Cell proliferation in Helicobacter pylori associated gastritis and the effect of eradication therapy.

Helicobacter pylori causes chronic (type B) gastritis. The 'intestinal' form of gastric cancer arises against a background of chronic gastritis, and prospective epidemiological studies have shown that H pylori is a major risk factor for this. An increase in mucosal cell proliferation increases the likelihood of a neoplastic clone of epithelial cells emerging where there is chronic epithelial cell injury associated with H pylori gastritis. In vitro bromodeoxyuridine labelling of endoscopic antral biopsy specimens was used to measure mucosal cell proliferation in H pylori associated gastritis before and after therapy for H pylori triple infection. Cell proliferation was increased in H pylori associated gastritis patients compared with normal controls and patients with H pylori negative chronic gastritis (p = 0.0001; Tukey's Studentised range). There was no difference in antral epithelial cell proliferation between duodenal ulcer and non-ulcer subjects infected with H pylori (p = 0.62; Student's t test). Antral mucosal cell proliferation fell four weeks after completing triple therapy, irrespective of whether or not H pylori had been eradicated (p = 0.0001). At retesting six to 18 months later (mean = 12 months), however, those in whom H pylori had not been successfully eradicated showed increased mucosal proliferation compared with both H pylori negative subjects at a similar follow up interval and all cases (whether H pylori positive or negative) four weeks after completion of triple therapy (p = 0.024). These findings suggest that H pylori infection causes increased gastric cell proliferation and in this way may play a part in gastric carcinogenesis.     

Helicobacter pylori in gastric corpus of patients 20 years after partial gastric resection

AIM: To determine the long-term prevalence of Helicobacter pylori (H pylori) gastritis in patients after partial gastric resection due to peptic ulcer, and to compare the severity of H pylori-positive gastritis in the corpus mucosa between partial gastrectomy patients and matched controls. METHODS: Endoscopic biopsies were obtained from 57 patients after partial gastric resection for histological examination using hematoxylin/eosin and Warthin-Starry staining. Gastritis was graded according to the updated Sydney system. Severity of corpus gastritis was compared between H pylori-positive partial gastrectomy patients and H pylori-positive duodenal ulcer patients matched for age and gender. RESULTS: In partial gastrectomy patients, surgery was performed 20 years (median) prior to evaluation. In 25 patients (43.8%) H pylori was detected histologically in the gastric remnant. Gastric atrophy was more common in H pylori-positive compared to H pylori-negative partial gastrectomy patients (P<0.05). The severity of corpus gastritis was significantly lower in H pylori-positive partial gastrectomy patients compared to duodenal ulcer patients (P<0.01). There were no significant differences in the activity of gastritis, atrophy and intestinal metaplasia between the two groups. CONCLUSION: The long-term prevalence of H pylori gastritis in the gastric corpus of patients who underwent partial gastric resection due to peptic ulcer disease is comparable to the general population. The expression of H pylori gastritis in the gastric remnant does not resemble the gastric cancer phenotype.     

Helicobacter pylori gastritis and gastric physiology

It is now recognized that Helicobacter pylori infection exerts profound and diverse effects on gastric acid secretory function and that the alterations in acid secretion depend on the pattern of gastritis caused by the infection. In patients with an antral predominant nonatrophic gastritis, there is acid hypersecretion leading to duodenal ulcer disease. In patients with an atrophic pangastritis, there is markedly reduced acid secretion and increased risk for gastric cancer. It is now recognized that acid secretion also modifies H. pylori gastritis and a person's premorbid acid secretory status may be an important factor in determining the pattern of gastritis that an individual develops. This two-way interaction between H. pylori gastritis and gastric acid secretion is important in understanding the role of H. pylori infection in the response to proton-pump inhibitor therapy: It explains the more profound control of gastric acid secretion in H. pylori-positive patients and why rebound acid hypersecretion is confined to H. pylori-negative subjects.     

Lymphocytic gastritis and Helicobacter pylori infection in gastric lymphoma.

Lymphocytic gastritis and primary gastric lymphoma are rare conditions with unknown aetiology. It has recently been suggested that Helicobacter pylori has a role in the pathogenesis of both of them. The occurrence of lymphocytic gastritis and H pylori was studied in a series of patients with primary gastric lymphoma. The cases of primary gastric lymphomas (n = 35) diagnosed in years 1970-1993 were identified. The specimens of 22 cases contained gastric mucosa sufficiently so that the number of intra-epithelial lymphocytes, severity of gastritis, and occurrence of H pylori could be studied. Lymphocytic gastritis was detected in seven of 22 patients (32%), and in most cases both in antral and body mucosa. Atrophy of the body glands was significantly more severe in lymphocytic gastritis patients. H pylori was detected in 13 of all 22 patients (59%); two of seven lymphocytic gastritis patients (29%), and 11 of 15 (73%) of patients without lymphocytic gastritis were H pylori positive. Patients with gastric lymphoma have significantly increased prevalence of lymphocytic gastritis. Rarity of H pylori in these patients might be connected with atrophic changes in body mucosa. Further studies are needed to show the significance of lymphocytic gastritis as a precursor of gastric lymphoma.     

Hyperplastic gastric polyps associated with persistent Helicobacter pylori infection and active gastritis

We report two cases of patients with 3-yr histories of upper gastrointestinal symptoms, hyperplastic gastric polyps, and active chronic gastritis. Biopsies retrospectively stained with Giemsa revealed the persistent presence of Helicobacter pylori (HP) in gastric biopsies of both patients throughout the 3 yr. After treatment with amoxicillin and bismuth subsalicylate, both became asymptomatic, one demonstrating disappearance and recurrence of the gastric polyps in conjunction with the HP. These cases demonstrate 3 yr of hyperplastic gastric polyps associated with HP and active gastritis.     

Helicobacter pylori and corpus gastric pathology are associated with lower serum ghrelin

AIM To evaluate the association of Helicobacter pylori(H. pylori), cag A genotype, and type of gastric pathology with ghrelin, leptin and nutritional status.METHODS Fasted dyspeptic adults(18-70 years) referred for an upper digestive endoscopy were enrolled in this crosssectional study. Height and weight were assessed for body mass index(BMI) calculation. A sociodemographic survey was administered and nutrient intake was evaluated with 24 h dietary recalls. Serum total ghrelin and leptin levels were analyzed by enzymelinked immunosorbent assay. 13 C-Urea Breath Test was performed and four gastric biopsies were obtained during endoscopy for histopathology and H. pylori DNA amplification and genotyping. Data analysis was performed using χ2, Mann-Whitney U, Kruskal-Wallis tests, Spearman's correlation and linear regression.RESULTS One hundred and sixty-three patients(40.8 ± 14.0 years), 98/65 females/males, were included. Overall, persistent H. pylori prevalence was 53.4%(95%CI: 45.7%-65.8%). Neither nutrient intake nor BMI differed significantly between H. pylori positive and negative groups. Serum ghrelin was significantly lower in infected patients [median 311.0 pg/m L(IQR 230.0-385.5)] than in uninfected ones [median 355.0 pg/m L(IQR 253.8-547.8)](P = 0.025), even after adjusting for BMI and gender(P = 0.03). Ghrelin levels tended to be lower in patients carrying cag A positive strains both in the antrum and the corpus; however, differences with those carrying cag A negative strains did not reach statistical significance(P = 0.50 and P = 0.49, respectively). In addition, the type and severity of gastric pathology in the corpus was associated with lower serum ghrelin(P = 0.04), independently of H.pylori status. Conversely, leptin levels did not differ significantly between infected and uninfected patients [median 1.84 ng/m L(0.80-4.85) vs 1.84 ng/m L(0.50-5.09),(P = 0.51)]. CONCLUSION H. pylori infection and severity of gastric corpus pathology are associated with lower serum ghrelin. Further studies could confirm a lower ghrelin prevalence in cag A-positive patients.     

Impaired production of gastric ghrelin in chronic gastritis associated with Helicobacter pylori

Ghrelin is primarily secreted from the stomach and has been implicated in the coordination of eating behavior and weight regulation. The effects of Helicobacter pylori infection on plasma ghrelin concentration and gastric ghrelin production still have not been well known. We determined plasma ghrelin concentration in a total of 160 consecutive individuals with normal body mass index including 110 H. pylori-infected and 50 H. pylori-negative subjects. The expression levels of ghrelin mRNA and ghrelin-producing cells in the gastric mucosa were quantified with real-time quantitative RT-PCR and immunohistochemistry, respectively. The severity of gastric atrophy was evaluated by serum pepsinogen concentrations. Plasma ghrelin concentration, gastric ghrelin mRNA, and ghrelin-positive cell numbers in gastric mucosa were significantly lower in H. pylori-infected subjects. The decrease in plasma ghrelin concentration in H. pylori-positive subjects was accompanied by an attenuation of ghrelin mRNA expression and a reduction of ghrelin-positive cell numbers in the gastric mucosa. Moreover, lower serum pepsinogen I concentrations and I/II ratio were significantly associated with lower plasma ghrelin concentrations in H. pylori-positive subjects. These findings suggest that impaired gastric ghrelin production in association with atrophic gastritis induced by H. pylori infection accounts for the decrease in plasma ghrelin concentration.     

Helicobacter pyloriin gastric corpus of patients 20 years after partial gastric resection

AIM:To determine the long-term prevalence of Helicobacterpylori(H pylori)gastritis in patients after partial gastricresection due to peptic ulcer,and to compare the severityof Hpylori-positive gastritis in the corpus mucosa betweenpartial gastrectomy patients and matched controls.METHODS:Endoscopic biopsies were obtained from 57patients after partial gastric resection for histologicalexamination using hematoxylin/eosin and Warthin-Starrystaining.Gastritis was graded according to the updatedSydney system.Severity of corpus gastritis was comparedbetween Hpylori-positive partial gastrectomy patients andHpylori-positive duodenal ulcer patients matched for ageand gender.RESULTS:In partial gastrectomy patients,surgery wasperformed 20 years(median)prior to evaluation.In 25patients(43.8%)Hpyloriwas detected histologically inthe gastric remnant.Gastric atrophy was more common inH pylori-positive compared to H pylori-negative partialgastrectomy patients(P<0.05).The severity of corpusgastritis was significantly lower in Hpylori-positive partialgastrectomy patients compared to duodenal ulcer patients(P<0.01).There were no significant differences in theactivity of gastritis,atrophy and intestinal metaplasiabetween the two groups.CONCLUSION:The long-term prevalence of Hpylorigastritisin the gastric corpus of patients who underwent partialgastric resection due to peptic ulcer disease is comparableto the general population.The expression of Hpylorigastritisin the gastric remnant does not resemble the gastric cancerphenotype.     

Light and electron microscopy study of Helicobacter pylori-associated gastritis and gastric carcinoma

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HOGG1 polymorphism in atrophic gastritis and gastric cancer after Helicobacter pylori eradication

AIM:To investigate the association between Ser326Cys human oxoguanine glycosylase 1(hOGG1) polymorphism and atrophic gastritis and gastric cancer after Helicobacter pylori(H.pylori) eradication.METHODS:A total of 488 subjects(73 patients with gastric cancer,160 with atrophic gastritis after H.pylori eradication and 255 controls) were prospectively collected.Polymerase chain reaction-restriction fragment length polymorphism analysis was performed to distinguish hOGG1 Ser326Cys polymorphism.Statistical analys...     

Gastric epithelial cell proliferation and cagA status in Helicobacter pylori gastritis at different gastric sites

OBJECTIVE: Helicobacter pylori infection causes hyperproliferation which is believed to predispose to the development of gastric carcinoma. The aim of this study was to analyze epithelial cell proliferation topographically in H. pylori gastritis in relationship to cagA status. MATERIAL AND METHODS: The proliferative index (PI: Ki-67-labeled nuclei/total number of foveolar nuclei) was determined in gastric mucosa biopsies taken at the antrum (lesser and greater curvatures), incisura, and corpus (greater curvature) from 78 patients with H. pylori gastritis and 20 H. pylori-negative patients. H. pylori and cagA status were determined by polymerase chain reaction (PCR) and serology. RESULTS: PIs were significantly higher in H. pylori- and cagA-positive patients, in comparison with H. pylori- and cagA-negative patients, at all sites (p相似文献   

Helicobacter pylori status and cell proliferation activity in chronic antral gastritis.

BACKGROUND: Helicobacter pylori is known to cause antral gastritis and multifocal atrophic gastritis. In addition to its inflammatory effect, H. pylori has a direct effect on gastric mucosa. Increased epithelial proliferation, which may be an early biologic change in the development of gastric carcinoma, can be measured using silver stain for nuclear organizer regions (AgNOR). AIM: To detect the relation between H. pylori colonization and AgNOR index. METHODS: One hundred and twenty consecutive antral endoscopic biopsy specimens from patients with dyspepsia were examined for H. pylori colonization, polymorphonuclear infiltrate, mononuclear infiltrate, germinal center formation, mucus depletion and AgNOR index. RESULTS: AgNOR indices were not significantly related to grades of H. pylori colonization and chronic and active inflammation. The index increased significantly (p=0.03; ANOVA) with increasing mucin depletion. CONCLUSION: H. pylori colonization and presence of gastric antral inflammation are not related to cell proliferation activity; the latter is associated with mucin depletion.     

Apoptosis in Helicobacter pylori gastritis and residual gastritis after distal gastrectomy

BACKGROUND/AIMS: Active gastritis, accelerated cell turnover followed by apoptosis, DNA damage and hyperplasia are often seen in the anastomosis area after gastrectomy. Recently, it has been reported that H. pylori induces apoptosis on gastric cells. Until now, the surgical effect itself and H. pylori infection have not been well differentiated as causes of apoptosis associated with gastritis. Our aim is to clarify the relationship of residual gastritis after gastrectomy and H. pylori gastritis. METHODOLOGY: Residual gastritis model using the Mongolian gerbil has been established with microsurgical technique. Residual gastritis with and without H. pylori infection was studied by histopathological examination and quantitated by Rauws' score. Elevation of pH in gastric juice after surgery was confirmed. Stimulation of downstream events leading to apoptosis, cleavage of poly-ADP-ribose polymerase as a result of activation of caspase-3, was evaluated using Western blotting. RESULTS: Histopathologically, H. pylori infection led to deterioration after surgery. The postoperative Rauws' score with infection was higher than without infection. Cleavage of poly-ADP-ribose polymerase was increased after surgery in gerbils with and without H. pylori infection. Densitometric study showed a greater increase in the animals with H. pylori infection than those without infection that was enhanced after surgery (0.59 vs. 1.04, 0.73 vs. 1.17, respectively). CONCLUSIONS: Apoptosis is increased both in residual gastritis and H. pylori gastritis. Both enterogastric reflux and H. pylori infection may be linked to tumorigenesis in anastomosis sites followed by accelerated epithelial cell turnover followed by apoptosis.     

Helicobacter pylori gastritis of the gastric cancer phenotype in relatives of gastric carcinoma patients.

OBJECTIVE: Infection with Helicobacter pylori is associated with gastric cancer. However, a hereditary risk of gastric cancer has also been reported. Hence, we decided to evaluate H. pylori gastritis in relatives of gastric cancer patients in comparison with matched controls. DESIGN: Case-controlled study. METHODS: A total of 237 patients with merely H. pylori gastritis (i.e. not associated with either peptic ulcer or gastric malignancy), and either first-degree (93.7%) or second-degree (6.3%) relatives with gastric cancer, were age- and sex-matched with 237 patients with H. pylori gastritis unassociated with a family history of gastric cancer. From each patient, antral and corpus biopsy specimens were obtained and investigated for degree (lymphocyte/plasma cell infiltration) and activity (polymorph infiltration) of gastritis (score: 0-4). Intestinal metaplasia was recorded as present or absent. RESULTS: The results show that relatives of gastric cancer patients have a significantly greater expression of gastritis due to a higher grade of gastritis in the antrum and corpus (P < 0.0001) and a greater activity of gastritis in the corpus (P < 0.0001). Intestinal metaplasia occurs more often in relatives of gastric cancer patients (antrum: P < 0.0001; corpus: P = 0.0237). CONCLUSION: Since the grade of H. pylori gastritis in relatives of gastric cancer patients is significantly higher than in controls, there appears to be a genetic susceptibility influencing the expression of H. pylori gastritis.     

Association of autoimmune type atrophic corpus gastritis with Helicobacter pylori infection

AIM:To study the association between Helicobacter pylori(H.pylori)infection and autoimmune type atrophic gastritis. METHODS:Twenty-three patients with different grades of atrophic gastritis were analysed using enzyme immunoassay-based serology,immunoblot-based serology,and histology to reveal a past or a present H.pylori infection.In addition,serum markers for gastric atrophy(pepsinogenⅠ,pepsinogenⅠ/Ⅱand gastrin)and autoimmunity[parietal cell antibodies(PCA), and intrinsic factor(IF),antibodies]were determi...     

Association of autoimmune type atrophic corpus gastritis with Helicobacter pylori infection

AIM:To study the association between Helicobacter pylori(H.pylori)infection and autoimmune type atrophic gastritis. METHODS:Twenty-three patients with different grades of atrophic gastritis were analysed using enzyme immunoassay-based serology,immunoblot-based serology,and histology to reveal a past or a present H.pylori infection.In addition,serum markers for gastric atrophy(pepsinogenⅠ,pepsinogenⅠ/Ⅱand gastrin)and autoimmunity[parietal cell antibodies(PCA), and intrinsic factor(IF),antibodies]were determi...