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At least 271 records · Page 15Linked to original sources
PubMed1996

Atrophic gastritis and Helicobacter pylori infection in patients with reflux esophagitis treated with omeprazole or fundoplication.

BACKGROUND: Helicobacter pylori infection plays an important part in the development of atrophic gastritis and intestinal metaplasia, conditions that predispose patients gastric cancer. Profound suppression of gastric acid is associated with increased severity of gastritis caused by H. pylori, but it is not known whether acid suppression increases the risk of atrophic gastritis. METHODS: We studied patients from two separate cohorts who were being treated for reflux esophagitis: 72 patients treated with fundoplication in Sweden and 105 treated with omeprazole (20 to 40 mg once daily) in the Netherlands. In both cohorts, the patients were followed for an average of five years (range, three to eight). After fundoplication, the patients did not receive acid-suppressive therapy. The presence of H. pylori was assessed at the first visit by histologic evaluation in the fundoplication group and by histologic and serologic evaluation in the omeprazole group. The patients were not treated for H. pylori infection. Before treatment and during follow-up, the patients underwent repeated gastroscopy, with biopsy sampling for histologic evaluation. RESULTS: Among the patients treated with fundoplication, atrophic gastritis did not develop in any of the 31 who were infected with H. pylori at base line or the 41 who were not infected; 1 patient infected with H. pylori had atrophic gastritis before treatment that persisted after treatment. Among the patients treated with omeprazole, none of whom had atrophic gastritis at base line, atrophic gastritis developed in 18 of the 59 infected with H. pylori(P<0.001) and 2 of the 46 who were not infected (P=0.62). CONCLUSIONS: Patients with reflux esophagitis and H. pylori infection who are treated with omeprazole are at increased risk of atrophic gastritis.

Adolescent↗
PubMed2004

Prognostic significance of antrum-predominant gastritis in functional dyspepsia.

BACKGROUND: The role of Helicobacter pylori infection in functional dyspepsia is still controversial, and subgroups of patients with functional dyspepsia who may benefit from H. pylori eradication should be identified. Patients with functional dyspepsia and antrum-predominant H. pylori-positive chronic gastritis, it has been argued, have fewer symptoms after eradication therapy. In the present study, we analysed the clinical significance of antrum-predominant gastritis on the long-term prognosis of functional dyspepsia. METHODS: Consecutive unselected dyspeptic patients were investigated in primary care and the patients with functional dyspepsia were enrolled in this long-term follow-up study. Altogether 182 patients were recruited: 65 with normal histology of the stomach, 36 with antrum-predominant gastritis, 21 with corpus-predominant gastritis and 60 with pangastritis. Patients' medical histories were reviewed after 6 to 7 years, with total number and outcome of repeated investigations analysed. At the end of follow-up, all patients were invited for voluntary gastroscopy. RESULTS: At the end of follow-up, the proportion of asymptomatic patients ranged from 21% (normal histology) to 26% (antrum-predominant gastritis). No statistically significant differences between groups appeared in regard to re-visits or to proportion of patients examined by sigmoideo- or colonoscopy during follow-up. Patients with antrum-predominant gastritis less often underwent upper endoscopy. Peptic ulcer was more frequent (P = 0.05) in patients with antrum gastritis than in other groups, but no other differences existed among any organic gastrointestinal findings. No significant differences between subgroups appeared among the 30% of patients using drugs for upper abdominal complaints during the previous year. CONCLUSIONS: Functional dyspepsia has an excellent long-term prognosis. Antrum-predominant gastritis in functional dyspepsia seems to carry an increased risk for peptic ulcer, and for this group in particular, H. pylori eradication should be considered. This finding requires confirmation in future studies performed in primary care.

Case-Control Studies↗
PubMed2005

Evolution of gastritis in patients with gastric erosions.

OBJECTIVE: Gastric erosions are mainly associated with Helicobacter pylori infection and non-steroidal anti-inflammatory drugs (NSAIDs), but there has been no information available on the long-term evolution of gastritis in subjects with erosions. MATERIAL AND METHODS: A series of 117 patients with gastric erosions without peptic ulcer disease and matched controls without erosions or ulcers were studied. Available subjects underwent endoscopy and biopsy 17 years later. Parietal cell antibodies were analysed at the first visit. RESULTS: Fifty-two patients and 67 controls were available for follow-up. Since H. pylori was a major determinant of gastritis, only subjects with unchanged H. pylori status were included in the evaluation of gastritis progression. At the follow-up visit, gastric erosions were present in 38% (16/42) of the patients and 11% (5/46) of the controls (p=0.005). In H. pylori-negative subjects, no evolution of histological changes was seen. In H. pylori-positive subjects, body gastritis was initially less active in the erosion group. With time, antral gastritis worsened only in the erosion group. Parietal cell antibodies were more common in the control group (23%; erosion patients 0%; p=0.01), which also showed worsening of gastritis (p=0.003) and aggravation of atrophy (p=0.002) in the body mucosa. CONCLUSIONS: Gastritis in H. pylori-positive subjects with gastric erosions shows evolution of antral predominance, body predominance including development of atrophic changes being rare. Accordingly, patients with erosions share the characteristics of gastritis of the duodenal ulcer phenotype. These findings support the importance of H. pylori and acid in the pathogenesis of gastric erosions in H. pylori-positive patients.

Biopsy, Needle↗
PubMed1980

Alkaline reflux gastritis. An objective assessment of its diagnosis and treatment.

The hypothesis that reflux of upper intestinal content, particularly of bile acids (BA), is responsible for a unique postgastrectomy syndrome, alkaline reflux gastritis, was tested on 28 occasions in 21 postoperative patients (14 symptomatic patients, 7 controls). Parameters evaluated: recumbent (rec.), upright, p.c. intragastric pH, {BA}, net BA reflux per hour, specific BA fractions, fasting and p.c. gastrin, maximal acid output (MAO), gastric emptying of solids by delta-scintigraphy), and the severity of nonstomal histologic gastritis, the "gastritis score," graded 0-15 by an independent senior pathologist. For the entire group, gastritis severity correlated positively with intragastric {BA} and net BA reflux per hour, both in recumbency and p.c. Five symptomatic patients demonstrated rec. and p.c. {BA} and net BA reflux per hour greater than two standard deviations from comparable mean values in control patients. They differed significantly from the remaining symptomatic patients as follows: increased intragastric {BA} and net BA reflux per hour, increased intragastric pH and decreased MAO. They also demonstrated a more severe grade of gastritis. Lithocholic acid was present in their reflux content significantly more often. Bilious vomiting was also more frequent. No other differences could be identified, either objectively or clinically, between the symptomatic groups. Four patients with excessive reflux underwent Roux-en-Y revision and restudy 6-22 months later. BA reflux was completely abolished, histologic gastritis improved, hematocrit rose, MAO increased, and gastric emptying slowed. Burning pain, bilious vomiting, and symptoms of esophageal reflux were eliminated. Vomiting and nausea were improved. Diarrhea was unchanged. The objective criteria outlined can identify symptomatic postgastrectomy patients with a greater than normal reflux and gastritis. Clinical criteria alone cannot. Revisional surgery in these patients eliminates reflux, improves gastritis, and produces symptomatic improvement. The hypothesis under consideration is strengthened but not proven.

Adult↗
PubMed1994

Duodenogastric reflux demonstrated by cholescintigraphy in peptic ulcer disease and chronic gastritis.

Duodenogastric (D-G) reflux is commonly associated with peptic ulcer disease and chronic gastritis. To determine D-G reflux in association with each disease entity, we studied 43 chronic gastritis patients and 21 peptic ulcer patients with cholescintigraphy. Scoring (0 to 3+) was judged by the amount of Tc-99m diethylacetanitanilido-IDA (EHIDA) in the stomach. In the chronic gastritis group, 5, 16, 10, and 12 patients scored 3+, 2+, 1+, and 0, respectively. In the peptic ulcer disease group 6, 2, and 13 patients scored 2+, 1+, and 0, respectively. Thirty-nine of the 64 patients (60.9%) were positive for D-G reflux. D-G reflux occurred in 31 of 43 (72.09%) of chronic gastritis patients and in 8 of 21 (38.1%) patients with peptic ulcer disease. D-G reflux was significantly higher in the chronic gastritis group (P = 0.0009). Chronic gastritis patients were more likely to have more marked D-G reflux than peptic ulcer disease (P = 0.048). The authors conclude that cholescintigraphy is noninvasive and objectively demonstrates D-G reflux in chronic gastritis and peptic ulcer disease and that chronic gastritis is more closely associated with D-G reflux than peptic ulcer disease.

Adult↗
PubMed1993

Helicobacter pylori-associated gastritis in Kuwait: endoscopy-based study in symptomatic and asymptomatic children.

Information is limited concerning the prevalence of Helicobacter pylori infection in asymptomatic children. Since January 1989, we have endoscoped 60 children for recurrent abdominal pain or for obtaining small-intestinal biopsy (their ages were a mean of 6.6 (range 9 months-13 years); there were 37 boys and 23 girls. Antral biopsies were obtained from all subjects and these were studied for the presence of gastritis and stained for H. pylori using modified Gram's stain. All biopsies were cultured for H. pylori. Children endoscoped for small-intestinal biopsy (n = 18) were used for comparison. Of the 42 children who had abdominal pain, 24 showed histological gastritis and 13 had H. pylori on microscopy (31% H. pylori-associated gastritis). In the compared group, five showed histological gastritis, and all had H. pylori on microscopy (27.7%). Culture was positive in 15; sensitivity was 85.7%. Six children, three pairs of siblings, had H. pylori gastritis supporting environmental etiology. Two had coinfection with intestinal giardiasis. Seven children were treated with daily oral amoxycillin (50 mg/kg) and tinidazole (20 mg/kg) for 6 weeks. In 3 (42.3%) H. pylori colonization cleared with healing of gastritis and resolution of symptoms. These results indicate that H. pylori gastritis is equally prevalent in symptomatic and asymptomatic children (31 and 27.7%, respectively; p > 0.05) in our population. It seems that the combination of oral amoxycillin and tinidazole is a poor choice in the treatment of H. pylori-associated gastritis in Kuwaiti children.

Abdominal Pain↗
PubMed1998

Inducible nitric oxide synthase, anti-oxidant enzymes and Helicobacter pylori infection in gastritis and gastric precancerous lesions in humans.

Chronic inflammation induced by Helicobacter pylori infection has been associated with an increased risk of stomach cancer. We have analysed 167 stomach biopsies from 99 patients for H. pylori infection and immunohistochemically for the expression of inducible nitric oxide synthase (iNOS), catalase and superoxide dismutases (SODs) as markers of oxidative stress. Biopsies were graded as follows on the basis of histology: normal, superficial gastritis, variable severity of atrophic gastritis with or without intestinal metaplasia, and dysplasia. iNOS was detected in inflammatory cells in all types of gastritis with or without H. pylori infection and independently of its severity. In foveolar cells, iNOS was observed in approximately 25% of all biopsies showing any type of gastritis, but in a markedly higher proportion of dysplastic samples. Catalase and Mn-type SOD in inflammatory cells and catalase in foveolar cells were more frequently observed in marked atrophic gastritis biopsies than in less severe gastritis. Individual differences were found in the expression of these enzymes within groups with the same severity of gastritis. Prolonged oxidative stress in severe gastritis and dysplasia may play an important role in gastric carcinogenesis, through increased damage of DNA and tissue by reactive oxygen and nitrogen species.

Adult↗
PubMed2003

Non-endoscopic diagnosis of atrophic gastritis with a blood test. Correlation between gastric histology and serum levels of gastrin-17 and pepsinogen I: a multicentre study.

BACKGROUND AND AIMS: Serum levels of gastrin-17 (S-G-17) and pepsinogen I (S-PGI) are biomarkers of gastric antral and corpus mucosa, respectively. In a prospective multicentre investigation, we determined whether these tests, together with the assay of Helicobacter pylori antibodies, are a non-endoscopic tool for the diagnosis of atrophic gastritis. MATERIALS AND METHODS: The series comprised 404 consecutive adult outpatients undergoing diagnostic upper-gastrointestinal endoscopy for various dyspeptic symptoms in five outpatient clinics. Gastric biopsies from the antrum and corpus (at least two biopsies from both sites) were available from all patients, and they were evaluated according to the guidelines of the updated Sydney system. S-PGI and S-G-17 were assayed with ELISA methods using monoclonal antibodies to pepsinogen I and amidated gastrin-17. In addition to the fasting level (S-G-17(fast)), a postprandial S-G-17 (S-G-17(prand)) level was measured 20 min after ingestion of a protein-rich drink. H. pylori antibodies were determined using a polyclonal EIA method. RESULTS: S-G-17(prand) (and S-G-17(fast)) and S-PGI levels decreased with increasing grade of atrophy of the antrum or corpus, respectively. S-G-17(prand) levels were significantly lower in patients with advanced (moderate or severe) atrophic antral H. pylori gastritis than in those with non-atrophic H. pylori gastritis. All patients with a resected antrum demonstrated S-G-17(prand) levels that were almost undetectable. Of the nine patients with an H. pylori-positive moderate or severe atrophic antral gastritis, six had S-G-17(prand) levels below 5 pmol/l. Similarly, S-PGI levels were significantly lower in patients with advanced corpus atrophy than in those without. Of the 45 patients with moderate or severe corpus atrophy in endoscopic biopsies, 35 patients had S-PGI levels < 25 microg/l. By using the cut-off levels for S-G-17(prand) and S-PGI with the best discrimination, the sensitivity and specificity of the blood test panel in delineation of patients with advanced atrophic gastritis (either in the antrum or the corpus, or both) were 83% and 95%, respectively. The predictive values of the positive and negative test results were 75% and 97%, respectively. In the diagnosis of atrophic gastritis, the application of S-G-17(fast) showed a slightly lower sensitivity and specificity than the application of S-G-17(prand) as a biomarker for antral atrophy. CONCLUSIONS: The diagnosis of atrophic gastritis obtained with the blood test panel of S-G-17, S-PGI and H. pylori antibodies is in good agreement with the endoscopic and biopsy findings. The panel is a tool for non-endoscopic diagnosis and screening of atrophic gastritis.

Adult↗
PubMed2006

Role of Helicobacter pylori and autoimmunity in serological atrophic corpus gastritis in a Dutch primary care community.

BACKGROUND: Atrophic corpus gastritis predisposes to vitamin B12 deficiency and gastric cancer. Little is known about the seroprevalence of atrophic corpus gastritis in the general population of Western Europe. AIM: To investigate the seroprevalence of atrophic corpus gastritis in a West-European primary care community in relation to Helicobacter pylori infection and autoimmunity. METHODS: Nine hundred and ninety-seven consecutive persons attending one general practice were asked to participate in the study by completing a questionnaire and donating fasting blood. Gastrin, pepsinogen A and C, and antibodies to H. pylori and parietal cells were measured by well-validated immunological methods. Criteria for serological atrophic corpus gastritis were pepsinogen A < 17 microg/l, pepsinogen A/C ratio <1.6, and gastrin >100 ng/l. RESULTS: Thirty-four participants (3.4%) fulfilled the serological criteria of atrophic corpus gastritis. Twenty-one of them (62%) and 17 of 34 (50%) age-matched and sex-matched nested controls were H. pylori positive [NS; odds ratio, 1.62 (0.62-4.24)], while 15 of them (44%) and one of 34 controls had antibodies to parietal cells [P < 0.005; odds ratio, 24.0 (3.00-201)]. CONCLUSIONS: The seroprevalence of atrophic corpus gastritis in this primary care community is 3.4%. When compared with controls, the approximate relative risk of having atrophic corpus gastritis was significantly higher (P < 0.025) for antibodies to parietal cells (24.0) than to H. pylori (1.62). In view of the decreasing risk of H. pylori infection in the western world, it is likely that the impact of H. pylori on the development of atrophic corpus gastritis will further diminish.

Adult↗
PubMed2006

Healing of lymphocytic gastritis after Helicobacter pylori eradication therapy--a randomized, double-blind, placebo-controlled multicentre trial.

BACKGROUND: An association between Helicobacter pylori infection and lymphocytic gastritis has been postulated. AIM: To assess the long-term effect of H. pylori eradication therapy on lymphocytic gastritis in a double-blind, placebo-controlled, multicentre trial. METHODS: Patients with lymphocytic gastritis were randomized to receive either 1-week triple therapy for eradication of H. pylori or omeprazole plus placebo. Endoscopy and histology was performed at baseline and after 3 and 12 months. Patients of the omeprazole/placebo group with persistent lymphocytic gastritis after 12 months received crossover open-label triple therapy. RESULTS: Fifty-one patients were randomized. Intention-to-treat analysis revealed a trend to a higher healing rate of lymphocytic gastritis 3 months after triple therapy compared with omeprazole/placebo (83.3% vs. 57.7%, 95% CI for RR: 0.8-2.8, P = 0.06). After 12 months, the healing rate of lymphocytic gastritis was significantly higher after triple therapy compared with omeprazole/placebo (intention-to-treat 95.8% vs. 53.8%, 95% CI for RR: 1.1-3.5, P = 0.01). All patients (n = 5) who received crossover triple therapy, showed healing of lymphocytic gastritis after further 12 months. CONCLUSION: Our study demonstrates that 1-week triple therapy aiming at eradication of H. pylori leads to a complete and long-lasting resolution of lymphocytic gastritis in the majority of patients.

Adult↗
PubMed1996

Cytotoxin and urease activities of Helicobacter pylori isolates from Japanese patients with atrophic gastritis or duodenal ulcer.

The vacuolating cytotoxin and urease secreted by Helicobacter pylori are thought to be virulent factors. Because vacuolation is potentiated by the presence of ammonium ion, which is produced by urease in vitro, it is of interest to examine whether cytotoxin and urease work reciprocally in the development of atrophic gastritis or duodenal ulcer. In the present study, patients (all H. pylori-positive) were divided into four groups: mild atrophic gastritis (group 1; nine patients), severe atrophic gastritis (group 2; 36 patients), duodenal ulcer with mild atrophic gastritis (group 3; 19 patients) and duodenal ulcer with severe atrophic gastritis (group 4; 12 patients). Cytotoxin production and urease activity of H. pylori isolated from these patients were analysed. Cytotoxin production was observed in four of nine (44.4%), 28 of 36 (77.8%), 11 of 19 (57.9%) and eight of 12 (66.7%) isolates from groups 1, 2, 3 and 4, respectively. Cytotoxin-producing H. pylori isolates were found significantly more in patients with severe atrophy than in patients with mild atrophy (P = 0.048). The mean of relative activity of cytotoxin in H. pylori isolate was 1.6 +/- 2.3, 7.9 +/- 7.4, 5.8 +/- 6.0 and 9.0 +/- 9.1 in groups 1, 2, 3 and 4, respectively. Helicobacter pylori isolates from severe atrophy or duodenal ulcer patients in groups 2 or 4 possessed significantly higher activity than those from non-ulcer patients in group 1 (P = 0.017 and 0.030, respectively). The mean of urease activity was 8.6 +/- 4.6, 10.0 +/- 5.9, 10.0 +/- 8.5 and 11.2 +/- 7.7 IU/mg in groups 1, 2, 3 and 4, respectively. These differences indicated no statistical significance. In each H. pylori isolate, the production of cytotoxin and urease were independent, which indicated that there was no reciprocal effect between them in vivo. Thus, cytotoxin-producing H. pylori isolates were more prevalent in patients with severe atrophic gastritis and the cytotoxin activities of H. pylori isolates from the patients with severe atrophic gastritis or duodenal ulcer were much higher than those from the patients with mild atrophic gastritis, which suggested that vacuolating cytotoxin may be a disease-inducing factor.

Bacterial Proteins↗
PubMed1971

Simple atrophic gastritis and gastric carcinoma.

Gastric carcinoma was detected nine, 10, 18, and 21 years after the biopsy diagnosis of atrophic gastritis in four patients of a group of 40. The gastritis was presumed to be of the simple type. Tests of vitamin B(12) absorption in three patients gave normal results, no gastric autoantibodies were detected in the two patients tested, in all patients histological examination of the gastrectomy specimens revealed a multifocal gastritis differing from the diffuse gastritis of pernicious anaemia and in three patients the gastritis affected the antrum, which is unusual in pernicious anaemia. The 10% incidence of gastric carcinoma in 40 patients with simple atrophic gastritis followed for a mean period of 15 years is equivalent to that previously described in pernicious anaemia. However, in view of the relative incidence of atrophic gastritis with and without pernicious anaemia in the general adult population, it emerges that atrophic gastritis without pernicious anaemia is numerically the more important precursor of gastric carcinoma.

Adult↗
PubMed1976

Gastritis duodenitis, and circulating levels of gastrin in duodenal ulcer before and after vagotomy.

Biopsy specimens have been taken from five standard sites in the stomach and from the duodenal bulb in order to investigate the association of gastritis and duodenitis with duodenal ulcer. Twenty patients with chronic duodenal ulcer were investigated in this manner and in addition had gastric secretion tests and a radio-immune assay of serum gastrin under differing conditions. The patients were then treated either by a truncal vagotomy and pyloroplasty (TVP) or by a highly selective vagotomy without a drainage procedure (HSV). All the investigations were repeated three months postoperatively. Duodenal ulcer was usually associated with gastriitis, although this varied in extent and severity from patient to patient. In nearly all the patients, gastritis was present at the pyloric end of the stomach and along the lesser curve. In more than half of the patients, gastritis was also present in the body of the stomach but the fundus was usually spared. Chronic duodenitis was found in the duodenal bulb in all these patients. After vagotomy there was a marked increase in both the extent and severity of the proximal gastritis in both treatment groups but the distal gastritis remain almost unchanged. There was little change in the incidence of duodenitis after vagotomy but its severity was lessened. No correlation was found between the peak acid output (PAO) in response to Histalog and the severity of the gastritis or the duodenitis either before or after operation, with one exception. The postoperative PAO was significantly less in those patients who developed a severe proximal gastritis after vagotomy. No relationship was found between the severity of the distal gastritis and the levels of serum gastrin. No correlation was found between either the basal or peak acid output and the corresponding serum gastrin levels before or after vagotomy.

Biopsy↗
PubMed1985

Gastric lesions in portal hypertension: inflammatory gastritis or congestive gastropathy?

This paper reports the incidence and natural history of macroscopic gastritis in a series of 127 consecutive patients with portal hypertension of various aetiologies. Gastritis was observed endoscopically in 65 patients (51%) and was of two main types. Twenty eight patients had severe or persistent gastritis which caused clinically significant bleeding on 80 occasions and accounted for 25% of the bleeds from all sources. The remainder had mild gastritis. The presence of gastritis seemed to be independent of the severity of liver disease or the degree of rise of wedged hepatic venous pressure and there was no difference in age, sex, or drugs prescribed in patients with or without gastritis. The mean follow up period and the mean number of sclerotherapy treatments was significantly greater (p less than 0.005) in patients with gastritis. Full thickness gastric biopsies in seven surgical patients and 11 autopsy specimens showed dilated and tortuous submucosal veins. Endoscopic biopsies in 14 patients showed vascular ectasia in the mucosal layer which was in excess of the degree of inflammatory infiltrate. Gastritis occurred in patients with portal hypertension of all common aetiologies and the clinical and pathological evidence supports the contention that it reflects a congested gastric mucosa and should be renamed congestive gastropathy. As injection sclerotherapy improves survival from variceal bleeding congestive gastropathy may become more common. The response to conventional ('anti-erosive') therapy is poor and measures aimed at reducing the gastric portal pressure may be the only effective means of treating this condition.

Adult↗
PubMed1988

Lymphocytic gastritis: a newly described entity: a retrospective endoscopic and histological study.

Lymphocytic gastritis is a histopathological entity characterised by the accumulation of small lymphocytes in the surface and foveolar epithelium. In order to investigate the correlation between endoscopy and histology in this condition, 192 observations selected on the basis of a presumed diagnosis of erosive or varioliform gastritis were reviewed. Ninety two instances corresponded to lymphocytic gastritis, while 100 did not show any particular microscopic feature and were labelled non-specific gastritis. There was a good correlation (48 of 58) between the diagnosis of the so-called varioliform gastritis and the histological evidence of lymphocytic gastritis. The correlation was even better when nodules, erosions, and enlarged folds were considered. Lymphocytic gastritis has a typical endoscopical appearance consisting of nodules, erosions, and large folds predominating in the gastric body. This contrasts with non-specific gastritis, which affects the antrum and produces erosions on a flat mucosa.

Duodenum↗
PubMed1989

Subclass distribution of mucosal IgG-producing cells in gastritis.

IgG-mediated immune reactions are probably involved in the maintenance of gastritis and glandular atrophy; the mucosal IgG-subclass pattern may therefore influence the effect of local hypersensitivity mechanisms. In this study the proportions of IgG1-, IgG2-, IgG3-, and IgG4-producing immunocytes were determined by paired immunofluorescence staining in specimens from simple gastritis, gastritis after Billroth II (BII) resection, and gastritis associated with dermatitis herpetiformis (DH). The results were related to histopathological degree of inflammation and atrophy. Generally, IgG1 immunocytes predominated (48-60%) in all types of gastritis. With increasing severity of inflammation, the IgG2-cell proportion was significantly increased from 4-6% to 26-34% in simple and BII gastritis, whereas the ratio of IgG1 immunocytes was correspondingly decreased from 58-69% to 38-43%. In the same types of gastritis the proportion of IgG3 cells was increased in association with severe (35-38%) compared with mild (15-23%) atrophy, whereas the proportion of IgG1 cells was correspondingly decreased. In severe gastritis associated with DH, the proportion of IgG1 cells was relatively high (60%) and that of IgG2 cells relatively low (13%), and severe atrophy did not seem to influence significantly the subclass proportions.

Antibody-Producing Cells↗
PubMed1992

Effect of Helicobacter pylori infection on 24 hour intragastric acidity in patients with gastritis and duodenal ulcer.

Helicobacter pylori status, gastric histology, and 24 hour acidity were studied in 35 gastritis patients, 21 duodenal ulcer patients, and 14 subjects with normal gastric mucosa. H pylori was identified in 21 of 35 patients with chronic active gastritis and in 19 of 21 duodenal ulcer patients, but in none of those with normal gastric mucosa. Mean scores of activity of gastritis were similar in H pylori positive gastritis and duodenal ulcer patients, but were significantly lower in H pylori negative gastritis patients (2.1 (0.8) and 2.3 (0.9) v 1.4 (0.7); p < 0.01, respectively). Median 24 hour hydrogen ion activity (interquartile range) was 21 (8.9-38.0) mmol/l in normal subjects and 23 (11.2-49.0) mmol/l, 19 (7.1-33.1) mmol/l, 44 (25.1-63.1) mmol/l, and 36 (31.6-39.8) mmol/l respectively in gastritis and duodenal ulcer patients with and without H pylori infection. During all predefined time periods, intragastric acidity was significantly higher in patients with H pylori positive duodenal ulcers compared with gastritis patients and normal subjects. However, there was no significant difference in intragastric acidity between the H pylori positive and negative gastritis patients. These results suggest that most of the subjects with chronic H pylori infection have normal gastric acidity.

Adult↗
PubMed1999

A genetic basis for atrophy: dominant non-responsiveness and helicobacter induced gastritis in F(1) hybrid mice.

BACKGROUND: The importance of host factors in helicobacter induced gastritis has been shown in animal models. Infection of most mouse strains with Helicobacter felis results in a functional atrophic gastritis, while other strains remain gastritis free. AIMS: To investigate these host factors further by using genetic crosses of responder and non-responder mice. METHODS: F(1) hybrids of the non-responder CBA/Ca strain and three strains of mice known to develop H felis induced gastritis were infected for three months with H felis. Gastritis was assessed by histopathology and serum antibody responses by ELISA. RESULTS: Infection of CBA/Ca mice and F(1) hybrids induced little or no gastritis. Analyses of the antibody responses in these mice revealed virtually undetectable anti-helicobacter antibody levels despite colonisation with high numbers of H felis. In contrast, infection of H felis responsive strains induced gastritis and a significant humoral immune response. CONCLUSIONS: The non-responsiveness of CBA/Ca mice to H felis infection is dominantly inherited. The lack of gastritis in CBA mice and their offspring is probably due to active suppression of the immune response normally mounted against H felis. Investigation of these mechanisms will provide important insights relevant to induction of gastric atrophy and cancer in humans.

Animals↗