Pylori-positive Gastric Ulcer Research Articles

Clinical observation of magnesium aluminum carbonate combined with rabeprazole-based triple therapy in the treatment of helicobacter pylori-positive gastric ulcer associated with hemorrhage.

Objectives:To evaluate the clinical effect of magnesium aluminum carbonate combined with rabeprazole-based triple therapy in the treatment of patients with Helicobacter pylori-positive gastric ulcer associated with hemorrhage.Methods:A total of 80 patients with Helicobacter pylori-positive gastric ulcer associated with hemorrhage admitted to the Baoding First Central Hospital from January 2019 to December 2020 were selected and randomly divided into two groups, with 40 cases in each group. The control group were given rabeprazole-based triple therapy, while the experimental group were treated with magnesium aluminum carbonate on the basis of the control group. The changes of symptoms and signs such as abdominal pain, abdominal distension, nausea, vomiting and hematochezia were compared between the two groups before and after treatment. Serological changes of the gastric mucosal microenvironment, such as the serum levels of extracellular regulatory protein kinase (ERK), superoxide dismutase (SOD) and epidermal growth factor receptor (EGFR), were compared between the two groups. Moreover, the differences in the results of gastroscopy between the two groups before and after treatment were compared and analyzed.Results:The scores of gastrointestinal symptoms in the experimental group after treatment were significantly improved compared with the control group (p=0.00). The levels of ERK and EGFR in the experimental group were significantly lower than those in the control group (ERK, p=0.01; EGRF, p=0.00), while the level of SOD was significantly increased (p=0.02). After treatment, the total effective rate of ulcer healing in the experimental group was 82.5%, which was significantly better than 60% in the control group (p=0.03). After treatment, moderate to severe gastric mucosal inflammation in the experimental group decreased to 10%, significantly better than that in the control group (decreased to 30%) (p=0.03).Conclusion:Magnesium aluminum carbonate combined with rabeprazole-based triple therapy is preferred for the treatment of patients with Helicobacter pylori-positive gastric ulcer associated with hemorrhage. With such a highly effective treatment regimen, the internal environment and blood supply of gastric mucosal cells can be significantly improved, gastric mucosal inflammation and gastrointestinal symptoms can be ameliorated, and the healing of ulcer surfaces can be accelerated.

Association of the functionally significant polymorphisms of the MMP9 gene with H. pylori-positive gastric ulcer in the Caucasian population of Central Russia.

Background and purposeThe study analyzed the association of functionally significant polymorphisms of matrix metalloproteinases (MMPs) genes with the development of gastric ulcer (GU) in Caucasians from Central Russia.MethodsThe 781 participants, including 434 patients with GU (196 Helicobacter pylori (H. pylori)-positive and 238 H. pylori-negative) and 347 controls (all H. pylori-negative) were recruited for the study. Ten SNPs of the MMP1 (rs1799750), MMP2 (rs243865), MMP3 (rs679620), MMP8 (rs1940475), and MMP9 (rs3918242, rs3918249, rs3787268, rs17576, rs17577, and rs2250889) genes were considered for association with GU using multiple logistic regression. The SNPs associated with GU and loci linked (r2≥0.8) to them were analyzed in silico for their functional assignments.ResultsThe SNPs of the MMP9 gene were associated with H. pylori-positive GU: alleles C of rs3918249 (OR = 2.02, pperm = 0.008) and A of rs3787268 (OR = 1.60–1.82, pperm ≤ 0.016), and eight haplotypes of all studied MMP9 gene SNPs (OR = 1.85–2.04, pperm ≤ 0.016) increased risk for H. pylori-positive GU. None of the analyzed SNPs was independently associated with GU and H. pylori-negative GU. Two haplotypes of the MMP9 gene (contributed by rs3918242, rs3918249, rs17576, and rs3787268) increased risk for GU (OR = 1.62–1.65, pperm ≤ 0.006). Six loci of the MMP9 gene, which are associated with H. pylori-positive GU, and 65 SNPs linked to them manifest significant epigenetic effects, have pronounced eQTL (17 genes) and sQTL (6 genes) values.ConclusionSNPs of the MMP9 were associated with H. pylori-positive GU but not with H. pylori-negative GU in Caucasians of Central Russia.

Correction: Low Prevalence of Helicobacter pylori-Positive Peptic Ulcers in Private Outpatient Endoscopy Centers in the United States.

Objectives During the past decades, the prevalence of gastric and duodenal ulcers, as well as Helicobacter pylori infection, has markedly declined. We hypothesized that the decline in H. pylori prevalence has decreased the fraction of H. pylori-positive gastric and duodenal ulcers. The present study was designed to test this hypothesis in a large US population undergoing esophagogastro-duodenoscopy in community-based endoscopy centers. Methods The Inform Diagnostics database is a national electronic repository of histopathologic records of patients distributed throughout the United States. A cross-sectional study among 1,289,641 individual esophagogastro-duodenoscopy patients analyzed the prevalence of peptic ulcers stratified by age, sex, ethnicity, H. pylori status, year of diagnosis, and ulcer type. The joint influence of multiple predictor variables on the occurrence of gastric and duodenal ulcers was analyzed using multivariate logistic regression analysis. Results Between 2009 and 2018, the general prevalence of H. pylori infection fell significantly from 11% to 9%. This decline was accompanied by a similar decline in the fraction of H. pylori-positive gastric ulcers from 17% to 14% and H. pylori-positive duodenal ulcers from 25% to 21%. Nowadays, only 17% of all patients with ulcer harbor H. pylori. The fraction of H. pylori-positive ulcers was significantly greater in duodenal than in gastric ulcers and in male than in female patients with ulcer. The prevalence of H. pylori was 2.6-fold higher among Hispanics and 3.2-fold higher among East Asians compared with the general population. The H. pylori prevalence fell from 24% to 22% among Hispanics and from 21% to 15% among East Asians. In East Asians and Hispanics, the fraction of H. pylori-positive gastric ulcers was 37% and 35%, respectively. Discussion H. pylori infection continues to fall in the general population. Nowadays, even among patients with ulcer only a small minority harbors H. pylori infection.

Low Prevalence of Helicobacter pylori-Positive Peptic Ulcers in Private Outpatient Endoscopy Centers in the United States.

During the past decades, the prevalence of gastric and duodenal ulcers, as well as Helicobacter pylori infection, has markedly declined. We hypothesized that the decline in H. pylori prevalence has decreased the fraction of H. pylori-positive gastric and duodenal ulcers. The present study was designed to test this hypothesis in a large US population undergoing esophagogastro-duodenoscopy in community-based endoscopy centers. The Inform Diagnostics database is a national electronic repository of histopathologic records of patients distributed throughout the United States. A cross-sectional study among 1,289,641 individual esophagogastro-duodenoscopy patients analyzed the prevalence of peptic ulcers stratified by age, sex, ethnicity, H. pylori status, year of diagnosis, and ulcer type. The joint influence of multiple predictor variables on the occurrence of gastric and duodenal ulcers was analyzed using multivariate logistic regression analysis. Between 2009 and 2018, the general prevalence of H. pylori infection fell significantly from 11% to 9%. This decline was accompanied by a similar decline in the fraction of H. pylori-positive gastric ulcers from 17% to 14% and H. pylori-positive duodenal ulcers from 25% to 21%. Nowadays, only 17% of all patients with ulcer harbor H. pylori. The fraction of H. pylori-positive ulcers was significantly greater in duodenal than in gastric ulcers and in male than in female patients with ulcer. The prevalence of H. pylori was 2.6-fold higher among Hispanics and 3.2-fold higher among East Asians compared with the general population. The H. pylori prevalence fell from 24% to 22% among Hispanics and from 21% to 15% among East Asians. In East Asians and Hispanics, the fraction of H. pylori-positive gastric ulcers was 37% and 35%, respectively. H. pylori infection continues to fall in the general population. Nowadays, even among patients with ulcer only a small minority harbors H. pylori infection.

Correlation between the cystathionine-γ-lyase (CES) and the severity of peptic ulcer disease.

The infection of Helicobacter pylori (H. pylori) is one of the most important causes of gastric ulcer disease. The role of hydrogen sulfide (H2S) production in H. pylori-induced gastric ulcer disease. The expression of cystathionine-γ-lyase (CSE) was determined, and correlated with the severity of gastric ulcer disease. One hundred and eight patients were selected based on the determination of gastric ulcer and the infection of Helicobacter pylori (H. pylori), including 36 normal control, 36 patients with H. Pylori-negative gastric ulcer, and 36 patients with H. Pylori-positive gastric ulcer. RT-PCR determination was performed to determine the expression of CSE, NF-κB and IL-8. The expression of CSE, NF-κB and IL-8 was higher in the gastric ulcer group than control group (p<0.05). Compared with the H. pylori-negative gastric ulcer, the expression of CSE, NF-κB and IL-8 was higher than H. pylori-positive gastric ulcer group (p<0.05). For H. pylori-negative gastric ulcer group, the expression of CSE positively correlated with the expression of NF-κB (r=0.98, p<0.05) and IL-8 (r=0.95, p<0.05). For H. pylori-positive gastric ulcer group, the expression of CSE also positively correlated with the expression of NF-κB (r=0.99, p<0.05) and IL-8 (r=0.85, p<0.05). The expression of CSE was positively correlated with the severity of gastric ulcer.

A Multicenter Prospective Observational Study of Triple Therapy with Rabeprazole, Amoxicillin and Metronidazole for &lt;i&gt;Helicobacter pylori&lt;/i&gt; in Japan

Triple therapy with rabeprazole (RPZ), amoxicillin (AMPC) and metronidazole (MNZ) (RPZ+AMPC+MNZ therapy: RAM therapy) has been approved by the Japanese Ministry of Health, Labour and Welfare as a second-line therapy for Helicobacter pylori-positive gastric and duodenal ulcers in Japan. The present multicenter prospective observational study aimed to investigate the safety and efficacy of RAM therapy in clinical practice. Patients with H. pylori-positive gastric or duodenal ulcers (including ulcer scars) in whom first-line therapy was unsuccessful were administered 10 mg of RPZ, 750 mg of AMPC and 250 mg of MNZ twice daily for seven days (total: 14 doses) based on an approved dose and regimen. Patient background factors, including complications, previous medical history, concomitant drugs, eradication results and adverse events were recorded by the investigator. The incidence of adverse drug reactions was 2.21% and the H. pylori eradication rate was 92.8%. Subgroup analyses performed to investigate the patient background factors affecting safety and efficacy revealed no factors that significantly affected the incidence of adverse drug reactions or the H. pylori eradication rate. Amid reports of decreased eradication rates with clarithromycin-based first-line therapy, the >90%H. pylori eradication rate achieved in the present study demonstrates the clinical efficacy of RAM therapy in subjects in whom first-line therapy is unsuccessful.

Strategies for peptic ulcer healing after 1 week proton pump inhibitor-based triple &lt;i&gt;Helicobacter pylori&lt;/i&gt; eradication therapy in Japanese patients: differences of gastric ulcers and duodenal ulcers

Helicobacter pylori (H. pylori) eradication therapy alone is insufficient to ensure healing of large ulcers with H. pylori-positive gastric ulcer (GU). The question of what is the optimum antiulcer treatment following H. pylori eradication therapy has not been fully elucidated. Furthermore, the ulcer healing effects of eradication therapy itself with H. pylori-positive duodenal ulcer (DU) have not been investigated. In GU study, the eradication therapy + proton pump inhibitor (PPI) group (group A) were administered eradication therapy followed by 7 weeks of a PPI, and the eradication therapy + gastroprotective drug (GP) group (group B) eradication therapy followed by 7 weeks of a GP. In DU study, the eradication therapy + PPI group (group C) were administered eradication therapy followed by 5 weeks of a PPI, and the eradication therapy only group (group D) was eradication therapy alone. In GU study, healing rates for ulcer of ≥15 mm in diameter were significant greater in the group A. In DU study, high healing rates were seen both the group C and D. In conclusion, a PPI could significantly heal GU than a GP after eradication therapy in GU. Meanwhile, the eradication alone is sufficient for DU.

Healing Effects of Rebamipide and Omeprazole in Helicobacter pylori-Positive Gastric Ulcer Patients after Eradication Therapy: A Randomized Double-Blind, Multinational, Multi-Institutional Comparative Study

Background and Aims: A recent placebo-controlled trial showed that rebamipide, which is a mucosal-protective antiulcer agent, promoted gastric ulcer healing without affecting the Helicobacter pylori status. We conducted a randomized, double-blind trial to compare the healing effects of rebamipide and the proton-pump inhibitor omeprazole in H. pylori-positive gastric ulcers after H. pylori eradication therapy. Methods: After completion of 1 week of eradication therapy, 132 patients with H. pylori-positive gastric ulcer were enrolled in 5 Chinese and 4 Korean institutions. Patients were randomly assigned to take either 20 mg of omeprazole (n = 63) or 300 mg of rebamipide (n = 65) daily for 7 weeks. Healing was defined as complete recovery and S1 and S2 stage ulcer according to the Sakita-Miwa classification. Results: Healing rates at 12 weeks were 81.5% (53/65) and 82.5% (52/63) in the rebamipide and omeprazole groups, respectively. There was no significant difference in treatment efficacy, as evidenced by gastric ulcer healing rates (absolute difference –1.0%; 95% confidence interval –10.7 to 8.7; p = 0.88). The H. pylori eradication rate and ulcer healing rate did not differ between the groups, the latter regardless of eradication outcome. Conclusions: Rebamipide is as effective as omeprazole in treating of H. pylori-positive gastric ulcer after eradication therapy.

Clinical trial: irsogladine maleate, a mucosal protective drug, accelerates gastric ulcer healing after treatment for eradication of Helicobacter pylori infection – the results of a multicentre, double‐blind, randomized clinical trial (IMPACT study)

Helicobacter pylori eradication therapy alone is not sufficient to heal all gastric ulcers. To verify the efficacy of treatment with irsogladine maleate between the termination and assessment of treatment for eradicating H. pylori in a double-blind study. Three hundred and twenty-two patients with a single H. pylori-positive gastric ulcer were given eradication treatment, then assigned randomly to a treatment group [given 4 mg/day irsogladine maleate (n = 150)] or a control group [given a placebo (n = 161)]. The gastric ulcer healing rates were compared after 7 weeks of treatment. The healing rate was significantly higher in the irsogladine maleate group (83.0%) than in the placebo group (72.2%; chi2 test, P = 0.0276). In the subgroup analysis of cases of eradication failure, the gastric ulcer healing rate was significantly higher in the irsogladine maleate group (57.9%) than in the placebo group (26.1%; chi2 test, P = 0.0366). Irsogladine maleate was effective for treating gastric ulcer after H. pylori eradication. The high healing rates observed in patients with or without successful eradication demonstrate the usefulness of irsogladine maleate treatment regardless of the outcome of eradication.

Gastric ulcer treatment: cure of Helicobacter pylori infection without subsequent acid-suppressive therapy: is it effective?

Whether it is a requirement to continue with anti-secretory therapy following anti-Helicobacter therapy in H. pylori positive gastric ulcers is an important question. As gastric ulcers tend to heal more slowly than duodenal ulcers, may be asymptomatic or only causing mild symptoms and success at curing H. pylori with current fist line therapies is 80% at best, clinicians will likely err on the side of caution and continue acid suppressive therapy to ensure healing of gastric ulcers. This is certainly recommended when dealing with bleeding ulcers.

Rebamipide, a gastro-protective and anti-inflammatory drug, promotes gastric ulcer healing following eradication therapy for Helicobacter pylori in a Japanese population: a randomized, double-blind, placebo-controlled trial

One week of Helicobacter pylori eradication therapy is insufficient for healing of gastric ulcers. We examined the efficacy of rebamipide in gastric ulcer healing following 1 week of eradication therapy in a randomized, double-blind, placebo-controlled trial. Patients with H. pylori-positive gastric ulcer were enrolled and received 1 week of eradication therapy, followed by 100 mg of rebamipide or placebo for 7 weeks. The primary end point was the gastric ulcer healing rate. Of the 309 patients entered in the trial, 301 completed H. pylori eradication therapy; 154 patients took rebamipide, and 147 took placebo. The healing rate in the rebamipide group was higher than that in the placebo group in the per-protocol analysis-80.0% (104/130) versus 66.1% (82/124) [95% confidence interval (CI), 3.1-24.7; P = 0.013)-and in a full analysis-70.1% (108/154) versus 60.5% (89/147) (95% CI, -1.1 to 20.3; P = 0.080). Compared with placebo, rebamipide significantly promoted gastric ulcer healing following 1 week of eradication therapy.

Interleukin-17 levels in Helicobacter pylori-infected gastric mucosa and pathologic sequelae of colonization.

To determine the role of interleukin (IL)-17 in gastric ulcerogenesis. Thirty-six gastric ulcer (GU) patients and 29 non-ulcer (NU) patients were enrolled in this study. Mucosal biopsy samples were obtained from the gastric antrum and GU site during endoscopy. Samples were used in in situ stimulation for 48 h in the presence of 10 microg/mL phytohemagglutinin-P (PHA), histological examination, and Helicobacter pylori (H pylori) culture. IL-17 and IL-8 protein levels in culture supernatants were assayed by ELISA. IL-17 mRNA expression was analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR). H pylori cagA and vacA status was assessed by reverse hybridization using a line probe assay (LiPA). IL-8 levels in culture supernatants were assayed after AGS cells were co-cultured with H pylori strain 26,695 or recombinant human (rh) IL-17. All 36 GU patients and 15 of 29 NU patients were found to be H pylori-positive, while 14 NU patients were H pylori-negative. All 51 H pylori strains from both GU and NU patients were cagA- and vacAs1/m1-positive. Antral mucosal tissues from H pylori-positive patients contained significantly (H pylori-positive NU patients: median 467 pg/mg/protein, range 53-2,499; H pylori-negative NU patients: median 104 pg/mg/protein, range 16-312, P< 0.0005) higher levels of IL-17 than those from uninfected patients. IL-17 levels at the ulcer site were significantly (ulcer site: median 1,356 pg/mg/protein, range 121-1,3730; antrum: median 761 pg/mg/protein, range 24-7,620, P< 0.005) higher than those at distant sites in the antrum. Biopsies from H pylori-positive GU and NU patients showed IL-17 mRNA expression in all samples whereas those from the antrum of the H pylori-negative controls showed no detectable expression. A significant correlation was seen between IL-17 and IL-8 levels at each biopsy site (ulcer: r = 0.62, P< 0.0001; antrum: r = 0.61, P< 0.0001) in GU patients. RhIL-17 and H pylori strain 26,695 each stimulated IL-8 production from AGS cells. IL-17 may play an important role in the inflammatory response to H pylori colonization, and may ultimately influence the outcome of H pylori-associated diseases that arise within the context of gastritis.

Helicobacter pylori eradication as the sole treatment for gastric and duodenal ulcers

It is uncertain whether eradication of Helicobacter pylori--without a prolonged suppression of acid secretion--is sufficient to allow healing of peptic ulcers. We evaluated whether eradication of H. pylori with no following anti-secretory medication then administered is sufficient for treatment of peptic ulcers. We also looked at the impact of non-steroidal anti-inflammatory drug (NSAID) and acetylsalicylic acid (ASA) use on ulcer relapses. The effect of eradication on ulcer healing and relapse rate was analysed in 115 patients, randomly allocated to four treatment groups: (1) quadruple therapy (28); (2) dual therapy (n-30); (3) triple therapy (n=27); and (4) lansoprazole and placebo (n=30). Endoscopic assessment was performed at 0, 8, and 52 weeks. The ulcer healing rate was 100% [95% confidence interval (CI), 95-100%] in H. pylori-negative and 83% (95% CI, 67-94%) in H. pylori-positive patients (P<0.01). In patients who used NSAIDS or ASA, the healing rates was 100% (95% CI, 73-100%) and 75% (95% CI, 19-99%) in H. pylori-negative (12 patients) and H. pylori-positive patients (four patients) (P = not significant). Ulcer relapses occurred in 5% (95% CI, 1-13%) of H. pylori-negative and in 36% (95% CI, 19-56%) of H. pylori-positive patients (P < 0.01). In H. pylori-negative patients who used NSAIDs or ASA the ulcer relapse rate was 30% (95% CI, 7-65%), whereas the ulcer relapse rate was 2% (95% CI, 0.4-10%) in patients who did not use NSAIDs or ASA (P < 0.05). No difference in ulcer relapse rate in H. pylori-positive patients who used or did not use NSAIDs or ASA was found. The eradication rate of H. pylori was 93% (95% CI, 76-99%) in the quadruple therapy group, 83% (95% CI, 64-94%) in the dual therapy group, 100% (95% CI, 87-100%) in the triple therapy group, and 0% (95% CI, 0-12%) in the lansoprazole and placebo group. Eradication treatment for H. pylori-positive gastric or duodenal ulcer is sufficient, with no need to follow it with anti-secretory medication. Cure of the infection reduces ulcer relapses in patients who did not use NSAIDs or ASA.

Gastric carcinoid tumors without autoimmune gastritis in Japan: a relationship with Helicobacter pylori infection.

In Japan, most cases of gastric carcinoid tumor (GCT) are unassociated with either autoimmune gastritis (AIG) showing type-A chronic atrophic gastritis (CAG-A) or Zollinger-Ellison syndrome (ZES). However, the pathogenesis of this tumor remains unknown. Recent studies have determined that Helicobacter pylori infection induces gastric carcinoid in Mongolian gerbils and that H. pylori lipopolysaccharide exerts a mitogenic effect on ECL cells. We examined five patients with histologically diagnosed GCT, 40 patients with H. pylori-positive gastric ulcer (Hp+GU), 24 patients with H. pylori-positive duodenal ulcer (Hp+DU), and 12 patients with AIG showing CAG-A topographically. We compared the prevalence of H. pylori infection, and the levels of gastrin and pepsinogen (PG) in the serum of patients with GCT with those of patients with Hp+GU, or Hp+DU, and AIG. We also investigated the histological characteristics of the tumor and the gastric corpus mucosa in the GCT patients. The levels of serum gastrin and PG I and II were measured using an RIA kit. In all five (100%) patients with GCT, H. pylori infection was present, without any evidence of AIG or ZES. The serum levels of gastrin in the GCT patients were higher than those in either Hp+GU or Hp+DU patients and lower than those in the AIG patients. In contrast, serum PG I levels and the PG I/II ratio were lower in the GCT group than in the Hp+GU or Hp+DU groups. Histologically, all GCTs were ECL cell tumors and peritumoral corporal mucosal atrophy was observed in four of the five patients with GCT. In conclusions, H. pylori infection and hypergastrinemia were found in the patients with GCT without AIG. This finding suggests that H. pylori infection may induce corporal mucosal atrophy and hypergastrinemia that can produce a GCT with time.

Increase in apoptosis and decrease in ornithine decarboxylase activity of the gastric mucosa in patients with atrophic gastritis and gastric ulcer after successful eradication of Helicobacter pylori

OBJECTIVE: Recent reports have shown that patients infected with Helicobacter pylori ( H. pylori) have a higher risk of gastric cancer. However, the mechanism of this increased risk is still unclear. In the gastric mucosa, the size of a continuously renewed population of cells is determined by the rates of cell production and of cell loss. Ornithine decarboxylase (ODC) activity is elevated in various gastrointestinal cancers and serves as a marker of mucosal proliferative activity. Apoptosis occurs throughout the gut and is associated with cell loss. Both cell proliferation and cell loss have important roles in H. pylori-associated gastric carcinogenesis. Therefore, we investigated the effect of H. pylori eradication on ODC activity and apoptosis in the gastric mucosa of patients with atrophic gastritis and gastric ulcers. METHODS: Biopsy specimens of the gastric antrum were obtained at endoscopy from 17 H. pylori-positive gastric ulcers patients and 15 H. pylori-positive gastritis patients before and 4 wk after eradication therapy with amoxicillin, omeprazole, and a new anti-ulcer agent, ecabet sodium, and from 10 gastric ulcer patients in whom ulcer healed but H. pylori was left untreated. ODC activity and induction of apoptosis were determined immunohistochemically. RESULTS: H. pylori was successfully eradicated with the triple therapy in 12 (80%) of 15 gastritis patients and 13 (76%) of 17 gastric ulcer patients. ODC activity was present in the gastric mucosa in 21 (84%) patients before eradication but in only four (16%) patients after successful eradication ( p = 0.0005). The apoptotic index increased significantly ( p = 0.0006) from 4.2% ± 0.4% before treatment to 7.4% ± 0.5% after successful eradication. CONCLUSIONS: Successful eradication of H. pylori decreases mucosal ODC activity and increases apoptosis in the gastric mucosa. These findings indicate that by decreasing mucosal cell proliferation and increasing epithelial cell loss, H. pylori eradication may help decrease the subsequent risk of gastric cancer.

Increase in apoptosis and decrease in ornithine decarboxylase activity of the gastric mucosa in patients with atrophic gastritis and gastric ulcer after successful eradication of Helicobacter pylori.

Recent reports have shown that patients infected with Helicobacter pylori (H. pylori) have a higher risk of gastric cancer. However, the mechanism of this increased risk is still unclear. In the gastric mucosa, the size of a continuously renewed population of cells is determined by the rates of cell production and of cell loss. Ornithine decarboxylase (ODC) activity is elevated in various gastrointestinal cancers and serves as a marker of mucosal proliferative activity. Apoptosis occurs throughout the gut and is associated with cell loss. Both cell proliferation and cell loss have important roles in H. pylori-associated gastric carcinogenesis. Therefore, we investigated the effect of H. pylori eradication on ODC activity and apoptosis in the gastric mucosa of patients with atrophic gastritis and gastric ulcers. Biopsy specimens of the gastric antrum were obtained at endoscopy from 17 H. pylori-positive gastric ulcers patients and 15 H. pylori-positive gastritis patients before and 4 wk after eradication therapy with amoxicillin, omeprazole, and a new anti-ulcer agent, ecabet sodium, and from 10 gastric ulcer patients in whom ulcer healed but H. pylori was left untreated. ODC activity and induction of apoptosis were determined immunohistochemically. H. pylori was successfully eradicated with the triple therapy in 12 (80%) of 15 gastritis patients and 13 (76%) of 17 gastric ulcer patients. ODC activity was present in the gastric mucosa in 21 (84%) patients before eradication but in only four (16%) patients after successful eradication (p = 0.0005). The apoptotic index increased significantly (p = 0.0006) from 4.2% +/- 0.4% before treatment to 7.4% +/- 0.5% after successful eradication. Successful eradication of H. pylori decreases mucosal ODC activity and increases apoptosis in the gastric mucosa. These findings indicate that by decreasing mucosal cell proliferation and increasing epithelial cell loss, H. pylori eradication may help decrease the subsequent risk of gastric cancer.

Contribution of major histocompatibility complex genes to susceptibility and resistance in Helicobacter pylori related diseases.

Although there have been numerous reports concerning the virulence factors of isolates for investigating the pathogenesis of Helicobacter pylori infection, few studies have been carried out regarding the association of HLA class II genes of the host with H. pylori related diseases. Two published studies have only analysed the HLA DQ locus alone. The aim of this study was thus to determine the association of HLA class II genes (DR, DQ and DP) with H. pylori related diseases using the DNA typing method. Fifty-eight patients with H. pylori positive gastric ulcers, 44 patients with H. pylori positive duodenal ulcers, 45 patients with H. pylori positive gastritis and 34 healthy subjects without H. pylori infection were typed for HLA class II genes by means of DNA typing with the polymerase chain reaction-sequence specific oligonucleotide probes method. A negative association with DRB1*1501, DQA1*01021 and DQB1*0602 alleles was noted in all three of the patient groups studied. Compared with the healthy controls, a positive association with DPA1*0201 (P= 0.032) and DPB1*0901 (P=0.005) in gastric ulcers, a positive association with DRB1*0405 (P=0.022) and DQB1*0401 (P=0.044) in duodenal ulcers, and a positive association with DPB1*0901 (P=0.016) in gastritis were observed. A haplotype analysis showed that the association of alleles with H. pylori related disease was with the haplotype rather than with either of the alleles individually. After correction for multiple comparisons, all the significant associations obtained between H. pylori related diseases and HLA class II genes disappeared. The interplay between host immunogenetic factors, bacterial virulence factors and environmental conditions may thus play a more important role in the outcome of H. pylori infection than immunogenetic factors alone.

A study of histopathological gastritis of &lt;i&gt;Helicobacter pylori&lt;/i&gt; infected peptic ulcer -difference of gastric ulcer and duodenal ulcer-

It is well known that there is a chronic active gastritis (CAG) in Helicobacter pylori (H. pylori) infected stomach. A characteristics of CAG between in H. pylori positive gastric ulcer and duodenal ulcer were studied. We found many differences as follows : 1) CAG was stronger in corpus than in antrum in H. pylori positive gastric ulcer. It was remarkable in cases accompany by gastric mucosal atrophy. 2) In H. pylori positive duodenal ulcer, CAG was stronger in antrum than in corpus. There was no relation in atrophic change of gastric mucosa.

Regional differences on production of chemokines in gastric mucosa between Helicobacter pylori-positive duodenal ulcer and gastric ulcer.

It is well known that antrum-predominant gastritis and pan-gastritis occurs in the patients with Helicobacter pylori-positive duodenal ulcer (DU) and gastric ulcer (GU), respectively. However, the role of chemokines in the pathogenesis of these pathologies is unclear. We examined the regional differences in mucosal chemokine production in patients with DU and GU. The production of interleukin-8 (IL-8), growth-related gene (GRO) alpha, and macrophage inflammatory protein (MIP)-1alpha was greater in the antrum than in the corpus in DU patients. In the patients with GU, monocyte chemoattractant protein (MCP)-1 levels in the mucosa adjacent to ulcer were greater than those away for the ulcer in the corpus. The reduction in chemokine production occurring in association with the eradication of H. pylori differed between DU and GU patients in the antrum (IL-8, P = 0.0394; GROalpha, P = 0.0149; MIP-1alpha, P = 0.0246; MCP-1, P = 0.0087). The data imply a different pathogenesis may exist for the gastritis present in patients with DU and GU occurring in H. pylori-positive individuals.

Helicobacter pylori感染と慢性活動性胃炎

A relation between Helicobacter pylori (H. pylori) infection and chronic active gastritis were studied with distinction of biopsy position. Gastric ulcer (313cases) , duodenal ulcer (187cases) and control group (160cases) , which has no lesion except atrophic gastritis, were used in this study. 1) There were no difference in activity score in H. pylori positive gastric ulcer and control group among biopsy positions ((1), (2) and (3)) . On the other hand, activity score in cases of H. pylori positive duodenal ulcer was higher in specimen number (1) and (3) than number (2). This tendency was different from gastric ulcer and control group. 2) A frequency of pan-gastritis was high in H. pylori positive cases. It was the highest in H. pylori infected duodenal ulcer. 3) We could analyse the relation between H. pylori infection and chronic active gastritis using biopsy specimen.