20 research outputs found

    Ulcer recurrence after gastric surgery: Is Helicobacter pylori the culprit?

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    Objectives: Helicobacter pylori is the most important cause of recurrent peptic ulcer disease. However, its role in ulcer recurrence after peptic ulcer surgery is unclear. We aimed at studying the prevalence and distribution of H. pylori in patients who had undergone peptic ulcer surgery, and any association between H. pylori infection and ulcer recurrence in these patients. Methods: Patients with previous vagotomy or partial gastrectomy presenting with dyspepsia or ulcer bleeding were recruited. Ulcer recurrence was documented by endoscopy. Biopsy specimens were taken from the gastric remnant and gastroenteric anastomosis in patients with previous partial gastrectomy, or from the antrum and corpus in vagotomized patients. H. pylori infection was detected by either a positive rapid urease test or the presence of the bacteria on histology. Results: Ninety-three patients were studied; 73 patients (78%) had partial gastrectomy and 20 (22%) had vagotomy with drainage. H. pylori infection was documented in 36 patients (49%) in the gastrectomy group and in 13 (65%) in the vagotomy group. Thirty-six patients in the gastrectomy group had recurrent ulcers and 15 (42%) of them had H. pylori infection. Twelve patients in the vagotomy group had recurrent ulcers and eight (67%) of them were H. pylori positive. The prevalence of H. pylori infection did not differ between patients with or without ulcer recurrence. Conclusion: H. pylori infection cannot account for ulcer recurrence after peptic ulcer surgery.link_to_subscribed_fulltex

    Effect of Helicobacter pylori eradication on treatment of gastro-oesophageal reflux disease: A double blind, placebo controlled, randomised trial

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    Background: The role of Helicobacter pylori eradication in the management of gastro-oesophageal reflux disease (GORD) is controversial. We hypothesised that H pylori eradication leads to worsened control of reflux disease. Methods: Consecutive patients with weekly reflux symptoms were prospectively recruited for endoscopy and symptom evaluation. Patients were enrolled if they had H pylori infection and required long term acid suppressants. Eligible patients were randomly assigned to omeprazole triple therapy (HpE group) or omeprazole with placebo antibiotics (Hp+ group) for one week. Omeprazole 20 mg daily was given for eight weeks for healing of oesophagitis and symptom relief. This was followed by a maintenance dose of 10 mg daily for up to 12 months. The primary study end point was the probability of treatment failure within 12 months, which was defined as either incomplete resolution of symptoms or oesophagitis at the initial treatment phase, or relapse of symptoms and oesophagitis during the maintenance phase. Predictors of treatment failure were determined by Cox's proportional hazards model. Results: A total of 236 GORD patients were screened and 113 (47.9%) were positive for H pylori; 104 (92%) patients were included in the intention to treat analysis (53 in the HpE group and 51 in the Hp+ group). Thirty one patients (30%) had erosive oesophagitis at baseline. H pylori was eradicated in 98% of the HpE group and in 3.9% of the Hp+ group. Overall, 15 patients (28.3%) in the HpE group and eight patients (15.7%) in the Hp+ group had treatment failure. The 12 month probability of treatment failure was 43.2% (95% confidence interval (CI) 29.9-56.5%) in the HpE group and 21.1% (95% CI 9.9-32.3%) in the Hp+ group (log rank test, p = 0.043). In the Cox proportional hazards model, after adjustment for the covariates age, sex, erosive oesophagitis, hiatus hernia, degree of gastritis, and severity of symptoms at baseline, H pylori eradication was the only predictor of treatment failure (adjusted hazard ratio 2.47 (95% CI 1.05-5.85)). Conclusion: H pylori eradication leads to more resilient GORD.link_to_subscribed_fulltex

    Noyori asymmetric hydrogenation

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    Is non-Helicobacter pylori, non-NSAID peptic ulcer a common cause of upper GI bleeding? A prospective study of 977 patients

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    Non-Helicobacter pylori, non-NSAID ulcer is relatively common in Western countries. Whether it is a significant problem in the Orient is unclear. The aim of this study was to investigate the incidence of non-H pylori, non-NSAID ulcers presenting with GI bleeding. A prospective study was done of 1675 consecutive patients presenting with upper GI bleeding over a period of 12 months. Upper endoscopy was performed with biopsy specimens taken from the antrum and body of the stomach for a biopsy urease test (BUT) and histology for detection of H pylori. Exposure to nonsteroidal anti-inflammatory drugs (NSAID) or aspirin within 4 weeks of hospitalization was carefully scrutinized. A 6-week course of treatment with an H2-receptor antagonist was prescribed for patients who did not use an NSAID and had a negative BUT result. Follow-up endoscopy was performed to confirm H pylori status with a BUT and histology. Positive histology at either initial or follow-up endoscopy was used as the standard for diagnosing H pylori infection. Among 977 patients who were found to have ulcer bleeding, 434 (44%) had exposure to aspirin or an NSAID. Of the 543 non-NSAID users, 431 (79.4%) had a positive BUT and 112 (20.6%) were BUT negative on initial endoscopy. Eighty-nine of 112 patients who were NSAID negative, BUT negative returned for follow-up endoscopy. Forty-nine of 89 (55.1%) were found to have a positive BUT and positive histology at follow-up endoscopy. Only 40 of 977 (4.1%) patients admitted with ulcer bleeding were confirmed to have non-H pylori, non-NSAID ulcers. Non-H pylori, non-NSAID bleeding ulcer is uncommon. A negative BUT is unreliable for exclusion of H pylori infection during the acute phase of ulcer bleeding.link_to_subscribed_fulltex

    Randomized trial of low-dose misoprostol and naproxen vs. nabumetone to prevent recurrent upper gastrointestinal haemorrhage in users of non-steroidal anti-inflammatory drugs

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    Background: Prophylactic misoprostol or non-steroidal anti-inflammatory drugs (NSAIDs) with low gastric toxicity (nabumetone) has been shown to reduce mucosal injury. Aim: To compare nabumetone vs. co-therapy of naproxen with low-dose misoprostol for secondary prevention of upper gastrointestinal bleeding in NSAID users. Methods: NSAID users presenting with upper gastrointestinal bleeding were enrolled if they required long-term NSAIDs. After ulcer healing, they were randomized to receive: naproxen (500-1000 mg/day) and misoprostol (200 μg b.d.), or nabumetone (1000-1500 mg/day) and placebo misoprostol for 24 weeks. The primary end-point was recurrent upper gastrointestinal bleeding. The secondary end-point was the proportion of patients suffering from major gastrointestinal events including ulcer bleeding, symptomatic ulcers and severe dyspepsia. Results: A total of 90 patients were included in the intention-to-treat analysis (misoprostol/naproxen 45, nabumetone 45). Recurrent bleeding occurred in 10 patients (22.2%) receiving misoprostol/naproxen compared with three (6.7%) receiving nabumetone (relative risk 3.33, 95% CI: 0.98-11.32, P = 0.069). The proportion of patients suffering from major gastrointestinal events at 24 weeks was 31.1% in the misoprostol/naproxen group and 28.9% in the nabumetone group. Conclusions: Misoprostol/naproxen is not superior to nabumetone for secondary prevention of upper gastrointestinal bleeding. Neither low-dose misoprostol nor nabumetone is adequate for high-risk NSAID users.link_to_subscribed_fulltex

    Atrophy and intestinal metaplasia one year after-cure of H. pylori Infection: A prospective, randomized study

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    Background and Aims: Helicobacter pylori-infected gastric mucosa evolves through stages of chronic gastritis, intestinal metaplasia (IM), glandular atrophy (GA), and dysplasia before carcinoma develops. We studied if H. pylori eradication would alter the course of premalignant histologic changes in the stomach. Methods: Volunteers from the Yantai County in China underwent upper endoscopy with biopsy specimens obtained from the antrum and corpus. H. pylori-infected subjects were randomized to receive either a 1-week course of omeprazole, amoxicillin, and clarithromycin (OAC) or placebo. At 1 year, endoscopies with biopsies were repeated. Results: A total of 587 H. pylori- infected subjects were randomized to OAC (n = 295) and placebo (n = 292). At 1 year, H. pylori was eradicated in 226 subjects assigned to OAC. In the placebo group, 245 patients remained H. pylori infected. Analysis of paired samples obtained from the same patients showed that acute and chronic gastritis decreased in both the antrum and corpus after H. pylori eradication (P < 0.001) and activity of IM decreased in antrum (P = 0.014). In the H. pylori-infected group, antral biopsy specimens had more pronounced acute gastritis (P = 0.01), whereas corpus specimens showed increased acute and chronic gastritis (P < 0.001) and a marginal increase in GA (P = 0.052). When histologic changes were compared between the 2 groups, decrease in acute and chronic gastritis was more frequent after H. pylori eradication (P < 0.001) but changes in IM were similar. In the H. pylori-infected group, increase in GA was seen in the corpus (P = 0.01). Conclusions: At 1 year, H. pylori eradication is beneficial in preventing progression of pathologic changes of the gastric mucosa.link_to_subscribed_fulltex

    Long-term outcome of Helicobacter pylori-negative idiopathic bleeding ulcers: A prospective cohort study

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    Background & Aims: Helicobacter pylori-negative idiopathic ulcers are increasingly recognized. The secular trend and long-term outcome of this condition are unknown. Methods: We prospectively studied consecutive patients with bleeding gastroduodenal ulcers from January to December 2000. The incidence and etiology of ulcers during this period were compared with that between September 1997 and August 1998. H pylori-negative idiopathic ulcers were defined as negative tests for H pylori, no exposure to analgesics within 4 weeks, and absence of other risk factors for ulcers. After the ulcers had healed, patients with H pylori-negative idiopathic ulcers and patients with H pylori ulcers who received eradication therapy were followed up for 12 months without anti-ulcer drugs. Results: Six hundred thirty-eight patients had bleeding ulcers: 213 (33.4%) were H pylori ulcers, and 120 (18.8%) were H pylori-negative idiopathic ulcers (vs 480 [50.3%] H pylori ulcers and 40 [4.2%] H pylori-negative idiopathic ulcers in 1997-1998; P <. 001). H pylori-negative idiopathic ulcers accounted for 16.1% of patients who were admitted for bleeding and 42.4% of patients who bled while in the hospital (P <. 0001); 28.3% of patients with H pylori-negative idiopathic ulcers had histologic evidence of past H pylori infection. The probability of recurrent ulcer complications in 12 months was 13.4% (95% CI: 7.3%-19.5%) in patients with H pylori-negative idiopathic ulcers and 2.5% (95% CI: 0.4%-4.6%) in patients with H pylori ulcers who received eradication therapy (P =. 0002). Conclusions: The incidence of H pylori-negative idiopathic bleeding ulcers is rising. These ulcers are prone to recurrent complications. © 2005 by the American Gastroenterological Association.link_to_subscribed_fulltex

    Incidence of gastroesophageal malignancy in patients with dyspepsia in Hong Kong: Implications for screening strategies

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    Background: A "test-and-treat" strategy for H pylori infection has been recommended in Europe and North America as safe and cost-effective for management of patients with dyspepsia. The primary aim of this study was to determine the frequency of gastroesophageal cancer in 2 groups of patients with dyspepsia: those 45 years of age or younger without "alarm" symptoms (low-risk group) and patients over 45 years of age or any patient with "alarm" symptoms (high-risk group). A secondary aim was to determine the frequency of gastric cancer among patients in the low-risk group with or without a positive serology for H pylori. Methods: Patients with persistent dyspepsia were recruited from 4 regional hospitals in Hong Kong. Those in the low-risk group were evaluated for H pylori by using a whole blood serology test; they underwent endoscopy within 1 week.Those in the high-risk group and those taking non-steroidal anti-inflammatory drugs (NSAIDs) underwent endoscopy promptly. Alarm symptoms were as follows: weight loss (10 or more pounds over 8 weeks), recurrent vomiting, dysphagia, bleeding, or anemia. Results: Of 2627 patients enrolled, 1017 were in the low-risk group and 1610 in the high-risk group. Twenty-three patients (0.9%) had gastroesophageal cancers (20 gastric, 3 esophageal). Four patients with cancer (17.4%) were in the low-risk group (3 gastric, 1 esophageal); all except the patient with esophageal cancer had a positive serology test. In the high-risk group, 19 patients had cancer (17 gastric, 2 esophageal). Conclusion: Gastric cancer is relatively frequent among young patients with dyspepsia who have no alarm features in Hong Kong.This finding raise concerns as to the safety of the "test-and-treat" strategy for the management of patients with dyspepsia in Asia.link_to_subscribed_fulltex

    Clopidogrel versus aspirin and esomeprazole to prevent recurrent ulcer bleeding

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    BACKGROUND: Concurrent therapy with a proton-pump inhibitor is a standard treatment for patients receiving aspirin who are at risk for ulcer. Current U.S. guidelines also recommend clopidrogel for patients who have major gastrointestinal intolerance of aspirin. We compared clopidogrel with aspirin plus esomeprazole for the prevention of recurrent bleeding from ulcers in high-risk patients. METHODS: We studied patients who took aspirin to prevent vascular diseases and who presented with ulcer bleeding. After the ulcers had healed, we randomly assigned patients who were negative for Helicobacter pylori to receive either 75 mg of clopidogrel daily plus esomeprazole placebo twice daily or 80 mg of aspirin daily plus 20 mg of esomeprazole twice daily for 12 months. The end point was recurrent ulcer bleeding. RESULTS: We enrolled 320 patients (161 patients assigned to receive clopidogrel and 159 to receive aspirin plus esomeprazole). Recurrent ulcer bleeding occurred in 13 patients receiving clopidogrel and 1 receiving aspirin plus esomeprazole. The cumulative incidence of recurrent bleeding during the 12-month period was 8.6 percent (95 percent confidence interval, 4.1 to 13.1 percent) among patients who received clopidogrel and 0.7 percent (95 percent confidence interval, 0 to 2.0 percent) among those who received aspirin plus esomeprazole (difference, 7.9 percentage points; 95 percent confidence interval for the difference, 3.4 to 12.4; P=0.001). CONCLUSIONS: Among patients with a history of aspirin-induced ulcer bleeding whose ulcers had healed before they received the study treatment, aspirin plus esomeprazole was superior to clopidogrel in the prevention of recurrent ulcer bleeding. Our finding does not support the current recommendation that patients with major gastrointestinal intolerance of aspirin be given clopidogrel. Copyright © 2005 Massachusetts Medical Society.link_to_subscribed_fulltex
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