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PubMed1996

[A sero-epidemiological study on atrophic gastritis and Helicobacter pylori infection].

The aim of this study is to clarify the relationship between the incidence of atrophic gastritis and Helicobacter pylori infection. A case control study was conducted in 1995. Cases and controls were selected among those who took an annual health examination in a rural area of Fukuoka Prefecture. Cases are those who were not diagnosed as having atrophic gastritis in 1991 or 1992 but were diagnosed as having atrophic gastritis in 1995 by the examination of serum pepsinogens. Controls are those who were not diagnosed as having atrophic gastritis between 1991, or 1992 and 1995. Helicobacter pylori infection was evaluated by anti Helicobacter pylori IgG in 1995. The odds ratio for atrophic gastritis was calculated using Logistic regression analysis. The odds ratio of age and sex was not significant, but the odds ratio of Helicobacter pylori infection was significantly elevated (5.2, 95% confidence interval: 2.08-13.17). As for the influence of sex difference on the incidence of atrophic gastritis by Helicobacter pylori infection, the odds ratio among males was not significant (1.4, 95% confidence interval: 0.30-6.10), but the odds ratio among females was significantly high (9.8, 95% confidence interval: 2.82-34.11). These results suggest that Helicobacter pylori infection is associated with the incidence of atrophic gastritis. There may be a risk difference between males and females in the incidence of atrophic gastritis caused by Helicobacter pylori infection.

Adult↗
PubMed2001

Screening markers for chronic atrophic gastritis in Chiapas, Mexico.

Intestinal-type gastric adenocarcinomas usually are preceded by chronic atrophic gastritis. Studies of gastric cancer prevention often rely on identification of this condition. In a clinical trial, we sought to determine the best serological screening method for chronic atrophic gastritis and compared our findings to the published literature. Test characteristics of potential screening tests (antibodies to Helicobacter pyloni or CagA, elevated gastrin, low pepsinogen, increased age) alone or in combination were examined among consecutive subjects enrolled in a study of H. pylori and preneoplastic gastric lesions in Chiapas, Mexico; 70% had chronic atrophic gastritis. English-language articles concerning screening for chronic atrophic gastritis were also reviewed. Sensitivity for chronic atrophic gastritis was highest for antibodies to H. pylori (92%) or CagA, or gastrin levels >25 ng/l (both 83%). Specificity, however, was low for these tests (18, 41, and 22%, respectively). Pepsinogen levels were highly specific but insensitive markers of chronic atrophic gastritis (for pepsinogen I <25 microg/l, sensitivity was 6% and specificity was 100%; for pepsinogen I:pepsinogen II ratio <2.5, sensitivity was 14% and specificity was 96%). Combinations of markers did not improve test characteristics. Screening test characteristics from the literature varied widely and did not consistently identify a good screening strategy. In this study, CagA antibodies alone had the best combination of test characteristics for chronic atrophic gastritis screening. However, no screening test was both highly sensitive and highly specific for chronic atrophic gastritis.

Adult↗
PubMed2001

[Clinical, endoscopic and histologic aspects of chronic Helicobacter pylori gastritis in Côte d'Ivoire: study of 102 patients].

BACKGROUND: Helicobacter pylori (H. pylori) is the most frequent aetiological factor of chronic gastritis (CG). The relationship between H. pylori gastritis, gastro-duodenal ulcer and some gastric cancers (adenocarcinoma, gastric MALT lymphoma) has now been proven. AIM: Describe clinical, endoscopical and histological aspects of H. pylori gastritis in Côte d'Ivoire. METHODS: Retrospective analysis of 1960 gastroscopy reports carry out between January 1994 and December 1995. Analysis of clinical and gastric histological results in 137 patients. FINDINGS: Among 137 patients with gastric biopsy, 102 had H. pylori gastritis (68 men, 38 women, mean age: 39.3 years) and 35 had chemical gastritis. Epigastric pain was the most frequent symptom. The mucosa was frequently erythematous or exsudative at endoscopy. Histological anomalies were located in the antrum, the fundus or generalised, respectively in 33.3%, 25.5% and 41.2% of cases. Mild atrophic CG was more frequent in various locations. Gastritis activity was present in 81.4%, intestinal metaplasia in 18.6% and follicular lymphoid hyperplasia in 36.3% of cases. CONCLUSION: Clinical and endoscopical aspects of H. pylori gastritis did not present any particularities. Fundic gastritis without antral localisation was not unusual. This situation could be the result of antibiotic and gastric acid secretion inhibitor treatments.

Adult↗
PubMed1975

Pentagastrin-stimulated gastric acid secretion in acute and chronic gastritis. Histological and secretory correlations.

Basal and pentagastrin-stimulated gastric acid secretion were determined in 122 patients with various types of gastritis and in 20 control subjects. All the gastritis patients and the control subjects were adult Chinese. The histological diagnosis was based on gastric biopsy specimens obtained through a fibergastroscope. Statistical analysis of the results in the various histological groups of gastritis and controls indicated that chronic superficial gastritis and chronic atrophic gastritis are not associated with reduced gastric acid secretion in Chinese subjects. In addition, analysis of combinations of the groups of patients with various types of gastritis showed no significant difference in the mean basal acid output but the mean peak acid output of patients with chronic gastritis was significantly higher than that of patients with chronic atrophic gastritis.

Acute Disease↗
PubMed2002

[Symptomatology and specific characteristics of chronic gastritis caused by Helicobacter pylori infection in children in the Czech population--epidemiologic, clinical, endoscopic and histomorphologic study].

BACKGROUND: H. pylori infection is associated with gastritis and peptic ulcer in children and adults. H. pylori acquisition seems to occur predominantly in childhood. Some data have reported H. pylori non-related chronic gastritis. Little information is available about the relationship between H. pylori, clinicopathologic features and long-term effects of infection in childhood. The purpose of this study was to compare the differences between chronic gastritis due to H. pylori with those of chronic gastritis not associated with H. pylori infection. METHODS AND RESULTS: 92 children (13.8 +/- 3.5 years) were take into they shaded group. 51 children were H. pylori positive, 41 children had no evidence of H. pylori. Epidemiological and clinical data, endoscopic appearance and histologic examination were evaluated. There were no differences in age and gender among the children. There was a significant correlation between H. pylori infection and parental education (p < 0.05) and habitat crowding (the number of rooms). There were no differences in clinical diagnosis and occurrence of any predominant symptom between the two groups. There was an association with a detrimental influence on daily life and activities in H. pylori patients (p < 0.01). Extradigestive symptoms (chronic urticaria, sideropenic anemia) were significantly more common in the H. pylori positive group (p < 0.05). 21 children (41.6%) were H. pylori positive/cagA positive, 15 of them (30.3%) were H. pylori positive/vacA positive. Findings of antral nodularity were more frequent in H. pylori positive children than in H. pylori negative (p < 0.000001). There were no differences in erythematous gastritis, haemorrhage and mucosal ulceration. H. pylori density score did not differ in various part of the gastric mucosa (antrum, corpus). Chronic gastritis was found to be more severe in patients with H. pylori infection compared with H. pylori-negative gastritis. Statistically significant was the increased presence of neutrophils, edema, monocytes, lymphoid follicles, the intensity of inflammation and mucosal oedema in the gastric mucosa in H. pylori positive children. There were no differences in the incidence of foveolar hyperplasia, mucosal atrophy, intestinal metaplasia and erosion. CONCLUSION: H. pylori related chronic gastritis may be considered as a specific form of inflammation and it may be associated with a typical clinical symptomatology in a subgroup of children in Czech population. Precautions in life style may diminish H. pylori-related disease in children.

Adolescent↗
PubMedDate not supplied

Helicobacter pylori-associated gastritis and gastric cancer in Nigeria.

BACKGROUND: The etiology of gastric cancer has not been clearly delineated. There is some evidence of an association of gastric cancer with Helicobacter pylori-induced chronic gastritis, atrophic gastritis and intestinal metaplasia. Previous studies report a high rate of H. pylori infection and chronic gastritis among Nigerians. METHODS: We retrospectively reviewed 84 tissue specimens with gastric cancer seen in our department over an 18-year period for for the presence of H. pylori infection, chronic gastritis, atrophic gastritis, and intestinal metaplasia in the adjacent non-cancerous gastric mucosa. RESULTS: H. pylori infection was detected in 15 (17.9%) of 84 specimens. Moderate to severe gastritis was found in non-cancerous areas in 77 (91.7%) specimens, and was equally frequent in patients with 'intestinal' and 'diffuse' types of cancer. Atrophic gastritis and intestinal metaplasia were observed in 22 (26.2%) and 35 (41.7%) specimens, respectively, and were more common in 'intestinal' type of gastric cancer. CONCLUSION: Chronic gastritis was seen in the adjacent non-cancerous mucosa in most specimens with gastric cancer. However, its severity did not correlate with the histological subtype of gastric cancer.

Adenocarcinoma↗
PubMedDate not supplied

Relationship between endoscopic nodular gastritis and Helicobacter pylori infection in children.

INTRODUCTION: The specificity of relationship of endoscopic evidence of nodular gastritis with Helicobacter pylori infection is unclear. AIM: To assess the relationship of endoscopic nodular gastritis and H. pylori infection among children. METHODS: 124 children (median age 8.2 years, range 1-15) undergoing upper GI endoscopy for abdominal pain underwent urease test and histological examination of gastric mucosa to determine the presence and density of H. pylori infection, and presence and severity of gastritis. RESULTS: H. pylori infection was detected in 57 (46%) children. Endoscopic nodular gastritis was present in 46 of these 57 patients (81%) and in 24 of 67 (36%) H. pylori-negative patients (36%). The frequency of endoscopic nodular gastritis was related to increasing age (p< 0.0001), presence of H. pylori, grade of histologic gastritis, and H. pylori density (p< 0.0001). CONCLUSION: Endoscopic finding of nodular gastritis is associated with presence of H. pylori infection and active chronic gastritis in children.

Adolescent↗
PubMed1990

Gastric campylobacter-like organisms and active antral gastritis in Puerto Rico.

We attempted to verify if the reported association of gastric campylobacter like organisms (GCLO) with active antral gastritis holds true in our population. All patients undergoing elective upper endoscopy were eligible for the study unless they had a history of gastric cancer or previous antrectomy. Biopsy specimens from 100 consecutive patients were examined blindly for the presence of inflammatory activity and/or intestinal metaplasia. The presence of GCLO was determined by the acridine orange fluorescence technique. A total of 131 antral biopsies examined were classified as either normal, active gastritis, chronic gastritis with activity and chronic gastritis without activity. GCLO were identified in 84% of the biopsies with inflammatory activity (active gastritis and chronic gastritis with activity). However, GCLO were found only in 11% of those biopsies with chronic gastritis without activity. It is therefore our conclusion that the previously reported association of GCLO with active gastritis holds true for our population.

Biopsy↗
PubMedDate not supplied

[Lymphocytic gastritis].

Lymphocytic gastritis is a new histopathological entity characterized by a dense lymphocytic infiltration of the gastric surface and pit epithelium. The diagnosis relies upon lymphocyte counts which are always far beyond the values obtained in other types of gastritis. The clinical presentation of lymphocytic gastritis is characterized, in the majority of cases, by weight loss and anorexia. Endoscopically it corresponds to a complex pattern of enlarged rugae and often eroded (aphthoïd) nodules. Our studies have shown a close correlation between lymphocytic gastritis and diffuse or corporeal varioliform gastritis. On the contrary, there is no relationship between lymphocytic gastritis and antral varioliform gastritis which exhibits heterogeneous histological features. Lymphocytic gastritis is a chronic disease which can evolve over long periods; it can however cure spontaneously (about half of the cases) after a delay of one to two years. The aetiology and pathogenesis are unknown. The histological similarity with coeliac disease suggests a possible role of immunological factors.

Chronic Disease↗
PubMed1989

No acid, no polys--no "active" gastritis, no dyspepsia. A proposal.

The current dilemma in characterizing non-ulcer dyspepsia (NUD) is due to the very nature of the term which has forced the dependence for diagnosis primarily on symptomatology and the absence of an ulcer crater as ascertained by radiographs or endoscopy. I propose a new classification which I believe is consistent and well founded, based on the presence of histologic gastritis and acid secretion of the stomach. Four categories are presented: (a) normal histology, (b) "active" gastritis, (c) "inactive" gastritis, and (d) atrophic gastritis with achlorhydria. Acid secretion is present in categories a-c. The classification is dependent on the presence of the "poly" to denote active gastritis, round cells to classify inactive gastritis, and the loss of parietal and chief cells with achlorhydria to define gastric atrophy. I propose that polys and acid, which characterize active gastritis, are necessary for producing dyspepsia and/or gastroduodenal mucosal injury, and provide a rationale for treatment. The accepted causes of active gastritis include acid-peptic disease, Campylobacter pylori, and aspirin/nonsteroidal anti-inflammatory drug (NSAID) medication.

Achlorhydria↗
PubMed1979

Significance of endoscopically visible blood vessels as an index of atrophic gastritis.

The endoscopic criteria for atrophic gastritis are. 1. pale mucosa; 2. shiny surface and 3. prominent submucosal vessels. To evaluate the diagnostic accuracy of circumscribed atrophic gastritis based on these findings, we studied 184 consecutive upper gastrointestinal endoscopies. The endoscopic diagnosis of atrophic gastritis was made only if two endoscopists both agreed on the findings and interpretation. The location of the atrophic pattern and whether it was circumscribed or diffuse were recorded. Two biopsy specimens were than obtained. Histologic material was interpreted by a pathologist who had no prior knowledge of the endoscopic findings. Twenty-five patients (13%) had atrophic gastritis endoscopically; in four it was diffuse and in 21 it was circumscribed. Utilizing the criteria of Whitehead, et al, atrophic gastritis was diagnosed histologically in three of four patients with diffuse gastritis but in one of those considered to have circumscribed atrophic gastritis. It is concluded from these preliminary data that a circumscribed atrophic mucosal pattern is a frequent endoscopic finding that does not necessarily represent atrophic gastritis histologically.

Adult↗
PubMed1976

Idiopathic chronic gastritis.

Idiopathic chronic gastritis is an autoimmune disease and the cause of this gastritis probably act through a final common immunologic pathway. Specific gastric antibodies are diagnostic of this gastritis and the tissue of the gastric mucosa is characterized by infiltrations of mononuclear cells damaging the glandular parenchyma with concomitant loss of gastric secretory function. With suitable predisposing factors operating, the patient with simple chronic gastritis can have pernicious anemia develop. Chronic gastritis is frequently associated with chronic gastric ulcer and carcinoma of the stomach but not with duodenal ulcer. Chronic gastritis clinically presents with vague dyspeptic symptoms. Females are more commonly affected than males and the incidence rises with advancing age. Treatment of chronic gastritis is supportive in nature and also similar to the treatment of other autoimmune diseases. The author has suggested a new treatment of duodenal ulcer whereby the patients are immunized against mucosal antigen with a view to induction of chronic gastritis. The resulting biochemical damage of the parietal cells will produce hypochlorhydria.

Adult↗
PubMedDate not supplied

A retrospective study on the incidence of lymphocytic gastritis in patients with Helicobacter pylori infection.

To investigate the relationship between lymphocytic gastritis and H. pylori infection, antral biopsy specimens from 162 patients with histological evidence of H. pylori infection, and from 177 subjects without colonization were retrospectively examined. Among patients with antral colonization, lymphocytic gastritis was identified in 8 cases (4.9%). Lymphocytic gastritis was not detected in specimens without H. pylori infection. Quantitation of the epithelial lymphocytic infiltration was carried out in all specimens and showed that cases with lymphocytic gastritis had a mean of 35.3 lymphocytes per 100 epithelial cells, compared with a mean of 2.6 and 2.4 respectively in chronic gastritis and normal mucosa. Among the 331 patients without lymphocytic gastritis, specimens colonized by H. pylori had a mean of epithelial lymphocyte counts significantly higher than those observed in both chronic gastritis and normal mucosa. These findings show a positive correlation between antral colonization by H. pylori and occurrence of lymphocytic gastritis, and suggest that the bacteria may have an important role in the induction of such particular form of antral inflammation.

Adult↗
PubMed1997

Treatment of gastritis in cheetahs (Acinonyx jubatus).

Three cheetahs (Acinonyx jubatus) had a clinical history of chronic spiral bacteria-associated gastritis and three cheetahs had no clinical history of gastritis. Gastric biopsies were obtained from all six cheetahs prior to treatment for gastritis and 3 wk and 1 yr posttreatment. The cheetahs were treated with tetracycline hydrochloride 500 mg p.o. q.i.d., metronidazole 250 mg p.o. q.i.d., and bismuth subsalicylate 300 mg p.o. q.i.d. Each drug was administered concurrently for 7 days. Following this treatment, each cheetah was maintained on 300 mg bismuth subsalicylate p.o. s.i.d. for 1 yr. The three cheetahs with a history of gastritis were culture positive for Helicobacter acinonyx and remained positive during the entire study. The three cheetahs with no clinical history of gastritis were culture negative for H. acinonyx, but gastric biopsies revealed Gastrospirillum-like bacteria (tentatively named Helicobacter heilmannii) pretreatment. Gastric biopsies were negative for H. heilmannii on subsequent examinations. Although the treatment did not eradicate H. acinonyx, it did provide symptomatic relief from the vomiting, anorexia, and weight loss associated with clinical gastritis. The use of endoscopically guided gastric mucosal biopsies for urease testing and histopathologic examination of Warthin-Starry-stained sections is a sensitive and specific method of diagnosing spiral bacteria-associated gastritis. Treatment of spiral bacteria-associated gastritis in cheetahs should include the rational use of antibiotics (tetracycline or amoxicillin and metronidazole), bismuth compounds, and omeprazole and evaluation of husbandry methods to reduce stress.

Acinonyx↗
PubMedDate not supplied

Who? When to treat? Gastritis, particular histological lesions, NSAID therapy and extradigestive diseases.

Indications of whom and when to treat Helicobacter pylori infection are reviewed in chronic atrophic gastritis, in particular types of gastritis (lymphocytic, giant fold, auto-immune gastritis), in hyperplastic polyps, before or during treatment with NSAIDs and in association with various extra-digestive diseases. Although there is no convincing evidence that Helicobacter pylori eradication may interrupt or reverse mucosal atrophy and intestinal metaplasia (potentially pre-cancerous lesions), indication for eradication could be considered in young patients if atrophic gastritis is considered as a consequence of chronic superficial gastritis which is reversible after Helicobacter pylori cure. The still evidence limited for a causal relationship between Helicobacter pylori and lymphocytic gastritis, giant folds gastritis and hyperplastic polyps suggests it is acceptable to eradicate Helicobacter pylori in infected patients presenting these special forms of gastritis. Despite the uncertainty on the interactions of Helicobacter pylori and NSAID in the genesis of peptic ulcer disease, it seems acceptable to prescribe eradication treatment in known Helicobacter pylori carriers before a long-term treatment with NSAID. The clinical evidence for an association between Helicobacter pylori and extra-digestive diseases is at the present time too limited to advocate routine eradication in these conditions before large prospective trials are performed.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1996

Gastric antioxidant, nitrites, and mucosal lipoperoxidation in chronic gastritis and Helicobacter pylori infection.

We have evaluated gastric juice pH, nitrites and vitamin C levels, mucosal glutathione, and malondialdehyde, a marker of lipid peroxidation, in patients with chronic gastritis undergoing endoscopy. Patients had chronic gastritis with (n = 28) or without (n = 60) atrophy and/or concomitant Helicobacter pylori infection. Nineteen healthy subjects, without major macroscopic or histologic changes, were included as controls. Ten subjects were studied before and after H. pylori eradication. Vitamin C levels were low in atrophic gastritis (p < 0.006) and H. pylori infection (p < 0.02). Nitrite concentrations and pH were significantly higher in atrophy (p < 0.005 and 0.0001). Glutathione turnover was higher than normal in gastritis, with higher levels of oxidized glutathione (p < 0.02). Gastric malondialdehyde levels were significantly increased by gastritis (p < 0.05) and H. pylori infection (p < 0.05). Overall, more active gastritis coincided with lower vitamin C levels and higher malondialdehyde levels. After H. pylori eradication a drop in mucosal MDA levels was observed (p = 0.04). In summary, chronic gastritis and H. pylori infection correlate with increased free-radical production, reduced gastric vitamin C levels, and increased glutathione turnover. The possible implications of these changes in the pathogenesis of gastric damage and in carcinogenesis are intriguing.

Adult↗
PubMed2004

Cure of Helicobacter pylori infection in patients with reflux oesophagitis treated with long term omeprazole reverses gastritis without exacerbation of reflux disease: results of a randomised controlled trial.

BACKGROUND: Helicobacter pylori gastritis may progress to glandular atrophy and intestinal metaplasia, conditions that predispose to gastric cancer. Profound suppression of gastric acid is associated with increased severity of H pylori gastritis. This prospective randomised study aimed to investigate whether H pylori eradication can influence gastritis and its sequelae during long term omeprazole therapy for gastro-oesophageal reflux disease (GORD). METHODS: A total of 231 H pylori positive GORD patients who had been treated for > or =12 months with omeprazole maintenance therapy (OM) were randomised to either continuation of OM (OM only; n = 120) or OM plus a one week course of omeprazole, amoxycillin, and clarithromycin (OM triple; n = 111). Endoscopy with standardised biopsy sampling as well as symptom evaluation were performed at baseline and after one and two years. Gastritis was assessed according to the Sydney classification system for activity, inflammation, atrophy, intestinal metaplasia, and H pylori density. RESULTS: Corpus gastritis activity at entry was moderate or severe in 50% and 55% of the OM only and OM triple groups, respectively. In the OM triple group, H pylori was eradicated in 90 (88%) patients, and activity and inflammation decreased substantially in both the antrum and corpus (p<0.001, baseline v two years). Atrophic gastritis also improved in the corpus (p<0.001) but not in the antrum. In the 83 OM only patients with continuing infection, there was no change in antral and corpus gastritis activity or atrophy, but inflammation increased (p<0.01). H pylori eradication did not alter the dose of omeprazole required, or reflux symptoms. CONCLUSIONS: Most H pylori positive GORD patients have a corpus predominant pangastritis during omeprazole maintenance therapy. Eradication of H pylori eliminates gastric mucosal inflammation and induces regression of corpus glandular atrophy. H pylori eradication did not worsen reflux disease or lead to a need for increased omeprazole maintenance dose. We therefore recommend eradication of H pylori in GORD patients receiving long term acid suppression.

Adult↗
PubMed1994

Histological study of chronic gastritis from the United Arab Emirates using the Sydney system of classification.

AIMS: To determine the prevalence of Helicobacter pylori in five main nationality groups with gastric ulcer, duodenal ulcer, and non-ulcer dyspepsia; and to determine the histopathological types of gastritis and assess the graded variables of Helicobacter associated gastritis. METHODS: Gastric antral and corpus biopsy specimens from 437 patients were examined for the prevalence of H pylori, 337 of which were classified and graded histologically according to the Sydney system. RESULTS: The overall colonisation rate of H pylori was 90%, and there was no significant difference between groups of different ethnic origins. The colonisation rates were 99%, 89%, and 78% in patients with duodenal ulcer, non-ulcer dyspepsia, and gastric ulcer, respectively. Helicobacter associated gastritis was the most common form of chronic gastritis (87%). H pylori density was greater in the antrum than the body. Gastric atrophy in helicobacter associated gastritis was seen in 54% of the cases (43% grade I, 10% grade II, 1% grade III) and increased the older the patients. Atrophy of the corpus alone was very rare (1%). Atrophy and intestinal metaplasia were more prevalent in patients with gastric ulcer than duodenal ulcer. CONCLUSION: The colonisation rate of H pylori was similar in the five groups studied and was almost invariably present in gastric biopsy specimens in patients with duodenal ulcer. H pylori associated gastritis was the most common form of gastritis. Atrophy was mainly of low grade and increased the older the patient.

Adolescent↗