SUMMARYBackground: Population-based data on gastro-oesophageal reflux disease in Chinese are lacking. The prevalence, clinical spectrum and health care-seeking behaviour of subjects with gastro-oesophageal reflux disease were studied. Methods: Ethnic Chinese (3605) were invited to participate in a telephone survey using a validated gastro-oesophageal reflux disease questionnaire and the Hospital Anxiety and Depression Scale. Results: A total of 2209 subjects (58% female; mean age, 40.3 years) completed the interview. The annual, monthly and weekly prevalence rates of gastro-oesophageal reflux disease were 29.8%, 8.9% and 2.5%, respectively. Gastro-oesophageal reflux disease symptoms were associated with non-cardiac chest pain [odds ratio (OR), 2.3; 95% confidence interval (95% CI), 1.7-3.1], dyspepsia (OR, 1.9; 95% CI, 1.4-2.5), globus (OR,

It is hypothesized that H. pylori-induced apoptosis may play a key role in gastric carcinogenesis by increasing cell proliferation and/or resulting in gastric atrophy.

SUMMARYAim: To test the efficacy of rabeprazole, levofloxacin and rifabutin triple therapy vs. quadruple therapy for the second-line treatment of Helicobacter pylori infection. Methods: One hundred and nine patients who had failed previous H. pylori eradication were randomized to receive: (i) rabeprazole, 20 mg b.d., rifabutin, 300 mg once daily, and levofloxacin, 500 mg once daily, for 7 days (triple therapy); or (ii) rabeprazole, 20 mg b.d., metronidazole, 400 mg t.d.s., bismuth subcitrate, 120 mg q.d.s., and tetracycline, 500 mg q.d.s., for 7 days (quadruple therapy). Endoscopy and culture were performed before treatment. Results:The clarithromycin (79% vs. 21%, P < 0.001) and metronidazole (89% vs. 40%, P < 0.001) resistance rates were significantly higher in patients with previous exposure than in those with no previous exposure. The intention-to-treat and per protocol eradication rates were 91%/91% for the triple therapy group and 91%/92% for the quadruple therapy group. For patients with double resistance to metronidazole and clarithromycin, the eradication rates were 85% (17/20) in the triple therapy group and 87% (13/15) in the quadruple therapy group. Compliance was greater than 95% for both regimens. Conclusion: Rabeprazole, levofloxacin and rifabutinbased triple therapy and quadruple therapy were equally effective as second-line treatments for H. pylori infection.

SUMMARYAim: To determine whether symptomatic response to lansoprazole predicts abnormal acid reflux in endoscopy-negative patients with non-cardiac chest pain. Methods: Patients who complained of chest pain, but had normal coronary angiography, were asked to undergo upper endoscopy. Those without gastric and oesophageal lesions were recruited for 24-h ambulatory oesophageal pH monitoring, and were randomly given lansoprazole 30 mg or placebo, both daily for 4 weeks. Chest pain symptoms were recorded before and 1 month after treatment on a locally validated questionnaire. The symptom score was calculated by multiplying the severity and frequency of the symptom, and symptom improvement was defined as > 50% reduction in symptom score.Results: Overall, 68 patients, 36 on lansoprazole and 32 on placebo, completed the trial. The symptom score was reduced significantly in both groups (P < 0.001). In the lansoprazole group, more patients with than without abnormal reflux showed symptom improvement (92% vs. 33%; odds ratio ¼ 22; 95% confidence interval, 2.3-201.8; v 2 ¼ 10.9; P ¼ 0.001), giving a sensitivity, specificity, positive predictive value, negative predictive value and accuracy of 92%, 67%, 58%, 94% and 75%, respectively. In the placebo group, the rates of symptom improvement were similar between those with and without abnormal reflux (33% vs. 35%, P ¼ N.S.). Conclusions: Treatment with lansoprazole is a useful test in diagnosing endoscopy-negative gastro-oesophageal reflux disease in Chinese patients with non-cardiac chest pain.

Helicobacter pylori is a major human pathogen that can cause peptic ulcers and chronic gastritis. Bismuth-based triple or quadruple therapies are commonly recommended for the treatment of H. pylori infections. However, the molecular mechanisms underlying treatment with bismuth are currently not fully understood. We have conducted a detailed comparative proteomic analysis of H. pylori cells both before and after treatment with colloidal bismuth subcitrate (CBS). Eight proteins were found to be significantly upregulated or downregulated in the presence of CBS (20 microg mL(-1)). Bismuth-induced oxidative stress was confirmed by detecting higher levels of lipid hydroperoxide (approximately 1.8 times) and hemin (approximately 3.4 times), in whole cell extracts of bismuth-treated H. pylori cells, compared with those from untreated cells. The presence of bismuth also led to an approximately eightfold decrease in cellular protease activities. Using immobilized-bismuth affinity chromatography, we isolated and subsequently identified seven bismuth-binding proteins from H. pylori cell extracts. The intracellular levels of four of these proteins (HspA, HspB, NapA and TsaA) were influenced by the addition of CBS, which strongly suggests that they interact directly with bismuth. The other bismuth-interacting proteins identified were two enzymes (fumarase and the urease subunit UreB), and a translational factor (Ef-Tu). Our data suggest that the inhibition of proteases, modulation of cellular oxidative stress and interference with nickel homeostasis may be key processes underlying the molecular mechanism of bismuth's actions against H. pylori.

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Summary Aims : To study the prevalence, clinical characteristics and long‐term outcome of oesophagitis in Chinese patients. Methods : Clinical and endoscopic data were collected prospectively from consecutive patients who underwent upper endoscopy between 1997 and 2001. Patients with endoscopic oesophagitis were graded according to the Los Angeles system and analysed according to their clinical presentation, endoscopic details, Helicobacter pylori status, non‐steroidal anti‐inflammatory drug history, co‐morbidity and mortality. Results : A total of 22 628 upper endoscopies were performed in 16 606 patients. Of these, 631 (3.8%) had endoscopic oesophagitis, 14 had benign oesophageal stricture (0.08%) and 10 had Barrett's oesophagus (0.06%). Most patients (94%) had either Los Angeles grade A or grade B oesophagitis. Patients who died during follow‐up had a significantly higher incidence of co‐morbid illness (100% vs. 63%, P < 0.001). By Cox regression analysis, the presence of gastrointestinal bleeding (P = 0.008), advanced age (P = 0.004) and the use of Ryle's tube (P = 0.043) were identified to be independent factors associated with mortality. Conclusions : Complicated gastro‐oesophageal reflux disease is uncommon in the Asian population. Advanced age, use of Ryle's tube and the presence of gastrointestinal bleeding are associated with a poor long‐term outcome, which is a reflection of the severe underlying co‐morbidity.

Aspirin-induced apoptosis is one of the important mechanisms for its antitumour effect against gastric cancer. We aimed at investigating the involvement of bcl-2 family members in the apoptotic pathway in gastric cancer. Gastric cancer cell line AGS and MKN-45 were observed as to cell growth inhibition and induction of apoptosis in response to treatment with aspirin. Cell proliferation was measured by MTT assay. Apoptosis was determined by 4'-6-diamidino-2-phenylindole staining. Protein expression was determined by western blotting. We showed that aspirin activated caspase-8, caspase-9 and capase-3, cleaved and translocated Bid, induced a conformational change in and translocation of Bax and cytochrome c release. In addition, suppression of caspase-8 with the specific inhibitor z-IETD-fmk, as well as the pan-caspase inhibitor z-VAD-fmk, prevented Bid cleavage and subsequent apoptosis. The caspase inhibitors failed to abolish the effects on Bax activation. In conclusion, our results identify a role of caspase-8/Bid and activation of Bax as a novel mechanism for aspirin-induced apoptosis in gastric cancer.