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PubMed1986

Enzyme activities in human gastric mucosa in gastritis and resected stomachs.

Biopsy specimens from the antral and body part of the stomach were studied for a range of marker enzymes in 11 patients with superficial gastritis, 9 patients with atrophic gastritis, and 31 Billroth-II-resected patients and compared with activities found in controls with normal gastric mucosa. In the antral part of the stomach increased gamma-glutamyltransferase activity was found in superficial (p less than 0.01) and atrophic gastritis (p less than 0.05), whereas monoamine oxidase activity was decreased in superficial (p less than 0.01) and atrophic gastritis (p less than 0.05). In the body part, increased activity of gamma-glutamyltransferase (p less than 0.01) and acid-beta-glucuronidase (p less than 0.01) was found in superficial gastritis. In atrophic gastritis increased activities for lactase (p less than 0.01), alkaline phosphatase (p less than 0.05), leucyl-beta-naphthylamidase (p less than 0.05), gamma-glutamyltransferase (p less than 0.05), 5'-nucleotidase (p less than 0.01), N-acetyl-beta-D-glucosaminidase (p less than 0.05), and acid-beta-glucuronidase (p less than 0.01) were found. Specimens from the gastric remnant showed an enzyme activity pattern similar to that seen in the body in atrophic gastritis, apart from a significantly decreased monoamine oxidase activity (p less than 0.004). Specimens with dysplasia in the gastric remnant showed decreased monoamine oxidase activity when compared with specimens without dysplasia (p less than 0.01).

Adult↗
PubMed1987

Classification principles and genetics of chronic gastritis.

Two family samples, (i) a sample considered to represent the population at large (431 subjects) and (ii) a sample of first-degree relatives of index subjects (IS) with overt pernicious anaemia (183 subjects) were analyzed in order to evaluate the onset and course of chronic gastritis (CG) and the pathogenetic factors involved with special reference to the effects of genetic variation. The analysis was based on data obtained from two generations: first generation (sibs of the IS) and second (children of the IS). Formulae derived from Poisson process were used for age-correction of the gastritic changes. Otherwise, conventional statistical methods were used in the genetic analysis and the calculation of prevalences of CG. This approach enabled us to achieve a classification of gastritis into more specific subgroups and to evaluate the natural course of the disease. The progression of gastritis in the second generation (children; mean age 35 years) was roughly similar in antrum and body, indicating that gastritis starts as a diffuse process affecting both areas of the stomach to a rather similar degree. The start of CG and its progression is at least to some degree influenced by genetic factors and probably regulated by the male sex. Thus nearly all children of male IS's with a non-atrophic mucosa (normal mucosa or superficial gastritis) showed a normal mucosa suggesting the existence of a particular sex-bound, genetic mechanisms. These mechanisms may prevent or delay the progression of gastritis up to middle age, when a change in dynamics occurs leading to formation of more specific subtypes of CG. In the first generation (mean age 60 years) CG dispersed into more specific subtypes (corresponding to types A and B of Strickland and McKay and type AB of Glass) and to more advanced stages, which were connected with a higher than expected prevalence of advanced stages also in the relatives. The families of IS's with type A atrophic gastritis (AG) (severe AG in the body but no AG in antrum), type B (AG in antrum but no AG in body) and type AB AG (AG in both antrum and body) showed typical dynamic patterns of the age-specific prevalences of AG. Genetic calculations showed that the type A of AG found in pernicious anaemia patients and their relatives is inherited by a simple dominant gene, while this type of inheritance is statistically unlikely in the type B of AG. The type B, on the other hand, exhibited characteristics that indicate a recessive Mendelian inheritance.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1980

[Chronic gastritis].

Chronic gastritis is a histological diagnosis, relying on separate biopsies from antral and fundic mucosa. According to Strickland type A gastritis corresponding to pernicious anemia should be differentiated from type B gastritis, maybe induced by duodeno-gastric reflux. Intensity of inflammatory infiltration and atrophy of the specific glands correlate by and large with acid secretion, however, not with alcohol or nicotine abuse or iron deficiency. Chronic atrophic gastritis may lead to gastric carcinoma of the intestinal type, in gastric ulcer patients localization of the ulcer crater is determined by the spread of gastritis. The histological diagnosis of chronic gastritis has no therapeutic consequences; however, in type A gastritis regular endoscopic follow-up studies in 2-5 year intervals seem advisable.

Anemia, Hypochromic↗
PubMedDate not supplied

[Prevalence of Helicobacter pylori and gastritis in southern Germany. Results of a representative cross-sectional study].

The recent discussions about the relationship between helicobacter-pylori-infection, gastritis and the occurrence of stomach cancer caused us to analyse blood sera of 543 participants randomly selected from the general population in the age of 25 to 34 and of 55 to 64 years from Mosbach (Neckar-Odenwald-Kreis), the county of Deggendorf (Lower-Bavaria) and Augsburg (Upper-Bavaria) regarding IgG-antibodies against helicobacter pylori and the concentrations of the pepsinogens A and C. The latter were used as markers for the presence of chronic gastritis without atrophy and with severe atrophy. The prevalence of helicobacter pylori infection and of forms of gastritis showed no particular differences regarding region or gender. Notable differences in the prevalences were observed with respect to the two age strata. The helicobacter pylori prevalence of the regions being studied ranged for males from 13% to 75% and for females from 22% to 76%. The prevalences of chronic gastritis without atrophy in the investigated areas, derived from the pepsinogen titers, were found to be for males between 24% and 70% and for females between 28% and 61%. Chronic gastritis with severe atrophy appeared mainly in the age group of 55 to 64 years, ranging from 2% to 11% in males and 4% to 10% in females, depending upon region. The helicobacter pylori prevalence and the prevalence of chronic gastritis without atrophy were found to be highly correlated. Chronic gastritis with severe atrophy was also found to be associated with helicobacter pylori prevalence. However, this association did not reach statistical significance.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2006

Prednisolone promotes remission and gastric mucosal regeneration in experimental autoimmune gastritis.

A cardinal feature of organ-specific autoimmunity is destructive pathology in the target organ. In human and experimental models of autoimmune gastritis, mononuclear cell infiltration and cellular destruction in the gastric mucosa are disease hallmarks. Strategies to cure autoimmune disease must not only establish immunological tolerance to autoantigen, but also rid the organ of pathogenic autoreactive cells. The present study has assessed the effect of prednisolone treatment in clearing the inflammatory infiltrate in experimental autoimmune gastritis and in preventing disease relapse in athymic compared with euthymic mice. Experimental autoimmune gastritis was induced by neonatal thymectomy or by transgenic expression of GM-CSF (PC-GMCSF mice). Groups of mice were treated with prednisolone (10 mg/kg per day) for 10 weeks or with prednisolone for 10 weeks followed by 10 weeks without prednisolone. Stomachs were examined for gross morphological changes, and by histology and immunohistochemistry for composition of inflammatory infiltrate and gastric mucosal integrity. Autoantibody to gastric H+/K+ ATPase was determined by ELISA. Prednisolone promoted remission of gastritis in both mouse models of experimental autoimmune gastritis, evident by reduction in stomach size, clearing of gastric inflammatory infiltrate, and regeneration of the gastric mucosa. Prednisolone withdrawal resulted in disease relapse in all PC-GMCSF mice, whereas approximately 40% of neonatal thymectomy mice retained normal stomach morphology and remained free of gastric pathology. It is concluded that prednisolone promotes remission and gastric mucosal regeneration in experimental autoimmune gastritis. Prolonged remission of autoimmune gastritis in some athymic mice suggests a role for the thymus in disease relapse.

Animals↗
PubMed1993

Helicobacter pylori, dietary factors, and atrophic gastritis in five Japanese populations with different gastric cancer mortality.

In a cross-sectional study of 634 men aged 40 to 49 years, randomly selected from five areas of Japan with different rates of gastric cancer mortality, 121 men of 624 evaluated were diagnosed as having atrophic gastritis through serum pepsinogen I < 70 ng/ml and the pepsinogen I (PGI)/pepsinogen II (PGII) ratio < 3.0. We examined the relation of Helicobacter pylori (H. pylori) antibodies and dietary factors, including plasma level of antioxidant micronutrients, to the presence of atrophic gastritis. Presence of H. pylori IgG antibodies was associated with increased risk of atrophic gastritis (odds ratio [OR] = 1.9, 95 percent confidence interval [CI] = 1.1-3.3). As the level of plasma beta-carotene increased, we found a steady decrease in the risk of atrophic gastritis (OR for second quartile = 0.7, third quartile = 0.6, fourth quartile = 0.4, with CI = 0.2-0.8). Frequent intake of yellow vegetables also was associated with lower risk, while frequent intake of soybean products was related to increased risk. Although H. pylori antibodies, beta-carotene level, and intake of soybean products were all significant in the multivariate analysis, these factors did not explain the differences in atrophic gastritis prevalence among the five regions. The analysis of these risk factors in relation to each pepsinogen marker showed that although both H. pylori infection and low plasma beta-carotene were associated with the decreased level of serum PGI/II ratio, the former was derived from the increase of PGII, which is common in early stage of atrophic gastritis, and the latter from the decrease of PGI, which is specific to severe atrophic gastritis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Gastritis in Barrett's esophagus.

Duodenogastric reflux has been implicated in the pathogenesis of complicated Barrett's esophagus and gastric ulceration. A group of 123 Barrett's patients were followed for a mean of 41 months; 9 (7%) developed gastric ulceration (GU). Of the Barrett's patients treated by antireflux surgery, 14% developed GU. We reviewed the gastric histology on 54 Barrett's patients (34 men, 20 women; average age 64 years) at presentation and classified the gastritis according to the Sydney system. A normal histologic pattern was present in seven patients; 15 patients had chronic pangastritis, 9 chronic antral gastritis, and 18 chronic gastritis of the corpus. Five patients had acute gastritis only, and in 74% there was reactive chronic gastritis. Of the patients with chronic gastritis, 45% (19 of 42) had histologic evidence of duodenogastric reflux, established by the bile reflux index. The presence of reactive chronic gastritis in Barrett's patients may have important pathophysiologic and therapeutic implications.

Aged↗
PubMed1995

Serological parameters in assessment of degree of gastritis in healthy volunteers.

This study was undertaken in healthy volunteers to determine the relation between serum levels of pepsinogen A, pepsinogen C, pepsinogen A:C ratio, and gastrin on the one hand and histology of the gastric mucosa on the other. The grade of gastritis was scored separately for antral and fundic mucosa by three different classifications: Whitehead, activity, and the Sydney score. Among 48 healthy volunteers studied, 17 were found to have gastritis according to the criteria of Whitehead. Fourteen of these 17 subjects with gastritis had H. pylori in gastric biopsies. In all 48 subjects serum pepsinogen A (r = 0.298-0.506; P < 0.01-P < 0.05), pepsinogen A:C ratio (r between -0.377 and -0.495; P < 0.001-P < 0.05) and gastrin (r = 0.38-0.695; P = 0.007-P < 0.01) were significantly correlated to the severity of both antral and body gastritis as assessed by all three classifications. In contrast, there was no significant correlation between serum pepsinogen C and any of the gastritis scores. When the 17 subjects with gastritis were analyzed separately, there were no correlations between the parameters studied and gastritis of the antrum. Regarding the corpus mucosa, serum PgA correlated significantly with the activity score (r = 0.520; P = 0.03), weakly with the Sydney score (r = 0.465; P = 0.06), but not with the Whitehead score. Serum PgC correlated with the Whitehead (r = 0.555; P = 0.02) and Sydney score (r = 0.523; P = 0.03), but only weakly with the activity score (r = 0.441; P = 0.08).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2004

Topography of chronic active gastritis in Helicobacter pylori-positive Asian populations: age-, gender-, and endoscopic diagnosis-matched study.

BACKGROUND: The incidence and mortality of gastric cancer is high among Japanese and Chinese populations but extremely low in Thailand and low in Vietnam. The aim of this study was to compare the degree of corpus-predominant gastritis, which is considered to be one of risk factors of gastric cancer, in Helicobacter pylori-positive Asian adult populations. METHODS: H. pylori-positive Chinese (Beijing and Fuzhou), Thai, and Vietnamese patients were paired with Japanese patients by age, gender, and endoscopic diagnosis to compare the ratio of corpus gastritis to antrum gastritis (C/A ratio) (105, 85, 195, and 154 pairs, respectively). RESULTS: The Japanese C/A ratio was significantly higher than that in other groups. Corpus-predominant gastritis (C/A ratio > 1.00) was characteristic in aged Japanese and Chinese (Fuzhou), but Chinese (Beijing), Thai, and Vietnamese were antrum predominant (C/A ratio < 1.00) in every age group except for the Vietnamese over-70 group. There was a similarity between degree of H. pylori colonization and neutrophil activity score. CONCLUSIONS: Corpus-predominant gastritis was found in aged Japanese and Chinese (Fuzhou) and antrum-predominant gastritis was found in Chinese (Beijing), Thai, and Vietnamese patients. These results correlate with the low incidence of gastric cancer in Thai and Vietnamese populations. The incidence and mortality of gastric cancer is high among Japanese and Chinese populations but extremely low in Thailand and low in Vietnam. The aim of this study was to compare the degree of corpus-predominant gastritis, which is considered to be one of risk factors of gastric cancer, in Helicobacter pylori-positive Asian adult populations.

Adult↗
PubMed2005

Influence of bile reflux and Helicobacter pylori infection on gastritis in the remnant gastric mucosa after distal gastrectomy.

BACKGROUND: Two main pathogenic factors, bile reflux and Helicobacter pylori infection, have been identified in the remnant stomach, but it is still unclear which factor is important in the pathogenesis of gastritis in the remnant stomach after distal gastrectomy. METHODS: In 184 patients who had had distal gastrectomy performed using the Billroth-I procedure (B-I; n-106), Billroth-II procedure (B-II; n-36), and jejunal interposition (J-I; n-42) we examined the severity of remnant gastritis endoscopically and carried out examinations for H. pylori infection and histological examination. RESULTS: The endoscopic severity of remnant gastritis was grade 1 or more in 101 of the 106 B-I patients (95.3%) and in all 36 B-II patients (100%). But, of the 42 J-I patients, the grade was 0 in 33 (78.6%). The endoscopic severity of remnant gastritis was significantly milder for J-I than for B-I (P < 0.001) and B-II (P < 0.001). H. pylori infection was confirmed in 59 of the 106 B-I patients (55.6%), 21 of the 36 B-II patients (58.3%), and 32 of the 42 J-I patients (76.1%). The rate of H. pylori infection was higher for J-I patients than for B-I (P < 0.05), but not for B-II patients (P = 0.1495). The severity of chronic and active inflammatory cellular infiltration tended to be inverse proportional relation with the endoscopic severity of the remnant gastritis. Furthermore, the histological inflammation and activity scores of H. pylori-positive patients were higher than those of H. pylori-negative patients, without regard to the endoscopic grade of gastritis. CONCLUSIONS: Reconstruction techniques play an important role in the prevention of bile reflux, and we found that endoscopically more severe remnant gastritis was associated with a lower rate of H. pylori infection and with a lower degree of inflammatory cellular infiltration.

Aged↗
PubMed2004

Tumor necrosis factor-alpha is required for gastritis induced by Helicobacter felis infection in mice.

Helicobacter pylori colonizes the gastric mucosa of human and causes chronic gastritis. The previous studies have demonstrated that gamma interferon (IFN-gamma) but not tumor necrosis factor-alpha (TNF-alpha) plays a critical role in pathogenesis of gastritis induced by H. pylori infection. In this study we investigated the induction of gastritis induced by H. felis infection in TNF-alpha-deficient mice, comparing with IFN-gamma-deficient mice. The scores of gastritis and epithelial changes of TNF-alpha-deficient mice and IFN-gamma-deficient mice were significantly lower than that of C57BL/6 mice. Moreover, the degrees of gastritis and epithelial changes of TNF-alpha-deficient mice were rather low compared with that of IFN-gamma-deficient mice. In spleen cell cultures stimulated with heat-killed H. felis, IFN-gamma production by TNF-alpha-deficient mice and TNF-alpha production by IFN-gamma-deficient mice were significantly reduced compared with those in C57BL/6 mice. These results suggested that TNF-alpha is involved in pathogenesis of gastritis induced by H. felis infection as IFN-gamma and that an interaction between TNF-alpha and IFN-gamma might be required in pathogenesis of gastritis induced by Helicobacter infection.

Animals↗
PubMed1999

Increased expression and cellular localization of inducible nitric oxide synthase and cyclooxygenase 2 in Helicobacter pylori gastritis.

BACKGROUND & AIMS: Inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 are important regulators of mucosal inflammation and epithelial cell growth. To determine the role of iNOS and COX-2 in Helicobacter pylori-induced tissue injury, we compared their gene expression in H. pylori-induced gastritis with that in normal gastric mucosa and in non-H. pylori gastritis. METHODS: In 43 patients, we assessed H. pylori infection status, histopathology, messenger RNA (mRNA) and protein expression, and cellular localization of iNOS and COX-2. RESULTS: By reverse-transcription polymerase chain reaction (RT-PCR), antral iNOS and COX-2 mRNA expression was absent to low in normal mucosa (n = 10), significantly increased in H. pylori-negative gastritis (n = 13), and even more markedly increased in H. pylori-positive gastritis (n = 20). Increased iNOS and COX-2 levels were confirmed by Northern and Western blot analysis and were both greater in the gastric antrum than in the gastric body of infected patients. Immunohistochemistry also showed increased expression of both genes in H. pylori gastritis: iNOS protein was detected in epithelium, endothelium, and lamina propria inflammatory cells, and COX-2 protein localized to mononuclear and fibroblast cells in the lamina propria. CONCLUSIONS: iNOS and COX-2 are induced in H. pylori-positive gastritis and thus may modulate the inflammation and alterations in epithelial cell growth that occur in this disease. Higher levels of iNOS and COX-2 in H. pylori-positive vs. -negative gastritis and in gastric antrum, where bacterial density is greatest, suggest that expression of these genes is a direct response to H. pylori infection.

Cyclooxygenase 2↗
PubMed2001

Light and electron microscopic immunohistochemical investigation on G and D cells in antral mucosa in Helicobacter pylori-related gastritis.

Recently, it has been recognized that Helicobacter pylori (H. pylori) infection is associated with an exaggeration of basal and meal gastrin secretion. We investigate whether there is a relationship between H. pylori-related chronic gastritis and G-cell and D-cell number and granule density index of G and D cells. - The number of antral G cells and D cells and granule density index of D and G cells are compared between thirty two patients with H. pylori-related chronic gastritis and twelve patients without H. pylori and inflammation. Antral mucosal biopsy specimens are examined using light and electron immunohistochemical techniques. - The number of G cells is the same in either infected or uninfected patients (98.40 +/- 11.39, 109.25 +/- 12.76 vs 101.17 +/- 7.72 for infected patients with non atrophic and with mild atrophic chronic gastritis and uninfected controls, respectively) except for the cases with moderate gastric mucosal atrophy, where G cells (58.22 +/- 5.63) decrease in number. The number of D cells is decreased in all patients with H. pylori-related gastritis. G cell granule density index is significantly (p < 0.05) increased in patients with H. pylori-related chronic gastritis than in controls (3.15 +/- 0.43 vs 2.528 +/- 0.01). D cell granule density index is similar between patients with H. pylori chronic gastritis and controls (3.18 +/- 0.05 vs 3.166 +/- 0.12). It is concluded that decreased D cells number in patients with H. pylori-related chronic gastritis might be one of the reasons for the existing hypergastrinaemia.

Adolescent↗
PubMed2005

Serum vitamin B12 concentrations and atrophic gastritis in older New Zealanders.

OBJECTIVE: To determine the serum vitamin B(12) status of older New Zealanders and to assess the impact of atrophic gastritis on vitamin B(12) status. DESIGN: A cross-sectional nationally representative population-based survey. METHOD: Serum vitamin B(12) concentrations were used to assess vitamin B(12) status. The presence and severity of atrophic gastritis was classified using serum pepsinogen I and II. SUBJECTS: A total of 466 noninstitutionalized urban and rural dwelling New Zealanders aged 65 y or older who participated in the 1997 National Nutrition Survey. RESULTS: The prevalence of deficient (<148 pmol/l) and marginal (148-221 pmol/l) serum vitamin B(12) concentrations was 12 and 28%, respectively. The prevalence of atrophic gastritis was 6.7% (severe 3.1%, mild-moderate 3.6%). While atrophic gastritis increased the relative risk (RR, 95% CI) of having a deficient or marginal serum vitamin B(12) concentration by 21-fold (6-67) and five-fold (1-17), respectively, those who had atrophic gastritis made up only 33 and 6% of the participants with deficient or marginal serum vitamin B(12) concentrations. An intake of vitamin B(12) from food that exceeded the recommended dietary allowance (2.4 mug/day) did not protect against deficient (RR 0.5; 95% CI: 0.2, 1.2) or marginal (RR 0.9; 95% CI: 0.5, 1.7) serum vitamin B(12) status. Vitamin B(12) supplement users had a reduced risk of having deficient and marginal vitamin B(12) status (RR 0.3; 95% CI: 0.1, 0.8). CONCLUSIONS: There is a relatively high prevalence of deficient and marginal serum vitamin B(12) concentrations among older New Zealanders. However, the prevalence of atrophic gastritis was low in the New Zealand elderly compared with other surveys. Although atrophic gastritis was a risk factor for low vitamin B(12) status, it did not fully explain the prevalence of low serum vitamin B(12).

Aged↗
PubMed2000

Changes in Helicobacter pylori-induced gastritis in the antrum and corpus during long-term acid-suppressive treatment in Japan.

BACKGROUND: Several studies have shown that acid-suppressive therapy aggravates corpus gastritis in patients with Helicobacter pylori infection, promoting the development of atrophic gastritis. AIM: To study the effects of long-term use of antisecretory agents on the H. pylori-positive gastric mucosa in Japan, a country with a high incidence of gastric cancer. METHODS: A total of 141 H. pylori-positive patients who had peptic ulcers or reflux oesophagitis were treated for 3 years with either omeprazole (20 mg/day) alone (n=7) or with omeprazole for primary therapy (8 weeks), followed by famotidine (40 mg/day) for maintenance therapy (n=134). Endoscopy was performed before, during, and after treatment. Biopsy specimens were taken from the greater curvature of the antrum and corpus and were examined histologically. RESULTS: The long-term use of famotidine after 8 weeks of treatment with omeprazole distinctly decreased H. pylori density and neutrophil infiltration in the antrum, but did not change H. pylori density in the corpus. The gastritis score increased in patients who had no, or only mild corpus gastritis before treatment (n=74), and significantly decreased in those who had moderate or severe gastritis before treatment (n=60). In four of the seven patients who received long-term treatment with omeprazole alone, neutrophil infiltration and H. pylori density decreased not only in the antrum but also in the corpus. There was no increase in intestinal metaplasia or mucosal atrophy as assessed endoscopically during follow-up. CONCLUSION: Changes in corpus gastritis in response to acid-suppressive therapy depend on the severity of gastritis before treatment. Long-term use of acid-suppressive therapy apparently does not accelerate the development of atrophy or intestinal metaplasia in Japanese patients.

Anti-Ulcer Agents↗
PubMed2001

Double gastric infection with Helicobacter pylori and non-Helicobacter pylori bacteria during acid-suppressive therapy: increase of pro-inflammatory cytokines and development of atrophic gastritis.

BACKGROUND: Long-term acid suppression may accelerate the development of atrophic gastritis in Helicobacter pylori-positive subjects. The pathogenetic mechanism remains unclear. AIM: To test the hypothesis that gastric double infection with H. pylori and non-H. pylori bacterial species-during acid suppression-may result in an enhanced inflammatory response, contributing to the development of atrophic gastritis. PATIENTS AND METHODS: A consecutive series of patients with gastro-oesophageal reflux disease undergoing treatment with proton pump inhibitors (n=113) or histamine2-receptor antagonists (H2-RAs) (n=37), and 76 non-treated dyspeptic controls were investigated. Gastric mucosal H. pylori and non-H. pylori bacteria, histological gastritis, H. pylori serology, and circulating interleukin (IL)-1beta, IL-6, and IL-8 were examined. RESULTS: Patients on acid suppression with either proton pump inhibitors or H2-RAs had a similar prevalence of H. pylori infection to the controls, but a higher prevalence of non-H. pylori bacteria (61% and 60% vs. 29%, P < 0.0001 and P < 0.002). Both the presence of H. pylori and non-H. pylori bacteria were independent risk factors of atrophic gastritis (antrum: relative risks (RRs), 10.1 and 5.07; corpus: RRs, 11.74 and 6.38). A simultaneous presence of H. pylori and non-H. pylori bacteria was associated with a markedly increased risk of atrophic gastritis (antrum: RR, 20.25; corpus: RR, 20.38), compatible with a synergistic effect. Furthermore, the simultaneous presence of both types of bacteria was associated with higher cytokine levels than in patients without any type of bacteria. This increase was also greater than in patients with H. pylori infection alone (P < 0.001, for both IL-1beta and IL-8). SUMMARY AND CONCLUSIONS: H. pylori-positive patients on long-term acid inhibition displayed three features: non-H. pylori bacterial growth; increased cytokine levels; and a higher risk of atrophic gastritis. We suggest that double infection with H. pylori and non-H. pylori bacteria is a major factor in the development of atrophic gastritis during gastric acid inhibition.

Adult↗
PubMed2002

Corpus gastritis in patients with endoscopic diagnosis of reflux oesophagitis and Barrett's oesophagus.

BACKGROUND: A high level of gastric acid secretion is considered to be a risk factor for reflux oesophagitis or Barrett's oesophagus. Corpus gastritis may have a protective effect on the oesophagus, because of decreased gastric acid output. AIM: To determine if corpus gastritis is associated with reflux oesophagitis or Barrett's oesophagus. METHODS: Three antral and two corpus biopsies were taken from consecutive patients in whom Helicobacter pylori testing was requested during endoscopy at a single centre between January 1995 and May 1997. Antral and corpus gastritis was studied by histology; H. pylori was studied by histology, culture and CLO test. A regression model was used to test for correlation between reflux oesophagitis, Barrett's oesophagus and risk factors. RESULTS: During the study period, 676 patients had biopsies taken during upper gastrointestinal endoscopy. Endoscopic signs of reflux oesophagitis and Barrett's oesophagus were observed in 125 and 23 patients, respectively. Corpus gastritis was found in 59% of patients without reflux oesophagitis or Barrett's oesophagus, 45% of patients with reflux oesophagitis and 30% of patients with Barrett's oesophagus. Two hundred and fifty-seven patients underwent follow-up endoscopy after H. pylori therapy. During a mean follow-up of 3 months, the incidence of reflux oesophagitis was not statistically different for patients with healing of corpus gastritis (10/98; 10%) and patients with persistent gastritis (8/97; 8%). CONCLUSIONS: Corpus gastritis was less common in patients with an endoscopic diagnosis of reflux oesophagitis or Barrett's oesophagus.

Barrett Esophagus↗
PubMed1996

Gastric mucosal phospholipids in dogs with familial stomatocytosis-hypertrophic gastritis.

In dogs, hypertrophic gastritis, which resembles Ménétrier's disease in man, has been demonstrated to be part of a hereditary syndrome called familial stomatocytosis-hypertrophic gastritis. In addition to hypertrophic gastritis, affected dogs exhibit abnormal blood phospholipid composition. Phospholipids may play a role in maintaining gastric mucosal integrity, and this may be compromised in gastritis. The question arises whether the differences in blood phospholipids may result from a disorder that might also be revealed in the composition of gastric mucosal phospholipids. We analysed the phospholipid composition of gastric mucosa from four dogs with familial stomatocytosis-hypertrophic gastritis. The general phospholipid composition and the molecular composition of phosphatidylcholine from mucosal tissue in the corpus of the stomach where hypertrophic gastritis was evident were not different from that of the antrum, where the tissue was normal. These results do not corroborate a relation between the gastric mucosal phospholipid composition and hypertrophic gastritis.

Animals↗