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PubMed1989

Topographic association between active gastritis and Campylobacter pylori colonisation.

One thousand biopsy specimens obtained from 10 sites in the stomachs of 50 patients were examined for the presence of active chronic gastritis and Campylobacter pylori. All 32 patients with active chronic gastritis at 234 out of 320 sites were positive for C pylori: 227 showed colonisation with C pylori by the Warthin-Starry stain; and 222 were positive by culture. C pylori was not found in 18 patients with inactive chronic gastritis or histologically normal mucosa. The area of C pylori colonisation was larger than the area of active chronic gastritis in 289 positive specimens on culture and 261 on staining, respectively, suggesting that C pylori colonisation may precede the development of active chronic gastritis. It is concluded that patchy distribution of active chronic gastritis and C pylori colonisation must be considered, particularly in serology or breath test studies where the histological examination serves as a reference. Furthermore, it may have important implications for the follow up of patients after antibacterial treatment. The topographic and specific association of C pylori and active chronic gastritis provides further evidence for the pathogenic role of C pylori in active chronic gastritis.

Adult↗

PubMed1992

Helicobacter pylori, gastritis, and peptic ulceration in the elderly.

AIMS: To determine the histopathological types of gastritis, presence of H pylori, and of peptic ulceration in patients aged 70 and over, compared with younger adults. METHODS: Gastric antral and corpus biopsy specimens from 112 elderly patients were classified and graded histologically according to the Sydney system. Details of recent antibiotic and non-steroidal anti-inflammatory drug use were recorded. Eighty four of the patients were positive for H pylori IgG antibodies and parietal cell antibodies. The results were compared with those from a series of 124 adult patients aged under 60. RESULTS: H pylori were visible at histological examination in only 57 of 87 (65.5%) elderly patients with chronic gastritis (excluding "special forms") compared with 72 of 79 (91.1%) of the younger patients with gastritis (p < 0.0002). Severe atrophy of the corpus mucosa was significantly associated with absence of H pylori (p < 0.002), and was present in eight of 30 elderly patients with helicobacter negative gastritis. Other explanations for absence of H pylori include recent antibiotic intake, more intestinal metaplasia, and lower bacterial load in elderly patients (p < 0.05). Autoimmune gastritis and NSAID use did not seem to be relevant. Serodiagnosis showed reduced sensitivity (81%) in patients who were helicobacter positive histologically, but was positive in 14 of 23 (61%) with H pylori negative gastritis histologically, suggesting either current infection that had been missed or previous infection. Peptic ulceration was significantly associated with NSAID use, but not with H pylori in the elderly. CONCLUSIONS: The spectrum of gastritis is different in the elderly, compared with younger adults, due to a significant group with chronic gastritis who are H pylori negative on histological examination. NSAID use, but not demonstration of H pylori (at histological examination) is associated with peptic ulceration in the elderly.

Adolescent↗

PubMed1995

Spectrotypic analysis of antibodies to Helicobacter pylori in patients with antral gastritis and duodenal ulcer.

AIMS: To investigate the anti Helicobacter pylori (H pylori) spectrotype associated with (a) antral gastritis and duodenal ulcer; (b) the H pylori eradicating treatment. METHODS: Spectrotypic analysis was performed by isoelectric focusing and reverse blotting (IEFRB) in a cross sectional study on sera from 70 patients with antral gastritis and duodenal ulcer. In addition, a longitudinal study was performed on 40 of these patients (20 with antral gastritis and 20 with duodenal ulcer) who underwent eradicating treatment. RESULTS: The cross sectional study showed that the oligoclonal spectrotype was present in 74% of antral gastritis patients and in 85% of duodenal ulcer patients. In only a minority of subjects (23% with antral gastritis and 3% with duodenal ulcer) was a polyclonal spectrotype observed. The longitudinal study showed a reduction in the intensity of the spectrotypic bands in 5/10 antral gastritis patients with eradicated H pylori as opposed to only 2/10 patients without eradication. A reduction was also observed in 6/11 eradicated v 0/9 non-eradicated patients with duodenal ulcer. Collectively, a reduction in the spectrotype was observed in 11/21 patients (52%) who--independently of the disease--underwent H pylori eradication, as opposed to 2/19 of the non-responder patients (10.5%). The polyclonal spectrotype was found exclusively in four patients with antral gastritis, all belonging to the group without eradication of H pylori after eradicating treatment. CONCLUSIONS: The anti H pylori oligoclonal spectrotype is the most common pattern observed in patients with antral gastritis and duodenal ulcer. After H pylori eradicating treatment the spectrotype does not change qualitatively, but the polyclonal pattern seems to be predictive of a poor response to eradication.

Adolescent↗

PubMed1995

The prevalence of lymphoid follicles in Helicobacter pylori associated gastritis in patients with ulcers and non-ulcer dyspepsia.

AIMS: To determine the prevalence of lymphoid follicles in Helicobacter pylori positive and negative gastritis in antral and body type gastric mucosa in patients with non-ulcer dyspepsia (NUD), duodenal ulcer, or gastric ulcer; to correlate follicle presence with patient age; to evaluate the correlation between the prevalence of lymphoid follicles and active and inactive gastritis and its severity; and to assess the positive predictive value of lymphoid follicle prevalence with respect to H pylori infection. METHODS: Gastric biopsy specimens, graded according to the Sydney system, from 337 patients were studied. RESULTS: Lymphoid follicles occurred more often in antral mucosa (78%) than in body type mucosa (41%) and were observed in 85% of patients with H pylori positive gastritis. There was no significant difference between NUD and gastric and duodenal ulcer disease with regard to the presence of lymphoid follicles. The positive predictive value of the presence of lymphoid follicles in H pylori infection was 96%. Lymphoid follicles were more commonly observed in patients aged between 10 and 29 years. Lymphoid follicles were more frequently found in pangastritis of all subtypes than in antral gastritis and also in active gastritis than in inactive gastritis. The presence of lymphoid follicles correlated strongly with the degree and severity of gastritis. CONCLUSION: Lymphoid follicles are a constant morphological feature of H pylori associated gastritis.

Adult↗

PubMed1999

The pattern of involvement of the gastric mucosa in lymphocytic gastritis is predictive of the presence of duodenal pathology.

AIM: To determine whether the pattern of involvement of the gastric mucosa in lymphocytic gastritis is predictive of the presence or absence of duodenal pathology. METHODS: 50 cases (M:F, 26:24; median age 57 years) diagnosed as lymphocytic gastritis between 1986 and 1998 with concurrent duodenal (D2) biopsies were identified from a computer search of the pathology records and validated by counting gastric intraepithelial lymphocytes. Gastric and duodenal intraepithelial lymphocyte counts were performed on haematoxylin and eosin (H&E) and anti-CD3 stained sections. D2 biopsies were assessed for villous atrophy and chronic inflammatory cell infiltration by subjective grading, and gastritis was classified and graded according to the updated Sydney system. A case was designated corpus predominant when the corpus chronic inflammation grade exceeded that of the antrum. If it was less, then the case was antrum predominant, and if they were equal it was diffuse (pan-) gastritis. The ratio between the corpus and antral intraepithelial lymphocyte count in individual patients was calculated. RESULTS: Of 50 cases of lymphocytic gastritis, 21 were classified as corpus predominant. With one exception (a case of mild villous atrophy), all were accompanied by normal duodenal morphology. Cases with a corpus predominant gastritis had median duodenal intraepithelial lymphocyte counts of 19 (H&E) and 14.1 (CD3), whereas 29 subjects with an antrum predominant or diffuse gastritis had median counts of 39.9 (H&E) and 37.9 (CD3). Fifteen of these 29 cases (52%) showed villous atrophy; all were graded as moderate or severe. Patients with any degree of villous atrophy had a mean corpus/antrum intraepithelial lymphocyte ratio (H&E) of 0.59 (representing antral predominance), while those with normal duodenal morphology had a ratio of 2.39 (p < 0.0001). CONCLUSIONS: The pattern of involvement of gastric mucosa in lymphocytic gastritis is closely related to the associated duodenal pathology. Those with the corpus predominant form are unlikely to have duodenal pathology, while those with an antral predominant or diffuse form should have distal duodenal biopsies taken to exclude villous atrophy.

CD3 Complex↗

PubMed2004

Growth factors associated with gastric mucosal hypertrophy in autoimmune gastritis.

A prominent pathological feature of murine autoimmune gastritis is a pronounced mucosal hypertrophy. Here, we examined factors that may be responsible for inducing this hypertrophy. Because gastrin is known to be both an inducer of gastric mucosal cell proliferation and is elevated in autoimmune gastritis, mice deficient in gastrin were thymectomised at day 3 and assessed for autoimmune gastritis. Gastrin-deficient mice showed all the characteristic features of murine autoimmune gastritis, including gastric unit hypertrophy due to hyperproliferation and accumulation of immature epithelial cells, decreases in the number of zymogenic and parietal cells, and autoantibodies to the gastric H+/K+-ATPase. Hence, gastrin is not required for either the establishment of chronic gastritis or development of the typical pathological features of this disease. We also examined mRNA levels of a number of gastric mucosal growth factors in RNA samples from mice with hypertrophic autoimmune gastritis. Members of the Reg family, RegIIIbeta and RegIIIgamma, were greatly elevated in mice with hypertrophic gastritis, whereas RegI and amphiregulin (an EGF receptor ligand) were more modestly and/or inconsistently induced. These data demonstrate that induction of gastric mitogenic factors, such as members of the Reg family, can be achieved in inflammatory situations by gastrin-independent pathways. Members of the Reg family, in particular RegIIIbeta and RegIIIgamma, are good candidates to be involved in inducing the mucosal hyperproliferation in autoimmune gastritis. These findings are likely to be of relevance to other gastric inflammatory conditions.

Amphiregulin↗

PubMed2000

Increased cell proliferation in chronic Helicobacter pylori positive gastritis and gastric carcinoma--correlation between immuno-histochemistry and Tv image cytometry.

BACKGROUND: [corrected] Epithelial cell proliferation activity has been reported both to be unaltered and increased in Helicobacter pylori (H. pylori) associated chronic gastritis. The proliferation rate decreased following H. pylori eradication, but results are controversial whether this change is dependent on the success of eradication. We compared the cell proliferation activity of H. pylori positive and negative gastric epithelial biopsies in chronic gastritis with and without intestinal metaplasia (IM) and gastric cancer by the expression of proliferation cell nuclear antigen (PCNA) and Tv image cytometry, and assessed the effect of H. pylori eradication on the cell proliferation rate in the gastric epithelium. METHODS: Brush smears and antral biopsies were taken from 70 patients (42 men, 28 women, mean age 58+/-15 y.o.) on routine endoscopy. Patients were divided into four groups according to the histology; normal epithelia (n = 10), chronic gastritis without IM (n = 24), chronic gastritis with IM (n = 20), and gastric carcinoma (n = 16). Thirty-three patients were H. pylori positive, and success of eradication was controlled in 24 cases. Cell proliferation was measured by immunohistochemistry using PCNA labeling index (LI) and by Tv image cytometry evaluating 12 morpho- and densitometric parameters of each nuclei and 6 additional parameters of each smear. RESULTS: PCNA LI, DNA index and S + G2 ratio were all higher in chronic gastritis than in the normal epithelium, and were further increased in carcinoma. The lower PCNA LI observed in chronic gastritis with IM corresponds to the lower S phase ratio determined by Tv image analysis. In H. pylori positive cases, the proliferation activity was 69.3+/-13.05% prior to the eradication and it decreased to 55.8+/-23.31% after the successful eradication therapy. When immunohistochemistry was compared with Tv image cytometry, PCNA LI significantly correlated with the percentage of cells in GL phase (r = -0.415) and S phase (r = 0.385), Integrated Optical Density mean (r = 0.598), density maximum (r'= 0.608), surface (r = 0.670), layers (r = 0.638), diameter minimum (r = 0.619), diameter maximum (r = 0.730) and perimeter (r = 0.501), respectively (p < 0.05). CONCLUSIONS: Epithelial cell turnover is increased in chronic gastritis with or without IM, and in gastric carcinoma. The lower PCNA LI observed in chronic gastritis with IM corresponds to the lower S phase ratio determined by Tv image analysis. Cell proliferation decreases after successful H. pylori eradication. Both methods proved to be reliable for the determination of epithelial cell proliferation.

Adult↗

PubMed1998

Activation of epithelial cells in gastritis.

BACKGROUND: Helicobacter pylori is now recognised to be the major cause of antral gastritis and a risk factor for further development of gastric cancer. This infection results in local inflammation and a modification of gastric mucosal epithelial cell characteristics. Systematic investigation for the expression of the secretory component by gastric epithelium in a personal historical series of biopsy specimens showed the expression of this activation marker in 38% of the cases, 19% also showing clear signs of H. pylori infection. AIMS: To further appreciate the activation of epithelial cells in the chronic gastric inflammation associated with H. pylori infection and other types of gastritis without consideration of the grade of gastritis. METHODS: Punch gastric biopsies from 36 patients (10 patients with confirmed H. pylori gastritis, 16 patients with non-H. pylori gastritis and 10 controls) were tested for the expression of ICAM-1/CD54, HLA-DP, -DQ, -DR, secretory component and bcl-2 by immunofluorescence. RESULTS: Up-regulation of most markers was observed both in H. pylori and non-H. pylori gastritis, although secretory component, CD54 and DP expression was more closely associated with H. pylori gastritis. CONCLUSION: H. pylori infection appears to activate gastric epithelial cells more strongly than other types of gastritis. This suggests an active relationship between this bacterium and epithelial cells. Investigation of the up-regulationship between this bacterium and epithelial cells. Investigation of the up-regulation of secretory component, ICAM-1/CD54 or DP in gastric biopsies may serve as extensive markers in search of H. pylori gastric infections.

Adult↗

PubMed2000

Relationship between ethanol-induced gastritis and gastric ulcer formation in rats.

BACKGROUND/AIMS: Patients with peptic ulcer diseases have a high prevalence of coexisting chronic gastritis. The mechanism of how gastritis leads to gastric ulcer formation is yet to be determined. The purpose of this study was to clarify the relationship between gastritis and gastric ulcer in rats. METHODS: Ethanol (80% v/v, p.o.) was given repeatedly in rats to induce subchronic gastritis. Gastric ulcer was then induced by 60% acetic acid. RESULTS: Findings showed that subchronic gastritis potentiated gastric ulcer formation. It also produced more apoptotic cells, together with an overexpression of tumor necrosis factor-alpha (TNF alpha) in the gastric mucosa. Inhibition of the production/release of TNF alpha by pentoxifylline prevented the increase in apoptosis and the enhancement of susceptibility to ulcerative damage by subchronic gastritis. However, such subchronic gastritis did not further affect the rate of ulcer healing in these animals. CONCLUSION: The induction of gastritis resulted in an activation of TNF alpha expression followed by apoptosis in the gastric mucosa. This could lead to an increase in the severity of ulcerative damage in the stomach.

Animals↗

PubMed1992

Gastric endocrine cells and gastritis in patients receiving long-term omeprazole treatment.

Both argyrophil endocrine cells and gastritis were investigated in 2,120 biopsies of gastric corpus mucosa from 443 out of 448 patients receiving long-term (for periods ranging from several months to 4 years) omeprazole treatment. None of the patients showed neoplasia or dysplasia, either endocrine or non-endocrine. In 123 out of 443 patients (27.8%), endocrine hyperplasia of diffuse (9.3%), linear (4.1%) or micronodular (14.4%) type was detected either before or at some time during treatment. Chronic atrophic gastritis was found in 45 (10.2%) patients, 60% of whom also showed micronodular hyperplasia. In patients with chronic atrophic gastritis, micronodular hyperplasia occurred in 49% of 96 biopsies, compared with 6% of 1,083 biopsies from patients with non-atrophic chronic gastritis and 2% of 941 biopsies from patients with no evidence of gastritis. In 202 patients treated with omeprazole for at least 330 days, the incidence of micronodular hyperplasia increased from 2.5% at the first biopsy to 10.4% at the final biopsy, while the incidence of chronic atrophic gastritis increased from 1.0% to 13.0%. The present and parallel studies suggest that progression of gastritis is inherent in the natural history of acid-related diseases, while endocrine cell changes are mostly secondary to gastritis-related gland atrophy and have no tumorigenic potential.

Adult↗

PubMedDate not supplied

Chronic gastritis and Helicobacter pylori in digestive form of Chagas' disease.

Patients with the digestive form of Chagas' disease frequently present chronic gastritis. As the microorganism Helicobacter pylori is now accepted as the most common cause of human chronic gastritis, the present work was undertaken to verify a possible relationship between the presence of this bacterium and inflammatory changes of antral mucosa in chagasic patients. Seventeen chagasics, with megaesophagus and or megacolon were studied. Fragments from two different regions of antral mucosa were obtained by endoscopy, fixed in 4% neutral formaldehyde and embedded in paraffin. The sections were stained by haematoxylin and eosin for histology analysis, and by carbolfuchsin for H. pylori identification. H. pylori was found in 16 (94.1%) chagasic patients, all of them presenting chronic gastritis. Superficial gastritis was seen in 9 (52.9%) while atrophic gastritis was present in 8 (47.1%) patients. H. pylori was present on gastric mucosa of 8 (100%) patients with atrophic gastritis and of 8 (88.8%) patients with superficial gastritis. We concluded that the microorganism H. pylori should be considered a possible factor connected with the etiopathogenesis of chronic superficial and atrophic gastritis frequently observed in patients with the digestive form of Chagas' disease.

Adult↗

PubMed1978

Long-term observation of subjects with normal mucosa and with superficial gastritis: results of 23--27 years' follow-up examinations.

261 subjects with a normal body mucosa or with superficial gastritis used as controls for an atrophic gastritis series have been followed up for 23--27 years. Of them, 41 died during the earlier and 63 during the present follow-up period. In all, 141 subjects were reexamined in 1976--1977 and 16 answered a questionnaire. None of the subjects had gastric carcinoma or an adenomatous polyp. One patient diagnosed and reported earlier had died of gastric carcinoma during the present period of observation. Of the subjects with normal body mucosa 58% had developed superficial and 14% atrophic gastritis. Of those with superficial body gastritis 42% had developed atrophic gastritis and 18% showed an improvement of the gastritic changes. It should be noted, however, that earlier examinations were performed with blind biopsy and the present with direct vision gastroscopic biopsy. The state of the antral and body mucosa was similar in 53%, antral changes dominated in 33% and the changes in the body in 14%. Intestinal metaplasia was found in 36%, atypical epithelium in 6%, parietal cell antibodies in 0.5% and intrinsic factor antibodies in 0.5%. The fasting serum gastrin level was above 100 ng/ml in 10%. Only 2 cases fulfilled the morphological, functional and immunological criteria of type A gastritis. The present controls differed from the atrophic gastritis series in that the topography of gastritis was different and in that the incidence of metaplasia, atypia, gastric antibodies and high serum gastrin levels was markedly lower.

Antibodies↗

PubMed1985

The Diagnosis and Therapy Survey October 1978-March 1983, health care consumption and current drug therapy in Sweden with respect to the clinical diagnosis of gastritis.

Demographic epidemiology, current drug therapy and the health care resources required by patients clinically considered to have gastritis were studied during a four and a half year period-October 1978 to March 1983. The investigation was based on data from the Diagnosis and Therapy Survey, an on-going nation-wide sample study covering all out-patient care in Sweden. Gastritis was found to account for 1.9% of all out-patient consultations and for 30% of those for gastrointestinal disorders. The corresponding figures for peptic ulcer disease were 0.2% and 4%, respectively. The estimated minimum number of annual consultations for gastritis was 47 per 1,000 inhabitants. The majority of the consultations were dealt with in general practice, where gastritis was the fifth most common diagnosis. Drug therapy was considered to be indicated in 92% of the consultations. Antacids were prescribed in 77%, anticholinergic/spasmolytic drugs in 36% and histamine H2-receptor antagonists in 4%. The clinical diagnosis of gastritis was found to be the major indication for antacids and anticholinergic drugs and accounted for a substantial proportion of H2-receptor antagonist prescriptions. The patient groups with gastritis and duodenal ulcer showed a similar age distribution, with a mean age of about 50 years. In the gastritis group, the two sexes were equally represented, but in the duodenal ulcer group there was a predominance of men. The results of the Diagnosis and Therapy Survey indicate that the patient group with symptoms traditionally denoted as gastritis in clinical practice constitutes a major health care problem in our community.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1989

Chronic antral gastritis, Lewis(a+) phenotype, and male sex as factors in predicting coexisting duodenal ulcer.

Chronic antral gastritis, Lewis(a+) phenotype (Le(a+)), and male sex are common in patients with peptic ulcer. To approximate the relative risks (RR) and possible interactions of these factors in predicting coexisting active duodenal (DU) or gastric ulcer (GU), a consecutive endoscopic series of 140 ulcer patients and 215 non-ulcer controls was examined. The Lea phenotype (Le(a+) versus Le(a-)) was determined immunohistochemically as binding of Le(a)+-specific monoclonal antibody to surface epithelial secretory mucosubstances in gastric biopsy specimens. The presence versus absence of the gastritis was determined histologically from antral specimens. The RRs of the factors in the prediction of ulcer were approximated as age-adjusted RRs when the risk of ulcer in the absence of the factors--that is, in the absence of gastritis, in female sex and in Le(a-) phenotype--was applied as a base line (RR = 1). A case-control design, logistic linear modelling, and the maximal likelihood method were used in estimation of the risks. The RR of coexisting distal ulcer (DU or pyloric or prepyloric GU) was increased in the presence of gastritis (RR = 10.2), in male sex (RR = 3.0), and in Le(a+) phenotype (RR = 1.8). The RR of proximal ulcer (angular or corpus GU) was increased in the presence of gastritis (RR = 35) but decreased in the presence of male sex (RR = 0.5) and Le(a+) phenotype (RR = 0.7). As predictors of both distal and proximal ulcer, gastritis, sex, and Le(a) phenotype were independent of each other; that is, their joint value in prediction of ulcer is a multiplicand of the marginal risks. Thus, a 50-fold difference in the joint RR could be approximated between the extreme risk groups for distal ulcer--that is, between Le(a+) males with gastritis and Le(-a) females with normal antrum. In a consecutive series of outpatient endoscopies, 45% of females and 8% of males could be categorized to these extreme 'low'- and 'high'-risk groups, respectively. We conclude that sex, Le(a) phenotype, and gastritis are factors that, at least in ordinary outpatient endoscopy material, divide subjects to subgroups with very different risks and probabilities for having coexisting peptic ulcer.

Adult↗

PubMed1992

Frequency of Helicobacter pylori and gastritis in healthy subjects without gastrointestinal symptoms.

To investigate the frequency of Helicobacter pylori and gastritis in asymptomatic adults, 30 healthy volunteers underwent upper endoscopy. Biopsy specimens were obtained from the corporeal and antral mucosa of the stomach. The specimens were examined by light microscopy for gastritis and the occurrence of H. pylori. In 12 subjects signs of gastritis were noted at endoscopy, but only in 7 of them was this diagnosis confirmed histologically. No other abnormalities were observed by the endoscopist. Histologic examination was normal in 17 subjects, but in 13 subjects (43%) inflammation was found in the gastric specimens. Ten had inflammation both in the corpus and in the prepyloric specimens, and in six of these subjects H. pylori was discovered. H. pylori was only found in subjects with inflammation in both the corpus and the antrum. Subjects with gastritis were slightly older than subjects with normal gastric mucosa (median age, 47 versus 37 years; not significant). In the group of subjects with gastritis, persons with H. pylori were older than those without (median age, 53.5 versus 36 years; p = 0.05). The results of our study indicate that gastritis is present before colonization with H. pylori occurs. This could imply that H. pylori is not the cause of gastritis but that the presence of gastritis is a prerequisite for colonization of the bacterium in the stomach.

Adult↗

PubMed1995

Serum gastrin and mucosal somatostatin in Helicobacter pylori-associated gastritis.

AIMS: The aims were to study gastrin concentrations and gastric mucosal somatostatin and gastrin concentrations in relation to the extent of gastritis in Helicobacter infection. METHODS: We measured basal serum gastrin concentrations in antral mucosal biopsy specimens and somatostatin concentrations in corpus biopsy specimens in 88 consecutive dyspeptic subjects undergoing endoscopy. These subjects were divided into three categories on the basis of histology, serology, and culture: H. pylori-positive pangastritis, H. pylori positive antral gastritis with normal body histology, and H. pylori-negative controls. Statistical evaluation was done with the Wilcoxon rank sum test. RESULTS: Basal serum gastrin concentrations were significantly increased only in subjects with pangastritis and not in those with antral gastritis only, as compared with controls (mean +/- SEM: 72 +/- 7, 46 +/- 10, and 42 +/- 7 ng/l, respectively). Subjects with pangastritis or antral gastritis had significantly lower antral somatostatin concentrations than controls (mean +/- SEM: 0.80 +/- 0.07, 1.03 +/- 0.15, and 2.40 +/- 0.31 micrograms/g(protein), respectively). We also found significantly lower antral gastritis only as compared with controls (mean +/- SEM: 62 +/- 13, 78 +/- 16, and 165 +/- 25 micrograms/g(protein), respectively). In subjects with pangastritis a significantly lower concentration of somatostatin was found in the corpus biopsy specimens than in those with antral gastritis only and controls. CONCLUSIONS: These results suggest that hypergastrinemia in H. pylori gastritis is not caused by antral gastritis and antral somatostatin deficiency alone but that corpus inflammation plays a key role in the origin of hypergastrinemia. Furthermore, in patients with pangastritis a corpus mucosal somatostatin deficiency was found.

Adolescent↗

PubMed2001

Non-invasive approach for diagnosing atrophic gastritis using the 13C-bicarbonate breath test.

The experiments presented here were done to evaluate whether the levels of CO2 in respiratory air during the 13C-bicarbonate breath test (13C-BBT) may be used as a marker of non-invasive diagnosis of the levels of atrophic gastritis. Twenty-eight patients with chronic gastritis and five healthy volunteers were enrolled in the study. Moreover, experimental gastritis was induced in rats by N-methy-N-nitro-N-nitrosoguanidine. In human, the levels of atrophic gastritis were evaluated from the vascular pattern of the gastric fornix. Total delta 13CO2 calculated from the 13C-BBT and the mucosal thickness ratio (MTR) were measured in rats with experimental gastritis. The levels of 13CO2 were significantly higher from patients with a vascular pattern at the fornix than in those without a vascular pattern (p<0.01). There was a good correlation between MTR and the levels of 13CO2, in rats with experimental gastritis (p<0.01). These findings indicate that the levels of 13CO2 during 13C-BBT reflect the levels of atrophic gastritis and show its clinical significance for non-invasive evaluation of atrophic gastritis. This has important clinical implications in selecting Helicobacter pylori-positive cases for therapy and follow-up.

Age Factors↗

PubMed1995

Influence of Helicobacter pylori colonization on histological grading of chronic gastritis in Korean patients with peptic ulcer.

OBJECTIVES: We conducted an analysis of correlation between histological grading of chronic gastritis and the presence of H. pylori infection to investigate if H. pylori influences histological severity of chronic gastritis in Korean patients with peptic ulcers. METHODS: Gastroscopic antral biopsy specimens and peripheral venous blood were taken from 80 patients with gastric or duodenal ulcers. H. pylori was identified microscopically in sections with Giemsa staining and quantitative grading of cultured H. pylori was reported on a scale 0 to 3. The histopathological features of biopsy specimens were reported according to the Sydney classification of chronic gastritis. Serum gastrin and pepsinogen concentrations were measured by radioimmunoassay. RESULTS: H. pylori was identified in 62.5%(20 of 32 GU, 30 of 48 DU) of the study group. Gastric clonization rate of H. pylori did not increased with age. Forty of 50 biopsy specimens with H. pylori and also 23 of 30 biopsy specimens without H. pylori showed active chronic gastritis. There was no significant correlation overall between the presence of H. pylori and histological grading of chronic gastritis, including activity, and also no association was found between the quantitative grading of H. pylori and the histological grading of chronic gastritis. With and without H. pylori, a mean of serum gastrin concentration(79.4 +/- 4.30 pg/ml and 80.2 +/- 31.9 pg/ml)showed no significant difference, but a mean of serum pepsinogen concentration(87.7 +/- 41.6 ng/ml and 119 +/- 34.4 ng/ml) showed significant difference between the populations with and without H. pylori(p = 0.001). CONCLUSIONS: The influence of H. pylori on histological grading of chronic gastritis in Korean is less than that in prior studies of Western countries, and further investigation of pathogenesis of H. pylori in chronic gastritis and peptic ulceration is necessary.

Adolescent↗