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BACKGROUND: Helicobacter pylori-associated gastritis has been linked to the pathogenesis of gastric adenocarcinoma (GA), especially when associated with intestinal metaplasia (IM) and atypia/dysplasia (A/D). We examined p53 expression, ploidy and proliferative activity and assessed H. pylori infection in relationship to IM and/or A/D in cases of gastritis not associated with GA and in cases of GA. METHODS: We examined 53 gastric biopsies from patients with gastritis not associated with GA, including patients with gastritis not associated with IM and/or A/D (n=35) and with gastritis associated with IM and/or A/D (n=21). Thirty-six distal gastrectomy specimens from patients with GA constituted a third group of patients. A scoring system that encompassed the presence or absence of H. pylori, degree of gastritis, IM and/or A/D, p53, MIB-1 proliferative index (MPI) and ploidy was estimated in the cases of gastritis and in cancer-associated mucosa (CAM) and the adenocarcinoma from patients with GA. RESULTS: Patients with GA had a higher median age than those with gastritis without IM and more were males (ratio, 2.2:1). H. pylori was detected in 75% (40/53) of gastritis specimens and in 55% (20/36) of GA cases. There was a statistically significant difference between the incidence of gastritis without IM and/or A/D and CAM (P=0.01). p53 expression was seen in 67% of cases (14/21) of gastritis with IM and/or A/D and in only 5% (2 cases) of gastritis without IM (P=0.0005). A statistically significant difference in MPI was seen between CAM and GA (P=0.01) and gastritis without IM and/or A/D and gastritis with IM (P=0.004). Cases of gastritis without IM and/or A/D had a median score of 8 while cases of gastritis with IM and/or A/D had a median score of 12 (P=0.0003). CAM had a median score of 13, which was significantly different than gastritis without IM and/or A/D (P=0.0003). CONCLUSIONS: The presence of IM and/or A/D can be used in H. pylori-associated gastritis as a starting point to further investigate high-risk lesions. Those showing p53 expression, high proliferative activity and aneuploidy require closer follow up and perhaps additional biopsies. Although aneuploidy is commonly seen in GA, its presence in cases of gastritis as an isolated finding should not indicate a high-risk lesion.
Bile reflux gastritis is due to an excessive reflux of duodenal contents into the stomach. The increased enterogastric reflux may provide the basis for increased mucosal injury. Bile reflux gastritis can appear in two circumstances: gastric resection with ablation of pylorus and primary biliary reflux due to the failure of pylorus. The aim of the study was to evaluate the endoscopical and histological changes caused by duodenal reflux on the gastric mucosa. The mucosal features were correlated with the risk factors involved in the development of bile reflux gastritis. Our study included 230 patients with alkaline reflux gastritis admitted in Medical Clinic no. 1, Emergency County Hospital Craiova. In all cases we performed an upper gastrointestinal endoscopy. Multiple biopsies were taken from gastric mucosa in 89 patients and the histological features were scored in accordance with the Sydney system. The average age of the patients with bile reflux gastritis was 58.387 years and the incidence of alkaline reflux gastritis was higher between 51 and 80 years. Reflux gastritis was noted to 138 males lpar;60%rpar; and 92 females (40%), ratio males/females was 1.5/1. The most frequent risk factors for bile reflux gastritis were gastric and biliary surgery. Alkaline reflux gastritis was observed in 167 cases (72.6%) after gastric surgery, consisting in gastric resection, pyloroplasty and gastroenteric-anastomosis. Gastroduodenal reflux after biliary surgery was noted in 17 cases (7.39%), 13 cases (5.69%) with cholecystectomy and four cases (1.73%) with biliary anastomosis. The average time interval from original operation to the discovery of the alkaline reflux gastritis was 14.91 years after gastric surgery and 15.29 years after biliary surgery. The commonest endoscopic alterations were: erythema of the gastric mucosa in 139 cases (64.43%), the presence of bile into the stomach in 133 cases (57.83%), the thicken of gastric folds in 22 cases (9.55%), erosions in 12 cases (5.22%), gastric atrophy in 12 cases (5.22%), petechiaes in five cases (2.17%), intestinal metaplasia one case (0.43%) and gastric polyp one case (0.43%). The histologic alterations observed from tissues collected during endoscopic examination were: chronic inflammation in 75 cases (84.06%), foveolar hyperplasia in 36 cases (40.44%), intestinal metaplasia in 31 cases (34.83%), acute inflammation in 16 cases (16.08%), Helicobacter pylori infection in 16 cases (16.08%), chronic atrophic gastritis in 12 cases (13.46%), gastric polyps in 12 cases (13.46%), dysplasia in 10 cases (11.23%), benign ulcerations in seven cases (3.04%), edema in six cases (6.74%) and neoplasia two cases (2.24%). Conclusions. Bile reflux gastritis was more frequent to male gender. The most frequent risk factors for alkaline reflux gastritis were gastric and biliary surgery. Reflux gastritis after gastric resection, pyloroplasty and gastroenteric-anastomosis were more frequent to male gender, while cholecystectomy and biliary anastomosis were predominantly to female gender. The average time interval from original operation to the discovery of the bile reflux gastritis was similar after gastric and biliary surgery. The commonest endoscopic alterations were: erythema of the gastric mucosa, the presence of bile into the stomach, thickens of gastric folds, erosions, gastric atrophy, petechiaes, intestinal metaplasia and gastric polyp. Acute inflammation, Helicobacter pylori infection, gastric polyps and benign ulcerations were more frequent in patients with bile reflux gastritis after gastric surgery, while edema and dysplasia were increased after biliary surgery.
Eosinophil granules contain cationic proteins, including the major basic protein, which are toxic to mammalian tissue. While eosinophils have been observed to comprise part of the inflammatory reaction in acute Helicobacter pylori gastritis, the role of the eosinophil in the pathogenesis of chronic gastritis is unknown. We evaluated whether eosinophil infiltration and degranulation are associated with chronic gastritis and H. pylori infection. We studied eight patients with chronic H. pylori antral gastritis, three with chronic antral gastritis in the absence of H. pylori, 11 healthy age-matched volunteers without antral gastritis, and eight patients with H. pylori-negative chronic specific gastritis (three Crohn's antral gastritis and five Ménétrier's disease). Serial sections were stained with hematoxylin and eosin, with Giemsa, and by a specific indirect immunofluorescence technique for eosinophil granule major basic protein. Specimens were graded independently by three observers and scores of 0-3 were given for eosinophil infiltration and degranulation (0 = none to 3 = confluent infiltration and/or degranulation). In H. pylori antral gastritis, significantly greater eosinophil infiltration and degranulation were found compared to the normal group, Ménétrier's disease, and chronic H. pylori-negative gastritis. There was no significant difference between gastric Crohn's disease and H. pylori gastritis. The severity of chronic gastritis was significantly correlated with the eosinophil score. Eosinophil degranulation did not appear to be greater at or near sites of bacterial colonization in the H. pylori gastritis specimens. The results suggest that eosinophil infiltration and degranulation may be associated with H. pylori gastritis. We postulate that the release of toxic cationic proteins from eosinophils contributes to the inflammatory changes present in H. pylori gastritis.
Chronic (atrophic) gastritis is a progressive disease which in a small proportion of patients leads to severe (total) atrophy (severe grade of chronic gastritis) of the antral or body mucosa or both. Chronic gastritis is a premalignant condition which favours the development of gastric cancer. Chronic gastritis precedes gastric cancer and shows a severalfold increase in the risk of gastric cancer compared to subjects with histologically normal stomach. Several tentative modifications to the estimate of the risks may be presented: (i) a severe risk of developing gastric cancer is restricted to subjects with a severe grade of chronic gastritis (ii) the risk of gastric cancer is increased in subjects who have either severe antral or body chronic gastritis, the risk being approximately three to five times higher in the antral chronic gastritis (B-type of gastritis) than in the body chronic gastritis (A type of gastritis); (iii) the antral and body chronic gastritis are independent risk factors for gastric cancer, the joint risks being multiplicands of the marginal risks i.e., the estimated risk is highest in those subjects who show severe chronic gastritis in both the antrum and the body (AB type of gastritis); (iiii) the chronic gastritis mediated gastric cancer risk is limited to gastric cancers of the intestinal type, and thus covers only a proportion of all cases of gastric cancer. In the highest risk groups it may be estimated that the probability of a subject developing gastric cancer in subsequent decades is up to 30% if the subject is a young man who has severe chronic gastritis in his antrum, or who has it coexistently in the antrum and body.
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.
The extent of fundal gastritis and the severity of antral gastritis in patients with duodenal ulcer and coexisting gastroduodenal ulcers were investigated using the endoscopic Congo red test. Forty-two patients with duodenal ulcer were followed-up by chromoendoscopy to investigate the location of gastric ulcers developed during the average observation period of 3.6 years in relation to the changes of fundal and antral gastritis. Duodenal ulcers were usually associated with extensive acid-secreting areas and moderate antral gastritis. In coexisting duodenal and antral ulcers, antral gastritis was usually severe, although fundal gastritis was of the same intensity as that seen with duodenal ulcers. In coexisting duodenal and high-lying ulcers, fundal gastritis was extensive and antral gastritis was severe. Follow-up studies showed that there was a significant relationship between the development of gastric ulcer and the changes of antral and fundal gastritis. Gastric ulcers developed in the antrum or the angulus in patients with duodenal ulcer when antral gastritis became worse, but no fundal gastritis spread. When fundal gastritis spread, ulcers developed in the gastric body. These findings suggested that development of increasing gastritis predicted the development of gastric ulceration and that the locations of gastric ulcer and duodenal ulcer were determined by the extent of fundal gastritis and the severity of antral gastritis.