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Upper Gastrointestinal Diseases (upper + gastrointestinal_disease)
Selected AbstractsInfluence of risk factors on endoscopic and clinical ulcers in patients taking rofecoxib or ibuprofen in two randomized controlled trialsALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 10 2001C. J. Hawkey Background: Highly selective inhibitors of the inducible cyclooxygenase-2 enzyme (coxibs) have been associated with less gastrotoxicity than nonselective NSAIDs in clinical studies. Aim: To evaluate the influence of risk factors for NSAID-induced gastrotoxicity on endoscopic and clinical ulcers in patients taking rofecoxib or ibuprofen. Methods: We analysed pooled data from two identical double-blind, randomized, 12-week endoscopy studies which compared the gastroduodenal toxicity of placebo (n=371), rofecoxib 25 mg (n=390), rofecoxib 50 mg (n=379), and ibuprofen 2400 mg daily (n=376) in patients with osteoarthritis. The potential risk factors evaluated were: age (< 65, , 65 years), sex, race (white, nonwhite), Helicobacter pylori status, presence of gastroduodenal erosions at baseline, a history of upper gastrointestinal disease, prior NSAID use within 30 days of study entry, and smoking. We also evaluated these factors for possible association with the development of clinically-evident gastrointestinal perforations, ulcers or bleeds over 12 weeks. Results: Across all treatment groups, the likelihood of detecting endoscopic ulcers, or of clinical presentation with a bleed, over 12 weeks was increased approximately 4,5-fold in patients with previous upper gastrointestinal disease (relative risk [95% confidence interval] of 4.2 [2.5, 7.1] for endoscopic ulcers; 3.8 [1.4, 10.6] for bleeds), or those with gastroduodenal erosions at baseline endoscopy (relative risk of 4.4 [2.6, 7.5] for endoscopic ulcers; 5.0 [1.9, 13.5] for bleeds). H. pylori infection did not increase the risk of endoscopic ulcers or bleeds (relative risk of 1.1 [0.8, 1.6] for endoscopic ulcers; 0.3 [0.1, 0.9] for bleeds). The risk factor sub-group effects were constant across all treatment groups, and the significantly higher incidence of ulcers with ibuprofen as compared to rofecoxib and placebo was maintained in all risk factor subgroups. Conclusions: Gastroduodenal erosions at baseline and a clinical history of upper gastrointestinal disease, but not H. pylori colonization, increased the risk for endoscopically-detected ulcers and clinical bleeds. Rofecoxib did not magnify the risk in any of the patient subgroups studied. [source] Overview of 50 years' progress in upper gastrointestinal diseasesJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 2009Neville D Yeomans Abstract There have been numerous and dramatic advances in our understanding of the mechanisms, causes and treatments of upper gastrointestinal diseases in the past 50 years. This review focuses on a few, not dealt with elsewhere in this special issue of the Journal. The early history of the recognition that nonsteroidal anti-inflammatory drugs are a major cause of peptic ulcer is described, with particular attention to the work of the pioneering Australian investigators. The story of the development of the histamine H2 -receptor antagonists and the proton pump inhibitors is also outlined. [source] Reflux esophagitis facilitates low Helicobacter pylori infection rate and gastric inflammationJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 8 2002Tae Jung Jang Abstract Background:Helicobacter pylori is regarded as an important pathogen in upper gastrointestinal diseases. However, little is known about the relationship between H. pylori infection and reflux esophagitis. Therefore, an investigation was undertaken in Korean subjects regarding the incidence of H. pylori infection, and a histopathological study of reflux esophagitis was also carried out. Methods: Analysis of gastric biopsy specimens was conducted for 73 patients with reflux esophagitis and 132 control subjects without reflux esophagitis. The H. pylori infection was assessed by using rapid urease test and the immunohistochemical method, and gastric mucosal morphologic change was analyzed according to the updated Sydney system. Results: The prevalence of H. pylori infection was significantly lower in patients with reflux esophagitis than in the non-reflux group. Grade of inflammation and glandular atrophy in the antrum and body were higher in patients in the non-reflux group compared with those in the reflux esophagitis group. Conclusions: It is suggested that H. pylori infection decreases the risk of reflux esophagitis by inducing atrophic gastritis. © 2002 Blackwell Publishing Asia Pty Ltd [source] Identification of the repeated number of C and D regions of tyrosine phosphorylation motifs in Helicobacter pylori cagA using multiplex PCRMICROBIOLOGY AND IMMUNOLOGY, Issue 10 2008Byungrak An ABSTRACT Various tyrosine phosphorylation motif regions of H. pylori cagA exist. The number of these regions was found to have some influence on cell signaling, which was found to be more pronounced when in D (ESS) region than in C (WSS) region. A molecular biological method with multiplex PCR was developed to distinguish C and D regions, and to identify the repetition number of tyrosine phosphorylation of the cagA gene. Multiplex PCR using novel primer sets was performed on 73 strains of H. pylori isolated from Korean patients with upper gastrointestinal diseases. The Western cagA was identified in only 3 strains (4.1%) whereas East Asia cagA was identified in 69 strains (94.5%). These results were reconfirmed through a sequencing analysis. The method developed in this study would be useful for monitoring the repeated number of C and D regions of tyrosine phosphorylation motifs in H. pylori cagA. [source] | ||||||||||