Recurrent symptoms and gastro-oesophageal reflux disease in patients with duodenal ulcer treated for Helicobacter pylori infection.
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BACKGROUND: Eradication of Helicobacter pylori has been shown to prevent relapse of endoscopically detected duodenal ulcers. There is controversy regarding symptom improvement after therapy. Some studies have suggested that a substantial number of patients remain symptomatic after eradication therapy. Other studies suggest that gastro-oesophageal reflux disease (GERD) may develop as a result of H. pylori eradication. AIM: To determine the relationship between symptoms and H. pylori eradication and to determine whether H. pylori eradication results in symptoms or endoscopic findings of GERD. METHODS: Two hundred and forty-two patients with endoscopically documented duodenal ulcer disease and evidence of H. pylori infection by rapid urease testing and histology were studied in four randomized, placebo-controlled, double-blind trials of H. pylori eradication therapy. All patients underwent symptom assessment and endoscopy with biopsy before therapy and 1 and 6 months after completing therapy. The rapid urease test and histology were used to determine H. pylori status. Interviewers were blinded to H. pylori status after eradication and were unaware of the endoscopic findings (interviews were performed prior to repeat endoscopy). RESULTS: The presence of epigastric pain was significantly associated with persistent H. pylori infection 1 month after therapy (odds ratio 2.3, 95% CI: 1.02-5.2; P=0.041), as was nausea (OR 7.1, 95% CI: 0.93-55.6; P=0.029). The presence of epigastric pain was significantly associated with ulcer relapse at 6 months (OR 7.5, 95% CI: 3.6-15.7; P < 0.001) as was nausea (OR 5.1, 95% CI: 1.7-16.0; P=0.002). Heartburn was not associated with eradication of H. pylori or ulcer relapse. New onset reflux symptoms were reported by 17% (17 of 101 patients) at 6 months and were not significantly different in patients with (15%) and without (22%) persistent H. pylori infection (P=0.47). Erosive oesophagitis was present at endoscopy in one of the 17 cases that developed new heartburn. CONCLUSIONS: One month after completion of therapy, the presence of epigastric pain or nausea is associated with persistent infection and these symptoms at 6 months are suggestive of duodenal ulcer relapse. The incidence of GERD is not increased in patients who have eradication of H. pylori. (+info)
Does eradication of Helicobacter pylori alone heal duodenal ulcers?
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BACKGROUND: Eradication of Helicobacter pylori infection prevents duodenal ulcer (DU) relapse, but it remains uncertain whether eradication of H. pylori alone heals duodenal ulceration. AIM: To test the hypothesis that eradication of H. pylori infection is accompanied by healing of duodenal ulcer. METHODS: A total of 115 consecutive patients with endoscopically confirmed H. pylori-infected duodenal ulcer were randomly assigned to one of two groups. Group BTC patients received a 1-week course of colloidal bismuth subcitrate 220 mg b.d., tinidazole 500 mg b.d., clarithromycin 250 mg b.d. Group OBTC patients received omeprazole 20 mg daily for 4 weeks with the BTC regimen during the first week. Endoscopy with antral biopsies and 13C-urea breath test (UBT) were performed before and 4 weeks after completion of the 7-day triple or quadruple therapy. RESULTS: Eight patients dropped out (four in BTC and four in OBTC). Duodenal ulcer healing rates on an intention-to-treat basis in BTC and OBTC were 86% (95% CI: 77-95%) and 90% (95% CI: 82-98%), respectively. The eradication rates of H. pylori on an intention-to-treat basis in BTC and OBTC were 88% (95% CI: 79-96%) and 91% (95% CI: 84-99%), respectively. There were no statistically significant differences in ulcer healing rates and eradication rates between these two groups (P > 0.05). Epigastric pain resolved more rapidly in patients assigned to OBTC compared with those assigned to BTC. Both of the two regimens were well tolerated with only minor side-effects (3% of the 115 patients) and the compliance was good. CONCLUSIONS: BTC is a very effective H. pylori eradication regimen. Almost all duodenal ulcers heal spontaneously after cure of H. pylori infection using a 1-week low-dose bismuth-based triple therapy. Treating duodenal ulcer with simultaneous administration of omeprazole achieves ulcer pain relief more rapidly. (+info)
Pantoprazole, amoxycillin and either azithromycin or clarithromycin for eradication of Helicobacter pylori in duodenal ulcer.
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BACKGROUND: Studies have shown that 1-week triple therapy consisting of a proton pump inhibitor, amoxycillin and clarithromycin may cure Helicobacter pylori infection in the majority of patients. AIM: To establish whether pantoprazole plus amoxycillin in association with either azithromycin or clarithromycin is useful in curing H. pylori infection in patients with a duodenal ulcer. METHODS: One hundred and ten patients with active duodenal ulcers and H. pylori infection were treated with pantoprazole (days 1-7, 40 mg b.d.; days 8-28 40 mg o.d.) plus amoxycillin 1 g b.d. for the first 7 days. Patients were randomly assigned to receive either azithromycin 500 mg o.d. for the first 6 days (PAAz group; n=55) or clarithromycin 500 mg b.d. for the first 7 days of treatment (PAC group; n=55). H. pylori status was determined by urease test and histology before the treatment, and again 4 weeks after cessation of any medication. RESULTS: One hundred and three patients completed the study. H. pylori infection was eradicated in 78% (39/50) of patients in the PAAz group (ITT analysis: 71%, 95% CI: 61-83%) vs. 81% (43/53) of patients in the PAC group (ITT analysis: 78%, 95% CI: 69-90%) (N.S.). All ulcers had healed. CONCLUSION: Our study shows that 1-week triple therapy with pantoprazole, amoxycillin and either azithromycin or clarithromycin is not satisfactory (<80% ITT H. pylori eradication rate). (+info)
Omeprazole or ranitidine bismuth citrate triple therapy to treat Helicobacter pylori infection: a randomized, controlled trial in Vietnamese patients with duodenal ulcer.
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AIM: To evaluate the effectiveness of triple therapy containing either omeprazole or ranitidine bismuth citrate (RBC) to treat H. pylori infection in Vietnamese duodenal ulcer patients. METHODS: Patients infected with H. pylori were randomized to receive either omeprazole (20 mg b.d.), clarithromycin (500 mg b.d.) and amoxycillin (1 g b.d.) for 10 days (OAC), or RBC (400 mg b.d.), clarithromycin (500 mg b.d.) and amoxycillin (1 g b.d.) for 10 days (RAC). H. pylori eradication and ulcer healing was established by a follow-up oesophagogastroduodenoscopy (EGD) at least 4 weeks after therapy. Side-effects and compliance were assessed. RESULTS: One hundred and four out of 108 (96%) patients with a duodenal ulcer were infected with H. pylori. Eighty per cent of infected patients had detectable CagA IgG antibodies. Fifty-seven patients received OAC and 47 received RAC. OAC eradicated H. pylori in 91 and 86% of patients by per protocol (PP) and intention-to-treat (ITT) analysis, respectively. PP and ITT eradication rates for RAC were 96 and 91%. Ulcer healing at the follow-up EGD was 89% with OAC and 100% with RAC. Side-effects were minor. No patient failed to complete the protocol due to side-effects. CONCLUSION: Triple therapy with either omeprazole or RBC is highly effective in eradicating H. pylori and healing duodenal ulcer in Vietnamese patients. (+info)
Relationship of blood group determinants on Helicobacter pylori lipopolysaccharide with host lewis phenotype and inflammatory response.
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As Lewis a (Le(a)) and Lewis b (Le(b)) blood group antigens are isoforms of Lewis x (Le(x)) and Lewis y (Le(y)) and are expressed in the gastric mucosa, we evaluated whether the patterns of expression of Le(x) and Le(y) on Helicobacter pylori lipopolysaccharides reflected those of host expression of Le(a) and Le(b). When 79 patients (secretors and nonsecretors) were examined for concordance between bacterial and host Le expression, no association was found (chi(2) = 5.734, 3 df, P = 0.125), nor was there a significant difference between the amount of Le(x) or Le(y) expressed on isolates from ulcer and chronic gastritis patients (P > 0.05). Also, the effect of host and bacterial expression of Le antigens on bacterial colonization and the observed inflammatory response was assessed. In ulcer patients, Le(x) expression was significantly related to neutrophil infiltration (r(s) = 0.481, P = 0.024), whereas in chronic gastritis patients significant relationships were found between Le(x) expression and H. pylori colonization density (r(s) = 0.296, P = 0.03), neutrophil infiltrate (r(s) = 0.409, P = 0. 001), and lymphocyte infiltrate (r(s) = 0.389, P = 0.002). Furthermore, bacterial Le(y) expression was related to neutrophil (r(s) = 0.271, P = 0.033) and lymphocyte (r(s) = 0.277, P = 0.029) infiltrates. Thus, although no evidence of concordance was found between bacterial and host expression of Le determinants, these antigens may be crucial for bacterial colonization, and the ensuing inflammatory response appears, at least in part, to be influenced by Le antigens. (+info)
Comparison of lansoprazole-based triple and dual therapy for treatment of Helicobacter pylori-related duodenal ulcer: an Asian multicentre double-blind randomized placebo controlled study.
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BACKGROUND: [corrected] In Asian countries with limited resources, clarithromycin-based triple therapy may not be readily available. There are also few direct comparisons of different regimens in Asia. AIM: To compare two lansoprazole-based non-clarithromycin triple therapies and one dual therapy in a prospective double-blind placebo-controlled study of Helicobacter pylori eradication and duodenal ulcer healing. METHODS: Fourteen centres in Asia participated in this study. Patients with acute duodenal ulcer who were H. pylori-positive were recruited. They were randomized to receive: (a) lansoprazole 30 mg b.d., amoxycillin 1 g b.d. and metronidazole 500 mg b.d. for 2 weeks (LAM-2 W), or (b) LAM for 1 week and placebo (LAM-1 W), or (c) lansoprazole 30 mg b.d., amoxycillin 1 g b.d. and placebo for 2 weeks (LA-2 W). Upper endoscopy was repeated at week 6 to check for duodenal ulcer healing. Symptoms and side-effects were recorded. RESULTS: A total of 228 patients were recruited, and two patients took less than 50% of the drugs. H. pylori eradication rates (intention-to-treat) were 68 out of 82 (83%) with LAM-2 W, 55 out of 71 (78%) with LAM-1 W and 43 out of 75 (57%) with LA-2 W. There were significant differences (P=0. 001) in eradication rates when comparing either LAM-2 W or LAM-1 W with LA-2 W. The eradication rate in patients with metronidazole resistant H. pylori strains were significantly lower than those with metronidazole sensitive strains (P=0.0001). The duodenal ulcer healing rates at week 6 were 85%, 85% and 72% in LAM-2 W, LAM-1 W and LA-2 W, respectively (P=0.065). Side-effects occurred in 13%, 11% and 9% in LAM-2 W, LAM-1 W and LA-2 W, respectively. H. pylori eradication and initial ulcer size were factors affecting duodenal ulcer healing. CONCLUSIONS: This Asian multicentre study showed that 1-week lansoprazole-based triple therapy without clarithromycin has similar efficacy in H. pylori eradication and ulcer healing compared with a 2-week regimen. Both triple therapies were significantly better than dual therapy in H. pylori eradication. Therefore, 1-week lansoprazole-based triple therapy is as safe and effective as 2-week therapy in eradication of H. pylori infection and healing of duodenal ulcer in these Asian centres. (+info)
Triple therapy in the eradication of Helicobacter pylori in patients with duodenal ulcer disease: results of a multicentre study in South-East Asia. South-East Asia Multicenter Study Group.
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BACKGROUND: The efficacy of proton pump inhibitor based triple therapy in patients from South-East Asia, where metronidazole resistance is reportedly high, has not been formally assessed in randomized, multicentre trials. AIM: To compare the eradication rates of Helicobacter pylori, ulcer healing rates and side-effects of three regimens of omeprazole triple therapy in patients with duodenal ulcer from South-East Asia and to study the impact of metronidazole resistance. METHODS: A single blind, randomized parallel group, comparative multicentre study. A total of 246 patients from 15 centres in four South-East Asian countries were randomized to receive OAC (omeprazole 20 mg b.d., amoxycillin 1 g b. d., clarithromycin 500 mg b.d.), OAM (omeprazole 20 mg b.d., amoxycillin 1 g b.d., metronidazole 400 mg b.d.) or OMC (omeprazole 20 mg b.d., metronidazole 400 mg b.d., clarithromycin 500 mg b.d.) for 7 days. After triple therapy, the patients were further randomized to receive either omeprazole or placebo for 7 days. Upper gastrointestinal endoscopy was performed before treatment and 4 weeks after treatment. Biopsies for culture and for histopathological examination for H. pylori were taken from corpus and antrum before treatment and 4 weeks after treatment. RESULTS: The eradication rates were intention-to-treat/per protocol (95% CI): OAC 87% (79-94%)/94% (89-100%); OAM 80% (70-89%)/91% (83-98%); OMC 85% (77-93%)/94% (88-100%). The difference in eradication rates between the three groups was not statistically significant (P=0.419). Pre-treatment metronidazole resistance, was found in 34% of isolates and was a significant prognostic factor in patients receiving OAM (odds ratio 5.26) but not in patients receiving OAC or OMC. CONCLUSIONS: All three treatment regimens were safe, well tolerated and highly effective for eradication of H. pylori and ulcer healing. Pre-treatment metronidazole resistance reduced the efficacy of OAM but did not affect the efficacy of OMC. (+info)
Randomized trial of omeprazole or ranitidine versus placebo in the prevention of chemotherapy-induced gastroduodenal injury.
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PURPOSE: Anticancer drugs may induce acute mucosal injury to stomach and duodenum. This study was planned to evaluate the efficacy of omeprazole or ranitidine in preventing such an injury. PATIENTS AND METHODS: Two hundred twenty-eight cancer patients with normal stomach and duodenum or with less than three erosions, who were selected to be treated with cyclophosphamide, methotrexate, and fluorouracil (90 breast carcinoma patients) or fluorouracil alone (138 colon carcinoma patients), were randomly assigned to treatment with omeprazole 20 mg, ranitidine 300 mg, or one placebo tablet a day. Seven days after the second course of chemotherapy (CT), the patients underwent a further esophagogastroduodenoscopy to evaluate the mucosal injury. Endoscopic findings were quantified on the basis of an arbitrary score, and the occurrence of epigastric pain or heartburn was assessed weekly. RESULTS: A significant difference was found among the three groups (P =.0032), as well as between pre- and postCT endoscopic findings (P =.00001). Endoscopic scores after CT were significantly higher than pretreatment scores in the placebo (P =.003) and ranitidine (P =.003) groups but not in the omeprazole group (P =.354). Acute ulcers were significantly less frequent in patients receiving omeprazole or ranitidine than in those receiving placebo (P =.0001 and P =.0315, respectively). Epigastric pain and/or heartburn were significantly less frequent in patients receiving omeprazole (P =.00124) or ranitidine (P =.038) than in those receiving placebo. CONCLUSION: Omeprazole is effective in preventing chemotherapy-induced gastroduodenal injury. Ranitidine is effective in reducing the frequency of ulcers and upper gastrointestinal symptoms but is not effective in preventing the global endoscopic worsening caused by chemotherapy. The different efficacy of omeprazole and ranitidine can be explained by their different pharmacodynamics. (+info)