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At least 19 recordsLinked to original sources
PubMed1995

Ten year follow up study of lymphocytic gastritis: further evidence on Helicobacter pylori as a cause of lymphocytic gastritis and corpus gastritis.

AIMS: To examine the course of lymphocytic gastritis and its relation to Helicobacter pylori (H pylori) infection in a 10 year follow up. METHODS: Ninety six patients were originally examined for dyspepsia in 1981. Gastroscopies with stepwise biopsies were performed on all the patients initially and after an interval of 10 years. RESULTS: Nine per cent of the patients (9/96) had features of lymphocytic gastritis in gastric biopsy at the first examination, and 12.5% (12/96) at the second examination; 7/9 patients (78%) had persistent lymphocytic gastritis during the follow up; in two the diagnostic features of lymphocytic gastritis had disappeared, and five had a new diagnosis of lymphocytic gastritis at the second examination. At the second examination 9/12 lymphocytic gastritis patients (75%) were H pylori positive histologically, while all had specific antibodies to H pylori. The lymphocytic gastritis patients had higher grades of gastritis (p = 0.009), neutrophilic and eosinophilic granulocytes, mononuclear inflammatory cells, and foveolar hyperplasia in the corpus mucosa, but smaller numbers of H pylori, than the H pylori positive patients without lymphocytic gastritis. The appearance of lymphocytic gastritis during the 10 year interval was associated with increases in the grades of corpus gastritis and neutrophilic granulocytes (p = 0.043 for both). During the follow up, the patients with lymphocytic gastritis, but not the H pylori positive patients without lymphocytic gastritis, appeared to have a significant increase in the grade of intestinal metaplasia in the corpus mucosa (p = 0.043). CONCLUSIONS: In some patients H pylori may cause a gastritis that predominates in the corpus and is associated with an increase in the intraepithelial lymphocyte count. This form of gastritis may cause progression of intestinal metaplasia.

Adult↗
PubMed2003

Interaction of Helicobacter pylori-induced follicular gastritis and autoimmune gastritis in BALB/c mice with post-thymectomy autoimmune gastritis.

BACKGROUND: There is still controversy about the relationship between Helicobacter pylori infection and autoimmune gastritis. The aim of this study was to clarify whether or not H. pylori infection interacts with the development of autoimmune gastritis. METHODS: Neonatally thymectomized BALB/c mice with autoimmune gastritis received orally administered H. pylori and were examined histologically and serologically. The T-helper (Th)1/Th2 immune balance in the microenvironment of the stomach was evaluated by reverse-transcriptase-polymerase chain reaction (RT-PCR) for interferon (IFN)-gamma and interleukin (IL)-4. RESULTS: Uninfected mice showed disappearance of parietal cells, and upregulation of IFN-Gamma, but no germinal center formation. The infected neonatally thymectomized mice showed follicular gastritis, preserved parietal cells, decreased serum anti-parietal antibodies, and upregulation of IL-4 and IFN-gamma. CONCLUSIONS: H. pylori infection changes the microenvironment of the gastric mucosa by inducing a Th2 immune response in addition to a Th1 response, and regresses autoimmune gastritis in neonatally thymectomized BALB/c mice.

Animals↗
PubMed1989

Can gastritis symptoms be evaluated in clinical trials? An overview of treatment of gastritis, nonulcer dyspepsia and Campylobacter-associated gastritis.

We carried out a review of the literature on Campylobacter pylori-associated gastritis and nonulcer dyspepsia (NUD) to determine whether or not symptoms related to these conditions can be measured reliably and whether or not any study to date has shown that treatment alters symptoms. Search strategies consisted of online Medline searching, a forward search of three articles using the Science Citation Index, a manual search of five gastroenterological journals, and a fully recursive search of cited references. Inclusion and quality criteria were applied to all retrieved studies. Nine of 23 studies did not fulfill the inclusion criteria. Of the 14 studies analyzed, two measured symptoms reliably. Neither showed a therapeutic benefit on symptoms. The difficulties encountered in conducting such studies and the methods of recording symptoms reliably are discussed. We conclude that to date, no treatment is of proven benefit in the relief of symptoms associated with C. pylori gastritis and NUD.

Campylobacter Infections↗
PubMed1996

Minimal chronic inactive gastritis: indicator of pre-existing helicobacter pylori gastritis?

Minimal chronic inactive gastritis is regularly observed in routine histopathology. Presently, it is not clear whether this type of gastritis should be regarded as a histopathological entity or a normal variant. The similarity to lesions observed after H.pylori eradication prompted us to look for an association between minimal chronic inactive gastritis and status post H.pylori eradication. In a prospective study of 110 consecutive patients undergoing upper gastrointestinal endoscopy, at least two mucosal biopsies were taken from the gastric antrum and body. Gastritis was classified according to the Sydney System. Antibodies to H.pylori were determined serologically by immunofluorescence test, ELISA, and complement binding reaction. A status post eradication of H.pylori was revealed by medical history and/or positive serology; H.pylori gastritis was found in 39.1%, reactive gastritis in 12.7%, and minimal chronic inactive gastritis in 29.1%. In 19.1% a combination of reactive/ minimal chronic gastritis was diagnosed according to morphology. Status post eradication was observed significantly more often in cases with minimal chronic inactive gastritis (43.8%) than in cases with reactive gastritis (7.1%, p < 0.004). Furthermore, positive ELISA and/or status after eradication was found in 50% of the cases with minimal chronic inactive gastritis (p < 0.005 vs reactive gastritis), in 42.9% of the cases with mixed reactive/chronic inactive gastritis (p < 0.03 vs reactive gastritis), and in 7.1% of the cases with reactive gastritis. Lymphoid aggregates, considered another sign of former H.pylori presence, were found significantly more often in minimal chronic inactive gastritis than in reactive gastritis (50% versus 7.1%, p < 0.005). Minimal chronic inactive gastritis is significantly associated with both positive H.pylori serology and status post eradication and is, therefore, an indicator of pre-existing H.pylori gastritis.

Biomarkers↗
PubMed2003

Expression of cyclooxygenases in Helicobacter pylori gastritis and residual gastritis after distal gastrectomy.

It has long been thought that duodenal reflux induces residual gastritis after distal gastrectomy. H. pylori infection appears to be another factor in residual gastritis; and H. pylori induced gastritis may exist preoperatively or may have been introduced postoperatively. Up until now, the surgical effect itself and H. pylori infection have not been well differentiated as causes of residual gastritis. Our aim in this study was to clarify the relationship between the surgical effect and H. pylori infection in residual gastritis. A residual gastritis model using the Mongolian gerbil has been established with microsurgical technique. Residual gastritis with and without H. pylori infection has been studied by histopathological examination and quantitated by Rauws' score. The expression of cyclooxygenase (both COX-1 and COX-2) has also been examined immunohistologically. Elevation of pH in gastric juice after surgery was confirmed. H. pylori infection led to deterioration after surgery. The postoperative Rauws' score with infection is higher than without infection. Levels of COX-1 were higher after surgery in both animals. COX-2 was not expressed in the animals without infection and only a little was expressed in the animals with infection. COX-2 was strongly expressed in the operated animals with infection, but the surgical effect was minute in the animals without infection. Residual gastritis consisted of both surgical gastritis and H. pylori gastritis. H. pylori gastritis is curable with eradication of the organism, but surgical gastritis is not. The COX inhibitor can be a good candidate in preventing residual gastritis after eradication of the H. pylori organism. The clinical implications of COX expression for patients with residual gastritis might deserve further study in the point of treatment of surgical and H. pylori gastritis.

Animals↗
PubMed1996

A clinicopathologic study of 42 patients with granulomatous gastritis. Is there really an "idiopathic" granulomatous gastritis?

Idiopathic granulomatous gastritis (IGG) is a diagnosis made only by excluding other causes of granulomatous gastritis, such as infection, foreign bodies, and systemic granulomatous diseases. Recently, several investigators have questioned the existence of IGG. We reviewed the slides and clinical data of all cases of granulomatous gastritis seen at the Cleveland Clinic between 1975 and 1994. In addition to routine hematoxylin and eosin stains, slides from all cases were stained with Ziehl-Neelsen, Gomori's methenamine silver, and Giemsa stains. Clinical information and follow-up were available for 42 patients. The clinicopathologic diagnoses of the 42 patients with granulomatous gastritis were as follows: Crohn's disease (n = 23), three of whom had concomitant chronic active gastritis with Helicobacter pylori infection; sarcoidosis (n = 9), four of whom had concomitant chronic active gastritis with H. pylori infection; chronic active gastritis with H. pylori infection and no other systemic illness (n = 2); distal esophageal adenocarcinoma and chronic active gastritis (n = 2); mucosa-associated lymphoid tissue (MALT) lymphoma with chronic active gastritis and presumed H. pylori infection (n = 2); peptic ulcer complications (n = 2); hypertrophic gastropathy with chronic active gastritis (n = 1); and possible Crohn's disease (n = 1). We conclude that (a) in most cases of granulomatous gastritis, a diagnosis of Crohn's disease or sarcoidosis could be established; (b) the background inflammatory pattern was helpful in suggesting a diagnostic category for granulomatous gastritis; (c) granulomatous gastritis is not associated with H. pylori per se; however, if known cases of Crohn's disease and sarcoidosis are excluded, an association between H. pylori and granulomatous gastritis cannot be ruled out; and (d) IGG, if it exists, is extremely rare.

Adenocarcinoma↗
PubMedDate not supplied

[Varioliform gastritis: frequency and relationship with lymphocytic gastritis].

Varioliform gastritis is currently recognized as a special kind of chronic gastritis characterized by nodules, thickened fugal folds and erosions. These features appear to be unusual and different from those seen in chronic gastritis. The frequency of varioliform gastritis rarely exceeds 3% and the diagnosis can be easily made by endoscopic examination. Very little is known about the etiopathogeny, clinical significance and evolution of this disease. The role of Helicobacter pylori still remains unknown, although a close relationship between this gastritis and lymphocytic gastritis was suggested to exist over the last few years. The aim of the present study was to investigate the frequency of varioliform gastritis and its possible correlation with lymphocytic gastritis. To our knowledge, this is the first systematic study of varioliform gastritis in South America. We studied endoscopically 200 consecutive patients and found only one case of varioliform gastritis (0.5%). In a second part of the study, we examined histopathologically mucosa biopsies from 24 patients with varioliform gastritis and studied the presence of intraepithelial lymphocytes to verify the presence of lymphocytic gastritis. No case was found. We conclude that there was no correlation between varioliform gastritis and lymphocytic gastritis in our patients.

Adolescent↗
PubMed2003

Endoscopic nodular gastritis: an endoscopic indicator of high-grade bacterial colonization and severe gastritis in children with Helicobacter pylori.

OBJECTIVE: To investigate the significance of endoscopic nodular gastritis associated with Helicobacter pylori infection. METHODS: This prospective study included 185 children (50.8% boys) aged 1 to 12 years (mean, 6.9 +/- 3.0 years) who underwent upper intestinal endoscopy during evaluation of chronic abdominal pain. The authors assessed the endoscopic appearance of the stomach, noting those patients with endoscopic nodular gastritis. Urease activity of gastric mucosal biopsies was measured. With histologic examination, the presence and density of H. pylori organisms, the presence of follicular gastritis, the nature of inflammation, and the gastritis activity grade and overall gastritis score were assessed. RESULTS: H. pylori infection was identified in 50 children (27%). Endoscopic nodular gastritis was significantly associated with active chronic gastritis and follicular gastritis. Nodularity in the stomach showed a high specificity (98.5%) and positive predictive value (91.7%) for the diagnosis of H. pylori infection and was observed in 22 of 50 (44%) H. pylori-positive patients and in 2 of 135 (1.5%) H. pylori-negative patients. A significant association was observed between older age and the prevalence of this finding (P< 0.001). There was a significant increase in endoscopic nodular gastritis with increased H. pylori density and a positive correlation (Pearson coefficient = 0.97) with increased gastritis score on histologic examination. Increase in gastritis score was dependent on increased H. pylori density in patients with gastric nodularity; this finding was independent of age. CONCLUSIONS: Endoscopic findings of antral nodularity in children suggest the presence of H. pylori infection and follicular gastritis and may identify cases of severe gastritis and marked bacterial colonization.

Abdominal Pain↗
PubMed1997

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↗
PubMed1989

Chronic gastritis and gastroduodenal ulcer: a case control study on risk of coexisting duodenal or gastric ulcer in patients with gastritis.

Chronic (atrophic) gastritis (AG) is common in active duodenal (DU) and gastric ulcer (GU) disease. In this case control study in consecutive prospective outpatients (571 cases and 1074 controls) who had undergone diagnostic upper gastrointestinal endoscopy and routine biopsies from both antral and body mucosa, we calculated the risk of coexisting active DU and/or GU in different gastritis of the antrum or body and according to grade (superficial gastritis, mild, moderate or severe atrophic gastritis). The risk of coexisting active gastroduodenal ulcer (ulcer in duodenum and/or stomach), as well as the risk of DU or GU, was dependent upon the presence and grade of gastritis in antrum and body mucosa. The risk of coexisting ulcer, as expressed as an age adjusted relative risk (RR) and calculated as odds ratio of gastritis in cases and controls, was significantly increased in the presence of superficial antral and body gastritis (RR = 8.5 (7.0-20.0) in men; RR = 5.8 (3.3-10.2) in women), as compared with the risk of ulcer in subjects with histologically normal mucosa (RR = 1). The risk of ulcer, and the risk of GU in particular, increased further with increasing severity of antral gastritis. In such patients with moderate or severe atrophic antral gastritis the RR of coexisting ulcer even exceeded 20 in men and 10 in women (RR = 25.6 (9.0-72.7) in men; RR = 11.7 (5.9-23.0) in women). On the other hand, the RR of ulcer, and the RR of DU in particular, was below 1 in the presence of atrophic gastritis in the gastric body, irrespective of the grade of gastritis in the antrum. We conclude that the type and grade of gastritis strongly predicts the risk of coexisting peptic ulcer, and that the risk of coexisting DU or GU increases with an increase in grade of AG of the antrum but decreases with an increase in grade of AG of the gastric body.

Adolescent↗
PubMed1999

Antigenic phenotyping of lymphoid cells and B cell gene rearrangement in type B gastritis and in gastritis not associated with Helicobacter pylori colonization.

Marginal-zone B cells of the mucosa-associated lymphoid tissue (MALT) are the normal counterpart of the neoplastic cells in MALT lymphoma. In both cases these lymphocytes express surface immunoglobulins, but are negative when stained for B cell associated antigens like CD10 and CD23. Furthermore, the B cell gene rearrangement has been found in Helicobacter pylori associated chronic gastritis and in extranodal type of marginal-zone lymphoma. The aim of this study was to quantify the number of IgM-, CD10-, and CD23-positive lymphocytes in patients with type B gastritis and to compare the results with the antigen profile of mononuclear cells in patients with gastritis not associated with H. pylori. Additionally, the immunoglobulin heavy-chain (IgH) gene rearrangement in H. pylori positive and H. pylori negative gastritis was studied. From 23 patients with a positive urease test and/or histologically proven H. pylori infection and chronic gastritis and from 22 patients with H. pylori negative chronic gastritis mucosa biopsy specimens were taken. Single-cell suspensions were obtained following enzymatic digestion. For immunocytochemistry, an alkaline phosphatase-antialkaline phosphatase method was applied. IgH gene rearrangement in formalin-fixed, paraffin-embedded specimens was determined by polymerase chain reaction in 11 patients with chronic gastritis. An increase in mu-positive plasma cells and B lymphocytes was detected in patients with H. pylori positive gastritis as compared with patients with H. pylori negative gastritis (10.0 vs. 3.9%, p < 0.001, and 4.3 vs. 1.6%, p < 0.01, respectively). In both groups, the proportion of CD10- and CD23-positive lymphocytes was <1%. IgH gene rearrangement was not restricted to type B gastritis; single bands were also present in 3 of 7 patients with H. pylori negative chronic gastritis. Our finding of IgH gene rearrangement in some of the patients with H. pylori negative chronic gastritis indicates that additional factors may be critical for these genotypical changes and for the pathogenesis of gastric MALT lymphoma.

Adolescent↗
PubMed2001

Level of serum cytokines in biliary gastritis and erosive gastritis with Helicobacter pylori coinfection.

The aim of this study was evaluation of serum cytokines level in patients with biliary and erosive gastritis. 50 patients were admitted to this study: 20 with biliary, 20 with erosive gastritis and 10 as the control group. In all patients serum levels of Il-8, Il-6R, Il-2R were evaluated. In each group half patients were infected by Helicobacter pylori, and the second half were uninfected. Mean level of Il-8 in patients with biliary gastritis was higher than in those in the control group, and was more increased in Helicobacter pylori infected patients than in uninfected ones. In erosive gastritis accompanied by Helicobacter pylori infection mean level of Il-8 was higher than in uninfected patients for which the level was normal. Serum Il-6R levels in biliary gastritis with infection by Helicobacter pylori were higher than in biliary gastritis without infection. These values were statistically significant vs. the control group. In erosive gastritis accompanied by Helicobacter pylori mean level of Il-6R was higher than in the control group, but was normal in patients without Helicobacter pylori. We noticed no influence of Helicobacter pylori infection on Il-2R levels in patients with biliary gastritis and erosive gastritis. These levels were normal in all groups of patients. In conclusion, in biliary gastritis we found the levels of Il-8, Il-6R higher than in erosive gastritis. Particularly significantly high levels of Il-8, Il-6R were observed in gastritis accompanied by Helicobacter pylori infection.

Adult↗
PubMed1993

Giant fold gastritis--a special form of Helicobacter pylori associated gastritis.

We investigated the question as to how frequently Helicobacter pylori gastritis is present in cases of endoscopically detected giant folds of the corpus and fundic mucosa, and whether this gastritis differs from Helicobacter pylori associated gastritis with no giant folds. Biopsy material obtained from 138 patients with giant folds (sex ratio: 1.0 men: 105 women; average age 61.0 years) was evaluated histologically and compared with that obtained from 1,196 patients with H. pylori associated gastritis without giant folds (1.1 men: 1.0 women; average age 51.9 years). Among the patients with giant folds, H. pylori colonisation of the gastric mucosa was found in 88.4% of the cases. The degree of H. pylori colonisation determines the degree and activity of the gastritis in the antrum and corpus (p < 0.001). A comparison of the degree of colonisation with H. pylori, the degree of gastritis and the activity of the gastritis in patients with giant folds and in H. pylori gastritis without giant folds revealed no statistically significant differences within the antrum. In contrast, in the case of the corpus, a comparison between the two groups showed that H. pylori colonisation, degree of gastritis, and activity of gastritis were statistically significantly more pronounced in patients with giant folds than in patients with H. pylori gastritis but no giant folds (p < 0.0001). A comparative analysis showed that giant fold formation in the fundus and corpus of the stomach may be a consequence of severe high-grade active H. pylori gastritis, that is, a special and rare form of reaction to the colonisation of the gastric mucosa with Helicobacter pylori.(ABSTRACT TRUNCATED AT 250 WORDS)

Biopsy↗
PubMed1991

Prevalence of Helicobacter pylori in specific forms of gastritis. Further evidence supporting a pathogenic role for H. pylori in chronic nonspecific gastritis.

Helicobacter pylori colonization of the gastric mucosa is strongly associated with chronic nonspecific gastritis; moreover, there is evidence to suggest that H. pylori may cause this form of gastritis. However, there is little or no information on the prevalence of H. pylori in specific forms of gastritis. Our hypothesis was that if H. pylori was pathogenic in chronic nonspecific gastritis, organisms would be found frequently in this type of gastritis but infrequently in specific forms of gastritis. Prevalence rates of H. pylori were determined independently in patients with eosinophilic and Crohn's gastritis, Menetrier's disease, and chronic nonspecific gastritis. The prevalence of H. pylori in patients with chronic nonspecific gastritis was 71%, whereas the organism was not identified in patients with any form of specific gastritis. This finding further supports the accumulating evidence that H. pylori is a primary pathogenic factor in chronic nonspecific gastritis.

Adolescent↗
PubMed1996

[Lymphocytic gastritis: autoimmune disease or variant of Helicobacter gastritis?].

Lymphocytic gastritis is characterized by the accumulation of small lymphocytes within the surface and foveolar epithelium, however its cause has not been proven. As compared with chronic active gastritis, the local immunoreaction of lymphocytic gastritis was immunohistochemically studied. Although many organisms of Helicobacter pylori (H. pylori) were immunohistochemically detected in all cases with chronic active gastritis, a few organisms were scattered only in 4 cases (28.6%) with lymphocytic gastritis. The extent of HLA-DR-expression in the foveolar epithelium was significantly higher in H. pylori-gastritis than in lymphocytic gastritis, and that of beta 2-microglobulin-expression in the surface epithelium was higher in lymphocytic gastritis than in H. pylori-gastritis. Numerous intraepithelial lymphocytes in lymphocytic gastritis were proved to be CD8-positive cytotoxic/suppressor T-lymphocytes. Our findings suggest that MHC-class I-expression is closely related to the pathogenesis of lymphocytic gastritis. Therefore, some intracellular autoantigens, molecularly mimicking viral antigens, may play a role in its pathogenesis. These autoantigens might occur probably associated not only indirectly with H. pylori-infection but also with unknown viral infection, food intake, bile reflux or stomach tumor.

Adult↗
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↗