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PubMed2003

Isolated granulomatous gastritis successfully treated by Helicobacter pylori eradication: a possible association between granulomatous gastritis and Helicobacter pylori.

We report two cases of granulomatous gastritis that resolved completely with Helicobacter pylori eradication. Two Japanese women, one 61 years old and one 58 years old, presented to our hospital with epigastralgia. Endoscopy revealed multiple shallow ulcerative lesions in the gastric corpus of both patients. Biopsy specimens demonstrated acute and chronic inflammation with multiple small, noncaseating granulomas at the level of the foveolar isthmi-the junction between the pits and the glands. Both specimens were positive for Helicobacter pylori. No other causes of organic granulomatous disease could be found. Both patients were diagnosed as having isolated granulomatous gastritis and were given triple therapy for Helicobacter pylorieradication, with their fully informed consent. The granulomatous gastritis resolved after successful Helicobacter pylorieradication therapy. This report describes a possible association between isolated granulomatous gastritis and Helicobacter pyloriinfection. To our knowledge, this is the first report describing isolated granulomatous gastritis successfully treated by triple therapy ( Helicobacter pylorieradication therapy).

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1993

Animal models of bacterial gastritis: the role of host, bacterial species and duration of infection on severity of gastritis.

Gastric bacteria from cheetahs with gastritis were used to inoculate specific-pathogen free kittens and conventional mice. Helicobacter sp. and Gastrospirillum sp. colonized kittens, while only Gastrospirillum sp. colonized mice. In kittens, both bacterial species induced mild lymphofolliclar gastritis which did not change over the course of the 11 months observation period. In mice, Gastrospirillum sp. induced lymphoplasmacytic and follicular gastritis which increased in severity over 6 months and persisted for the 12 month observation period. Gastric ulcers and gastric mucosal hypertrophy were present in chronically infected mice. These results indicate that host but not bacterial factors influence the severity of gastritis, and that in mice, bacterial gastritis increases in severity with time and may lead to gastric ulceration in some individuals.

Animals↗
PubMed1997

Focally enhanced gastritis: a frequent type of gastritis in patients with Crohn's disease.

BACKGROUND & AIMS: Gastric histology is not well studied in patients with Crohn's disease. The aim of this study was to analyze the histological appearance of gastric mucosa in patients with Crohn's disease. METHODS: In a prospective study, biopsy specimens taken from the antrum and body of 75 patients with known Crohn's disease of the large and/or small bowel and 200 Crohn's disease-free controls were evaluated by histology and immunohistochemistry. RESULTS: Helicobacter pylori-associated gastritis was found in 25 patients with Crohn's disease (33.3%) and 78 controls (39%). In H. pylori-negative patients with Crohn's disease, a characteristic type of gastritis was found in antral biopsy specimens of 36 patients (48%) and in body biopsy specimens of 18 patients (24%). It was characterized by a focal infiltration of CD3+ lymphocytes, CD68R+ histiocytes, and, in 80% of cases, of granulocytes. Granulomas were found in 11 patients. Overall, granulomas and/or focally enhanced gastritis were observed in 76% of H. pylori-negative patients with Crohn's disease and in 0.8% of controls. There were no correlations between the occurrence of focally enhanced gastritis and clinical and laboratory findings. CONCLUSIONS: Focally enhanced gastritis is common in Crohn's disease. Its recognition should guide the clinician into further investigations in patients not yet known to have Crohn's disease.

Adolescent↗
PubMed1996

Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994.

The Sydney System for the classification of gastritis emphasized the importance of combining topographical, morphological, and etiological information into a schema that would help to generate reproducible and clinically useful diagnoses. To reappraise the Sydney System 4 years after its introduction, a group of gastrointestinal pathologists from various parts of the world met in Houston, Texas, in September 1994. The aims of the workshop were (a) to establish an agreed terminology of gastritis; (b) to identify, define, and attempt to resolve some of the problems associated with the Sydney System. This article introduces the Sydney System as it was revised at the Houston Gastritis Workshop and represents the consensus of the participants. Overall, the principles and grading of the Sydney System were only slightly modified, the grading being aided by the provision of a visual analogue scale. The terminology of the final classification has been improved to emphasize the distinction between the atrophic and nonatrophic stomach; the names used for each entity were selected because they are generally acceptable to both pathologists and gastroenterologists. In addition to the main categories and atrophic and nonatrophic gastritis, the special or distinctive forms are described and their respective diagnostic criteria are provided. The article includes practical guidelines for optimal biopsy sampling of the stomach, for the use of the visual analogue scales for grading the histopathologic features, and for the formulation of a comprehensive standardized diagnosis. A glossary of gastritis-related terms as used in this article is provided.

Animals↗
PubMed1980

Necrotizing gastritis and phlegmonous gastritis--are they separate entities?

Phlegmonous gastritis, although a rare condition, is a submucosal bacterial infection strictly confined to the stomach with characteristic macroscopic and histological findings. A case of necrotizing gastritis with perforation is presented, and another similar case is reviewed, in which the gross and microscopic features are considerably different from those ascribed to classical phlegmonous gastritis. There was no evidence of an infectious aetiology in either case, and the predominant feature was necrosis. It is proposed that this variant may represent a separate disease entity of unknown aetiology. A combination of early radical gastric resection and vigorous antibiotic therapy appears to be the treatment of choice in both classical phlegmonous gastritis and necrotizing gastritis.

Adult↗
PubMed2004

Focal-enhanced gastritis in regressive autism with features distinct from Crohn's and Helicobacter pylori gastritis.

BACKGROUND: Immunohistochemistry allowed recent recognition of a distinct focal gastritis in Crohn's disease. Following reports of lymphocytic colitis and small bowel enteropathy in children with regressive autism, we aimed to see whether similar changes were seen in the stomach. We thus studied gastric antral biopsies in 25 affected children, in comparison to 10 with Crohn's disease, 10 with Helicobacter pylori infection, and 10 histologically normal controls. All autistic, Crohn's, and normal patients were H. pylori negative. METHODS: Snap-frozen antral biopsies were stained for CD3, CD4, CD8, gammadelta T cells, HLA-DR, IgG, heparan sulphate proteoglycan, IgM, IgA, and C1q. Cell proliferation was assessed with Ki67. RESULTS: Distinct patterns of gastritis were seen in the disease states: diffuse, predominantly CD4+ infiltration in H. pylori, and focal-enhanced gastritis in Crohn's disease and autism, the latter distinguished by striking dominance of CD8+ cells, together with increased intraepithelial lymphocytes in surface, foveolar and glandular epithelium. Proliferation of foveolar epithelium was similarly increased in autism, Crohn's disease and H. pylori compared to controls. A striking finding, seen only in 20/25 autistic children, was colocalized deposition of IgG and C1q on the subepithelial basement membrane and the surface epithelium. CONCLUSIONS: These findings demonstrate a focal CD8-dominated gastritis in autistic children, with novel features. The lesion is distinct from the recently recognized focal gastritis of Crohn's disease, which is not CD8-dominated. As in the small intestine, there is epithelial deposition of IgG.

Autistic Disorder↗
PubMed1994

[Varioliform gastritis or lymphocytic gastritis? Anatomoclinical study. Apropos of 14 cases].

The authors report 14 cases of lymphocytic gastritis, 13 of which correspond to an endoscopic appearance of varioliform gastritis. Epigastric pain was present in 91.6% of cases. Varioliform pattern corresponded to an antral site in 69.2% of cases and to the body in 30.8% of cases. Lymphocytic gastritis was diagnosed in 7 cases (46%), 6 of which corresponded to a varioliform gastritis. An associated duodenal ulcer was noted in 28.5% of our cases of lymphocytic gastritis.

Adolescent↗
PubMed2005

Upregulation of cathepsin W-expressing T cells is specific for autoimmune atrophic gastritis compared to other types of chronic gastritis.

AIM: To investigate a pathophysiological role of cathepsin W (CatW), a putative thiol-dependent cysteine protease, which is specifically expressed in cytotoxic lymphocytes, in different types of chronic inflammation of the gastric mucosa. METHODS: Gastric and duodenal biopsies of patients with Helicobacter pylori (H pylori)-associated active gastritis (Hp, n = 19), chemically induced reactive gastritis (CG, n = 17), autoimmune atrophic gastritis (AIG, n = 20), lymphocytic corpus gastritis (LG, n = 29), celiac disease (CD, n = 10), and corresponding controls (n = 24) were analyzed by immunohistochemistry for the expression of CatW and CD45. Furthermore, immunohistochemical double staining with anti-CD3 and anti-cathepsin was performed for the samples of AIG. RESULTS: Median values of CatW-expressing cells among CD45-positive immune cells were between 2% and 6% for normal gastric mucosa, CG, and LG, whereas the corresponding value was significantly increased for AIG (24.7%, P<0.001) and significantly decreased for HP (0.7%, P<0.05). Double staining with anti-CD3 and anti-CatW antibodies revealed that >90% of CatW-expressing cells in gastric mucosa of AIG were T cells. Duodenal mucosa had significantly more CatW/CD45-positive cells than normal gastric mucosa (median: 17.8% vs 2%, P<0.01). The corresponding proportion of CatW/CD45-postive cells was decreased in CD compared to duodenal mucosa (median: 2.1% vs 17.8%, P<0.05). CONCLUSION: The opposite findings regarding the presence of CatW-positive cells in AIG (increase) and CD (decrease) reflects the different cellular composition of immune cells involved in the pathogenesis of these diseases.

Autoimmune Diseases↗
PubMed1989

Lymphocytic gastritis versus varioliform gastritis. A historical series revisited.

A historical series of varioliform gastritis published in 1978 by Lambert et al. (Digestion 1978; 17: 159-167) was revisited by two pathologists. The histological preparations from 35 patients were reread and interpreted in the light of endoscopic data found in the files. The results demonstrate a strict correlation between clinical diffuse varioliform gastritis and a recently recognized histopathological entity--lymphocytic gastritis, which is characterized by intense lymphocytic infiltration of the surface and foveolar epithelium. The rare discrepancies occur in Crohn's disease and in varioliform gastritis limited to part of the stomach, mostly the antrum.

Crohn Disease↗
PubMed1998

Gastric cancer and premalignant lesions in atrophic gastritis: a controlled trial on the effect of supplementation with alpha-tocopherol and beta-carotene. The Helsinki Gastritis Study Group.

BACKGROUND: Vitamin E and beta-carotene are considered to decrease the risk of gastric cancer both in humans and in laboratory animals. We studied the effect of dietary supplementation with alpha-tocopherol and beta-carotene on the end-of-trial prevalence of premalignant and malignant lesions of the stomach in older men with atrophic gastritis. METHODS: The study was carried out within the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study (ATBC study) in Finland, in which 29,133 male smokers aged 50-69 years were randomly assigned to receive daily 50 mg alpha-tocopherol, 20 mg beta-carotene, both of these agents, or placebo, for 5-8 years. Serum pepsinogen was determined at base line and after 3 years' supplementation to find men with atrophic gastritis. A low serum pepsinogen I level, indicating atrophic gastritis of the corpus area of the stomach, was found in 2132 men. These men were invited to have upper gastrointestinal endoscopy (gastroscopy), which was performed on 1344 subjects after a median supplementation time of 5.1 years. RESULTS: Neoplastic alterations were found in 63 of the men (4.7%): 42 with definite dysplasias of low grade (moderate dysplasia), 7 with definite dysplasias of high grade (severe dysplasia), 11 with carcinomas (of which 7 were 'early' cancers), and 3 with carcinoid tumors. Neither alpha-tocopherol (relative risk, 0.98; 95% confidence interval, 0.57-1.69) nor beta-carotene (relative risk, 1.13; 95% confidence interval, 0.65-1.95) supplementation had any association with end-of-trial prevalence of gastric neoplasias after adjustment for other possible risk factors. The effect was not modified by base-line serum level or dietary intake of vitamins, prevalence of Helicobacter pylori infection, or other covariates. CONCLUSIONS: We thus conclude that supplementation with alpha-tocopherol or beta-carotene for 5 years has no major impact on the occurrence of neoplastic changes of the stomach in older male smokers with atrophic gastritis.

Aged↗
PubMed1999

An 18-year follow-up study of chronic gastritis and Helicobacter pylori association of CagA positivity with development of atrophy and activity of gastritis.

BACKGROUND: We wanted to evaluate the course of chronic gastritis and its association with Helicobacter pylori and CagA seropositivity in an adult sample from Saaremaa (Estonia) during an 18-year follow-up. METHODS: Seventy persons (31 men, 39 women; median age, 57.5 years) from a primary sample of 304 subjects endoscoped in 1979 were reinvestigated by endoscopy and biopsy in 1997. The state of the gastric mucosa and the presence of H. pylori in histologic sections from the antrum and corpus were assessed both in 1979 and 1997 in 66 subjects in accordance with the Sydney system, and H. pylori status in all 70 subjects was determined with the enzyme-linked immunosorbent assay (ELISA). Anti-CagA IgGs were determined with the ELISA, using the recombinant fragment of CagA. RESULTS: During an 18-year follow-up 11% of the subjects developed atrophy in the antrum, whereas 35% developed it in the corpus. Development of atrophy in the corpus and the appearance of intestinal metaplasia in the antrum were associated with increased activity of gastritis both in the initial and last follow-up biopsies. Anti-CagA positivity was found in 71% of H. pylori-seropositive persons (94% of subjects). There was a significant association between CagA positivity and the activity of gastritis, the presence of atrophy or damage to surface epithelial cells in the antrum and in corpus mucosal biopsy specimens at the last follow-up endoscopy. CONCLUSION: The CagA-positive strains of H. pylori enhance the development of atrophic gastritis compared with CagA-negative strains.

Antigens, Bacterial↗
PubMed1988

Naturally occurring chronic gastritis and C pylori infection in the rhesus monkey: a potential model for gastritis in man.

Histological examination of the stomachs of Rhesus monkeys at autopsy showed chronic gastritis in a high proportion of all ages. Lesions consisted of mild to heavy infiltration of the lamina propria by lymphocytes, plasma cells, and histiocytes. The antrum was most consistently affected, but lesions were also present in the fundus and pylorus. Gastric Campylobacter-like organisms (GCLO) apparently identical to human C pylori were cultured and/or detected immunohistologically in several animals. Electron microscopy showed the spiral bacteria on the epithelial surface and in gastric pits. They did not penetrate the cells but were intimately attached to the apical plasma membrane and caused loss of microvilli. Antibodies to C pylori were detected in serum of the monkeys by ELISA. The immunospecificity of this antibody response was confirmed by Western blotting techniques. A small number of cynomolgus monkeys examined had gastritis, which may also be associated with the presence of C pylori. Baboons did not have gastritis, nor was C pylori cultured from their stomachs. The study indicates that the Rhesus monkey has a naturally occurring gastritis associated with C pylori infection and may therefore be a suitable experimental animal for the human disease.

Animals↗
PubMed2001

Collagenous gastritis associated with lymphocytic gastritis and celiac disease.

Collagenous gastritis is a rare disorder, with only 8 cases reported in the literature, 2 in children and 6 in adults. We report an additional case of collagenous gastritis in a 42-year-old man with celiac disease. A thickened (>10 microm) subepithelial collagen band with entrapped capillaries, fibroblasts, and inflammatory cells was seen in the stomach, associated with lymphocytic gastritis. The duodenal mucosa showed severe villous atrophy but no subepithelial collagen deposition. No evidence of lymphocytic or collagenous colitis was found in the colon. The patient became symptom-free on a gluten exclusion diet and showed partial improvement of histopathologic findings after 3 months. Collagenous gastritis is a rare disease, but a wider recognition of its histopathologic features and clinical associations may bring more cases to light and provide additional clues in determining its etiology and pathogenesis.

Adult↗
PubMed2002

A study of the concordance between endoscopic gastritis and histological gastritis in an area with a low background prevalence of Helicobacter pylori infection.

The concordance between endoscopic and histological gastritis was determined in 52 patients referred for upper gastrointestinal endoscopy. The study was conducted in Northeastern Peninsular Malaysia, an area with a low background prevalence of H. pylori infection. Endoscopic and histological gastritis were assessed in accordance with the Sydney System. The results showed poor concordance between endoscopic and histological gastritis even after reclassifying mild endoscopic gastritis as normal. The low prevalence of H. pylori was validated in this study.

Adolescent↗
PubMed1989

[Effect of gastritis-granule on 52 cases of chronic gastritis infected with Campylobacter pyloridis].

52 patients with chronic gastritis infected by campylobacter pyloridis (CP) were selected for random observation. The course of treatment was 4 weeks. In the group treated with granule-gastritis, the effective rate for CP was 81.3% (26/32), and the improvement rates of the symptoms and histopathological lesion were 87.5% (28/32) and 40.6% (13/32) respectively. In the group treated with Wei-Mei-Su as the control group, the figures were 25%, 40% and 10% respectively. These differences were statistically significant (P less than 0.01-0.000). The results showed that the effect of granule-gastritis on chronic gastritis infected with CP was better than that of Wei-Mei-Su.

Adult↗
PubMed1983

Therapeutic effects of cetraxate against acute gastritis and acute aggravation of chronic gastritis. Endoscopic investigation by the double-blind method.

To determine the efficacy of cetraxate against acute gastritis and acute aggravation of chronic gastritis, a comparison was made with aldioxa as the standard drug by the double-blind method based mainly on observations by gastroscopy. There were four types of gastroscopic findings used: hemorrhage, erosion, redness and edema. Observations were performed whenever possible before and 1, 2 and 4 weeks after administration, and the cure and improvement rates were investigated. The cure rates for each finding except edema after 1 and 2 weeks were better (in the order of redness, erosion and hemorrhages) in the cetraxate group than in the aldioxa group, and there was a significant difference for redness in the 1st week (p less than 0.05). The no change and aggravating rates were also lower for redness in the 1st week (p less than 0.05) and edema in the 1st week (p less than 0.10) in the cetraxate group than in the aldioxa group. There were almost no differences in the effects of both drugs on subjective symptoms. The safety based on type and incidence of side effects was considered to be high for both drugs. From these results, it appeared that cetraxate is effective against acute gastritis and acute aggravation of chronic gastritis.

Acute Disease↗
PubMed1998

[Histopathological study of the role of Helicobacter pylori in the occurrence and development of chronic active gastritis, acute erosive gastritis and gastric ulcer].

A total of 773 gastric mucosas taken from 653 patients who were endoscopically diagnosed as normal, or having reddening, irregular mucosa, erosion, small ulcer or scar were examined pathologically according to the Sydney system to study the role of H. pylori in the occurrence and development of chronic active gastritis, acute erosive gastritis and ulcer. H. pylori were detected in higher frequency in lesions showing active inflammation with neutrophil infiltration and necrosis of the mucosa. The presence of H. pylori was correlated with the degree of lymphocyte infiltration, but not with the degree of intestinal metaplasia, mucosal atrophy and location in the stomach. Reddening and irregular mucosas were found histologically to be chronic active gastritis. These results suggested that H. pylori causes active inflammation in the gastric rucosa, and that milder inflammation causes reddening or irregularity of the mucosa, whereas severer inflammation causes erosion and ulcer. There is no essential difference between chronic active and acute erosive gastritis.

Adult↗
PubMed1987

Local immunoglobulin production is different in gastritis associated with dermatitis herpetiformis and simple gastritis.

The degree of inflammation and atrophy in gastric body mucosal specimens (n = 38) from 28 patients with dermatitis herpetiformis (DH) was graded histologically. Immunoglobulin (Ig) producing cells were enumerated by paired immunofluorescence staining in a 500 microns wide section area from the muscularis mucosae to the lumen (mucosal 'tissue unit'). The number of immunocytes of the three main classes (IgA, IgM, and IgG) was significantly raised with increasing degree of gastritis. All three classes were increased in specimens showing atrophy compared with those without atrophy. IgA cells predominated as in simple gastritis, but a striking difference was a marked increase of IgM cells in specimens with the most pronounced DH-associated gastritis. Relative class distribution of immunocytes within different mucosal zones showed that the percentage of IgA cells was significantly higher in the luminal than in the basal zone, whereas the contrary was true for IgG cells. IgM cells did not show any zonal preference. No relation was seen between small bowel and gastric lesions. The disproportionate increase of gastric IgM producing cells in DH might nevertheless reflect seeding of precursor cells of the secretory immune system generated in the proximal small intestine where the local IgM response is relatively pronounced.

Adolescent↗