatic reflux gastritis following partial gastrectomy for duodenal ulcer by determining the gastric mucosal mast cell count before and after Roux-en-Y biliary diversion. Following diversion, the histological picture changed from that of reflux gastritis to type B chronic gastritis in all cases. The mean mucosal mast cell count in all patients was 47.57/mm2 before diversion and 123.33/mm2 after diversion (P less than 0.05). Analysis of the paired data, in which eight out of nine patients showed a rise in mucosal mast cell numbers following bile diversion, also showed a significant difference before and after surgery (P less than 0.01). The gastric mucosal mast cell count is significantly less in reflux gastritis than in type B chronic gastritis. This is most likely to be due to increased degranulation, which would explain why striking vascular changes occur in the absence of inflammatory cell infiltration in reflux gastritis.

Anastomosis, Roux-en-Y↗
PubMed2003

Intragastric ascorbic but not uric acid is depleted in relation with the increased pH in patients with atrophic body gastritis and H. pylori gastritis.

BACKGROUND: Helicobacter pylori gastritis induces reversible lowering of Ascorbic Acid (AA) intragastric concentrations. No studies have been aimed at determining the gastric juice AA concentration of atrophic body gastritis (ABG) patients. Uric Acid (UA), is another potent hydro-soluble scavenger of ROS and its possible modification in the gastric juice of patients with H. pylori gastritis have never been investigated. This study was aimed at investigating the levels of AA and UA in the plasma and gastric juice of ABG patients, compared with H. pylori positive patients without corporal atrophy, and with healthy individuals. MATERIALS AND METHODS: Thirteen ABG patients (Group 1); 32 Chronic non-atrophic H. pylori gastritis patients (Group 2); and 13 healthy stomach controls (Group 3) attending gastroscopy with gastric biopsies (antrum=3, corpus=3) had plasma and intragastric levels of AA and UA measured. RESULTS: Intragastric AA concentration was significantly lower in group 1 (median 0.21 microg/ml, range 0.1-24) compared both with groups 2 (median 5.5 microg/ml, range 0.1-33.2) (p=0.043) and 3 (median 14.9 microg/ml, range 0.34-44.8) (p=0.0028). Intragastric UA was not different between the three groups. Intragastric AA concentration resulted negatively correlated with the intragastric pH (Spearman r=-0.47, p=0.0003). In patients with gastritis (groups 1 and 2) there was a significant negative correlation between the sum of the Sydney Score variables in the body mucosa, and AA in the gastric juice (Spearman r=-0.55; p=0.0001). CONCLUSION: The study shows that intragastric pH is the key factor for the depletion of gastric juice AA observed in patients with corporal atrophy and to a lower extent with nonatrophic H. pylori gastritis.

Adolescent↗
PubMed2002

Animal models of human disease: experimental autoimmune gastritis--a model for autoimmune gastritis and pernicious anemia.

Human autoimmune gastritis is an organ-specific autoimmune disease of the stomach. It is characterized by the development of disease-specific autoantibodies and a pathology that specifically targets specialized cells within the gastric environment. The autoantigens associated with this disease have been defined as the gastric H+/K+ ATPase and intrinsic factor. The development of experimental disease models has been pivotal in our contemporary understanding of autoimmunity. Here we review mouse models of autoimmune gastritis and their relevance to human autoimmune gastritis associated with pernicious anemia. We appraise some historical as well as recent studies of experimental autoimmune gastritis (EAG), highlighting key findings that have formed the basis of our current understanding of the etiology and mechanism(s) associated with autoimmune gastritis. A precise understanding of the pathogenesis of autoimmune gastritis will permit the design of innovative and rational therapeutic strategies to prevent, arrest, ameliorate or reverse the disease.

Anemia, Pernicious↗
PubMed1977

Gastric acid secretion in chronic atrophic gastritis and chronic (superficial) gastritis.

Basal and pentagastrin-stimulated peak acid outputs were determined in 21 subjects with chronic atrophic gastritis and 10 subjects with chronic superficial gastritis. All subjects were Caucasian. The histological diagnosis was based on multiple gastric biopsy specimens obtained through a fibregastroscope. Comparison of the results with those of a previously reported Caucasian control group show that the mean basal acid outputs of subjects with chronic (superficial) gastritis were significantly higher than that of controls and subjects with chronic atrophic gastritis. No significant difference was found in the mean peak acid outputs of controls and subjects with chronic atrophic gastritis or chronic (superficial) gastritis.

Atrophy↗
PubMed1987

[Atrophic corpus gastritis and autoimmune gastritis].

The authors tried to clarify relations between autoimmune gastritis and isolated atrophic corpus gastritis by bioptic corporal and antral examinations from 150 probands as well as examinations of gastrin in serum and parietal cell antibody tests. Only 30% of all patients examined with isolated atrophic gastritis of the corpus part revealed criteria of an autoimmune gastritis. Therefore investigations of antibodies against parietal cells are necessary to mark off both clinical pictures. This differentiation seems to be necessary regarding the high risk of gastric cancer following an autoimmune gastritis.

Autoantibodies↗
PubMed1993

Serum and gastric mucosal pepsinogens in atrophic gastritis, particularly in type A gastritis associated with pernicious anemia in Japanese.

The levels of serum pepsinogen I (PG I) and pepsinogen II (PG II) were determined by IRMA (immunoradiometric assay) and the ratio of PG I/II calculated in 37 patients with type A gastritis and concomitant pernicious anemia (PA) and in 97 with chronic gastritis (type B gastritis) among Japanese. In several patients from each group, PG I and PG II in the gastric mucosa were stained by an enzyme antibody assay to compare the percentage of positively stained cells with levels of serum PG I and PG II. The levels of serum PG I and PG II in chronic gastritis decreased as the degree of atrophy increased. Serum PG I and PG II levels in PA were lower than those of patients with severe atrophy. Most of serum PG I levels in PA were less than 10 ng/ml. The PG I/II ratio also decreased as the severity of atrophy increased, distinctly showing that in PA, the ratio were quite low and most of them are less than 1.0. Gastric mucosal pepsinogen showed a tendency similar to that of serum levels and also refrected the degree of atrophy. Therefore, by measuring these parameters it should be easier to determine the extent of atrophy, and to establish a serological diagnosis of type A gastritis associated with PA.

Anemia, Pernicious↗