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Background : Helicobacter pylori, especially the CagA-positive strains, are closely associated with peptic ulcers and gastric cancers. We performed a large scale gastric cancer screening project and examined the prevalence of H. pylori and CagA-positive strains in Changle, China, an area with one of the World’s highest gastric cancer mortality. We also compared the prevalence with that in Hong Kong which has one-tenth of the gastric cancer mortality of that in Changle. Methods : A total of 2424 subjects in Changle and 523 subjects in Hong Kong had endoscopic examination and venesection. Sera were tested for anti-H. pylori antibody and anti-CagA antibody and correlated with endoscopic findings. Results : In Changle, 80.9% of the subjects were H. pylori carriers. Out of 551 carriers, 408 (74%) were positive for anti-CagA antibody. A total of 76% and 87% of the asymptomatic and gastric cancer patients were positive for anti-CagA antibody, respectively (P > 0.05). Compared to Hong Kong, there was a significantly (P

Nonsteroidal anti-inflammatory drug (NSAID)-induced apoptosis is considered to be an important mechanism in the antineoplastic effects and damage produced by the drugs in the gastrointestinal tract. In this study, two different gastric cancer cell lines, MKN28 (mutant-type p53) and AGS (wild-type p53), were compared as to growth inhibition, apoptosis, and cell cycle and apoptosis-related gene expression in response to indomethacin treatment. Cell growth was measured by MTT (3-(4,5-dimethylthiazole-2-yl)-2,5-diphenyl tetrazolium bromide) assay. Apoptosis was characterized by acridine orange staining and DNA fragmentation, and cell cycle kinetics by flow cytometry. The mRNA and protein levels of p53, p21waf1/cip1, and c-myc were determined by Northern and Western blotting. The results showed that indomethacin initiated growth inhibition and apoptosis in both cell lines without cell cycle shifting. AGS cells were more sensitive to growth inhibitory activity and apoptosis of indomethacin than MKN28 cells. In MKN28 cells, the levels of p53, p21waf1/cip1, and c-myc mRNA remained unchanged over the 24-hr treatment with indomethacin, but the p53 protein level was elevated after 4 hr. There was no change in the p21waf1/cip1 and c-myc protein levels in the MKN28 cells. In AGS cells, a progressive increase in c-myc mRNA and protein levels was noted, while p53 and p21waf1/cip1 remained unchanged. It can be concluded that wild-type p53 and/or up-regulation of c-myc is associated with indomethacin-mediated differential apoptosis in gastric epithelial cells.

Background : The effectiveness of Helicobacter pylori eradication treatment and long term acid suppression maintenance in the natural course of duodenal ulcer has not been directly compared. Aim : To compare in a prospective randomized study the effectiveness of H. pylori eradication on the prevention of recurrence of duodenal ulcer with long-term maintenance acid suppression therapy. Methods : One hundred and fourteen duodenal ulcer patients were randomized to the treatment over a 12-month period. Fifty-seven of them received triple therapy consisting of 1 g sucralfate q.d.s. for 28 days, 300 mg metronidazole q.d.s. for 14 days and 250 mg clarithromycin q.d.s. for 14 days. Another 57 received 20 mg omeprazole q.d.s. for 12 months. An upper endoscopy was performed before treatment, at 6 weeks, and 2, 6 and 12 months after the first endoscopy. Side-effects were self-recorded and clinical follow-ups were arranged for up to 4.25 years. Results : The ulcer healing rate was 90.2% (95% confidence interval (95% CI): 79–97%) in the omeprazole group at 6 weeks as compared to 83.3% (95% CI: 70–93%) in the triple therapy group (P = 0.38). There was a higher success rate of pain control in the omeprazole group. Side-effects were more frequently reported and compliance was poorer in the triple therapy group during the first 4 weeks. During follow-up, more relapses were seen in the omeprazole group (9.8%, 95% CI: 3–21%) than the triple therapy group (4.2%, 95% CI: 1–13%) at 1 year (P = 0.44). All relapses were due to the persistence of H. pylori infection. At the 1 year follow-up, none of the patients who were H. pylori negative had an endoscopic relapse compared to 7 out of 56 patients who remained H. pylori positive (12.5%, 95% CI: 5–24%, P = 0.018). After a mean follow-up of 4.07 years, none of those who remained H. pylori negative had an ulcer relapse while the 11 out of 41 who remained H. pylori positive had an ulcer relapse (26.8%, 95% CI 14–43, P = 0.0005). Conclusions : Both regimens were highly effective in healing ulcers. The eradication of H. pylori infection was associated with more side-effects and poor compliance but was more effective than the maintenance therapy in reducing the recurrence of duodenal ulcers. For the prevention of ulcer recurrence, testing of H. pylori status after triple therapy is more important than maintenance therapy.

There are suggestions that duodenal ulcer protects individuals from gastric cancer and that rice is ulcerogenic while wheat is gastro-protective. We aimed to examine the relationship of gastric cancer, duodenal and gastric ulcers in different geographical regions in China and identified dietary risk factors for duodenal ulcer and gastric cancer. The prevalence of peptic ulcer and gastric cancer among symptomatic patients in eight major cities, four each from the north and the south representing all the six defined regions of China were studied. Endoscopy and case records over a 10 year period were reviewed and cases of confirmed duodenal and gastric ulcer and gastric cancer, together with the total number of endoscopies performed per year, were recorded. Rates were expressed as cases/1000 endoscopies. Results were compared to another epidemiological study on diet and mortality in the same regions in China conducted at the same time. Duodenal ulcer rates were 2.4-fold higher in southern China than northern China, whereas gastric cancer rates were 1.6-fold higher in the north than in the south. Correlation studies showed for the first time an inverse linear relationship between the gastric cancer rates and the duodenal ulcer rates (r=-0.8076, P=0.015), as well as the duodenal ulcer: gastric ulcer ratios (r=-0.9133, P=0.002). Gastric ulcer rates were higher in southern China but did not correlate with the gastric cancer rates (r=0.1455, P=0.731). Duodenal ulcer rates were found to be related to daily rice intake (r=0.8554, P=0.029) and inversely related to daily wheat flour intake (r=-0.8472, P=0.033). Gastric cancer rates were not related to any dietary risk factors tested. We concluded there was an inverse relationship between gastric cancer rates and duodenal ulcer rates. Although duodenal ulceration and gastric cancer are both linked to Helicobacter pylori infection, the findings of this study indicate independent additional aetiological factors for the pathogenesis of these conditions. Dietary factors such as rice or wheat intake may play a role.

Background: Low risk of rebleeding has been observed in patients with gastrointestinal bleeding due to peptic ulcer without high-risk stigmata of recent hemorrhage. We aimed to evaluate the safety and acceptability of an aggressive early discharge policy in those patients admitted with upper gastrointestinal bleeding due to duodenal ulcers without high-risk stigmata of recent hemorrhage. Method: Retrospective analysis was carried out in bleeding ulcer patients less than 60 years of age with stable vital signs and no stigmata or only flat spots on endoscopy. A prospective study was then performed that included only duodenal ulcer patients less than 60 years of age with stable vital signs, no concomitant serious medical illness, and no stigmata of recent hemorrhage. These patients were discharged on the same day that endoscopy was performed. Results: During a period of 18 months, 72 patients satisfied the criteria in the retrospective study. The mean hospital stay was 1.4 days (range, 1 to 5). There were no episodes of rebleeding nor significant drops in hemoglobin level 2 weeks after discharge (10.8 gm/dL ± 1.4 vs 11.0 gm/dL ± 1.5). Seventy-five patients were recruited into the prospective study. None of them had rebleeding nor significant drops in hemoglobin 1 week after discharge (12.1 gm/dL ± 1.8 vs 11.7 gm/dL ± 2.5). Conclusion: We conclude that patients with gastrointestinal bleeding who have clean-based duodenal ulcers and are stable on admission can be safely discharged on the same day as endoscopy. (Gastrointest Endosc 1997;45:26-30.)

Amoxycillin in combination with anti-ulcer agents has been shown to prolong duodenal ulcer remission. While this effect can be related to the eradication of Helicobacter pylori, it is not known if amoxycillin might possess cytoprotective properties. Protection against ethanol-induced gastric mucosal damage by intragastric instillation of amoxycillin suspension (prepared from capsule form) and solution (from injection form, 100% pure amoxycillin), and by intraperitoneal injection of amoxycillin solution was studied using an ex vivo gastric chamber in the rat. Intragastric and intraperitoneal administration of amoxycillin dose-dependently protected the rat gastric mucosa from damage by absolute ethanol. This protection was lost when the rats were pretreated with indomethacin. Gastric mucosal blood flow as measured by laser Doppler flowmetry and gastric acid output were unaffected by amoxycillin. Amoxycillin imparts gastric cytoprotection, and one possible mechanism is by the release of prostaglandins.

ContextAlthough chronic Helicobacter pylori infection is associated with gastric cancer, the effect of H pylori treatment on prevention of gastric cancer development in chronic carriers is unknown.ObjectiveTo determine whether treatment of H pylori infection reduces the incidence of gastric cancer.Design, Setting, and ParticipantsProspective, randomized, placebo-controlled, population-based primary prevention study of 1630 healthy carriers of H pylori infection from Fujian Province, China, recruited in July 1994 and followed up until January 2002. A total of 988 participants did not have precancerous lesions (gastric atrophy, intestinal metaplasia, or gastric dysplasia) on study entry.InterventionPatients were randomly assigned to receive H pylori eradication treatment: a 2-week course of omeprazole, 20 mg, a combination product of amoxicillin and clavulanate potassium, 750 mg, and metronidazole, 400 mg, all twice daily (n = 817); or placebo (n = 813).Main Outcome MeasuresThe primary outcome measure was incidence of gastric cancer during follow-up, compared between H pylori eradication and placebo groups. The secondary outcome measure was incidence of gastric cancer in patients with or without precancerous lesions, compared between the 2 groups.ResultsAmong the 18 new cases of gastric cancers that developed, no overall reduction was observed in participants who received H pylori eradication treatment (n = 7) compared with those who did not (n = 11) (P = .33). In a subgroup of patients with no precancerous lesions on presentation, no patient developed gastric cancer during a follow-up of 7.5 years after H pylori eradication treatment compared with those who received placebo (0 vs 6; P = .02). Smoking (hazard ratio [HR], 6.2; 95% confidence interval [CI], 2.3-16.5; P

Background: Sucralfate monotherapy has been shown to suppress but not eradicate Helicobacter pylori. The combination of sucralfate with antibiotic(s) has been evaluated recently in the treatment of H. pylori-positive duodenal ulcer. The aim of this article is to review the efficacy of sucralfate-containing duotherapy and triple therapy in duodenal ulcer healing and H. pylori eradication rates. Methods: Reports on duotherapy and triple therapy including sucralfate as the mediating agent were analysed to assess the duodenal ulcer healing and H. pylori eradication rates. Results: One study on duotherapy with sucralfate and amoxycillin achieved an ulcer healing rate of 86% and H. pylori eradication rate of 40%, which compared favourably with sucralfate monotherapy that resulted in duodenal ulcer healing and H. pylori eradication rates of 65% and 0% respectively. A total of six studies have examined triple therapy using sucralfate with two antibiotics. The duodenal ulcer healing rates were generally over 90% a...

Glycoconjugates on cell surfaces are known to have important physiological and biological functions. The oligosaccharide components of the cell surface glycoconjugates are recognized as important mediators of cellular interaction and interaction of cells with ligands such as hormones and growth factors (1,2). In normal tissues, such molecules (receptors) form part of the transmembrane structures linking extracellular signals with intracellular transducers of the received information (3) Disruption of these receptors results in loss of transmembrane communication and hence cellular dysfunction Oligosaccharide domains of cellular glycoprotems and glycohpids are synthesized by a series of hierarchically organized glycosyltransferase enzymes within the Golgi apparatus. Structural modifications to oligosaccharide domains of these glycoconjugates occur during ontogeny and oncogenests (4,5). It is increasingly recognized that these modified oligosaccharide domains (antigens) on cancer cells may represent the accumulation of precursor chains with absence of more complex structures because of decreased activity of synthesizing enzymes for terminal components of the carbohydrate chains. In addition, neosynthesis of new saccharide structures may occur because of enhanced synthesis of new components, often because of aberrant fucosylation or sialylation or a combination of both It has been postulated that altered glycoconjugates interact in vivo with lectins associated with the membrane of corresponding cells, as is thought to be the case in the interaction between tumor cells and endothelium in the course of seeding of metastases (6). Increasing awareness of the major significance of cell surface glycoconjugates has led to a rapid expansion in techniques for their analysis.

Eradication of Helicobacter pylori (H. pylori) in patients with uncomplicated duodenal ulcers prevents long-term recurrence of ulcers. We aimed to study whether treatment of H. pylori prevents the long-term recurrence of duodenal ulcer hemorrhage.Patients with duodenal ulcer bleeding and confirmed H. pylori infection were recruited. A total of 120 patients were randomly assigned to triple therapy (DeNoltab 120 mg, amoxycillin 500 mg, and metronidazole 300 mg four times daily) or DeNoltab 120 mg four times daily alone. No maintenance therapy was given during the follow-up period. The endpoints were the cumulative rates of symptomatic and bleeding duodenal ulcer recurrences.Of the patients receiving the triple regimen, 85.1% had H. pylori eradicated as compared to 2.0% of patients receiving DeNoltab (p0.05). More patients in the DeNoltab group than those in the Triple group had recurrence of ulcer bleeding, but this did not reach statistical significance (12/60 vs 6/60, p = 0.20). Logistic regression analysis on clinical, personal, and endoscopic characteristics identified persistent H. pylori infection as the only independent predictor of recurrence of duodenal ulcer bleeding.Treatment of H. pylori alone with the present bismuth-based triple therapy in patients with duodenal ulcer hemorrhage did not result in significant reduction in further bleeding episodes, although a trend was seen for the group that was given triple therapy. On the other hand, posttreatment H. pylori status was found to be an independent predictor of bleeding recurrence.

Antacids have served us well for over a century. In terms of peptic ulcer disease, the attitude in the late 1950s to 1970s that antacids should be taken only on demand was unjustified and erroneous. 13 recent endoscopic controlled studies have confirmed the efficacy of antacids in the healing of duodenal ulcer, achieving about 75% healing in 4 weeks. The efficacy of antacids in promoting gastric ulcer healing has been less well studied and the results are controversial. The most appropriate and economical antacid regimens for the treatment of duodenal ulcer disease should include tablets or liquid that have acid neutralising capacity of 400 mmol/day given at least an hour after meals. As a long term therapy, antacids appear to work, but need be taken in multiple daily doses, a regimen which is unlikely to meet with long term patient compliance. Patients with gastro-oesophageal reflux disorders or pregnancy-related reflux have also benefited from the usage of antacids ad libitum. Early previous studies have clearly demonstrated the efficacy of antacids in reducing gastro-oesophageal reflux and healing of reflux oesophagitis. The acidity of the gastric contents is the major determining factor in the outcome of the aspiration pneumonitis occurring during delivery. The prophylactic use of antacids during delivery has helped to reduce the severity of this complication. Similarly, the prophylactic administration of antacid aiming to maintain gastric pH between 3.5 to 7.0 has resulted in significant reduction of bleeding due to stress associated ulcers and/or erosive haemorrhagic gastritis in critically ill patients. Antacid therapy, however, is controversial in the management of nonulcer dyspepsia or nonsteroidal anti-inflammatory drug related upper gastrointestinal mucosal damage. Undoubtedly, antacids have major roles to play in the treatment of gastric acid related disorders. They have clear advantages and disadvantages when compared with the antisecretory agents. New proton pump inhibitors in particular have certainly superseded antacids and even the H2-receptor antagonists in many respects. However, the long term safety record of antacids remains unsurpassed by any of the new antisecretory agents.

Peptic ulcer disease is twice as common in people living in South China when compared with those in North China. However, the gastric cancer rate in North China is three times that of South China. The overall Helicobacter pylori prevalence rate is similar in North and South China populations and it is higher than Caucasians living in Western societies. However, there is a significantly higher prevalence of H. pylori seropositivity among those who live in the high gastric cancer areas of China. On the other hand, there is no significant difference in the H. pylori positive rate in the peptic ulcer disease patients between the two regions of China. Other permissive/associated co-factors in the development of peptic ulcer disease or gastric cancer remain unknown at this stage.

To the Editor.— I share the views of Greenberg and Bank 1 that when considering the etiopathological role of Helicobacter pylori in nonulcer dyspepsia one needs to take into account the age of the patients surveyed. However, I fear that the authors might have underestimated the true prevalence of H pylori colonization in their study population by using a single antral biopsy urea broth test. The biopsy urea broth test has recently been compared in a pilot study 2 with a modified technique, cytological brushing urea broth test, and histologic examination used in our unit and has been shown to underestimate H pylori colonization by 15% (85% sensitivity of biopsy urea broth test and 100% sensitivity of cytologic brushing urea broth test, respectively). The false-negative rate has increased to about 20% in a subsequent larger study (unpublished results). No mention has been made in the article by Greenberg and Bank