bluuebunny/crossref_metadata_2025_split huggingface dataset:
Second‐line treatment of Helicobacter pylori infection after dilution agar methods and PCR‐RFLP analysis
Authors: Masaoka T. , Suzuki Kurabayashi H., K. , Kamiya A. G. , Ishii H. 
Published: December 2004

SummaryBackground : After unsuccessful first‐line treatment of Helicobacter pylori infection, the percentage of clarithromycin‐resistant strains has been reported as between 30% and 70% in Japan and other countries. A high prevalence of clarithromycin‐resistant strains is reported to be associated with eradication failure.Aim : We examined antibiotic susceptibility testing using a combination of dilution agar methods with PCR‐restriction fragment length polymorphism (RFLP) analysis.Methods : We enrolled 41 patients in whom first‐line treatment with LAC (lansoprazole, amoxycillin and clarithromycin) was unsuccessful. Endoscopic biopsied specimens were used to examine antibiotic susceptibility to clarithromycin by dilution agar methods. PCR‐RFLP analysis was performed to determine the presence of point mutations, which are primarily responsible for resistance to clarithromycin.Results : Clarithromycin‐resistance rate after failure of the LAC regimen was 73.2%. Drug susceptibilities of three strains obtained by PCR‐RFLP analysis were different from those by dilution agar methods. One strain with MIC values to clarithromycin of 0.05 µg/mL had a point mutation, A2144G. This strain was not eradicated by repeating LAC, but was eradicated by substituting metronidazole for clarithromycin.Conclusions : Dilution agar methods should be combined with PCR‐RFLP analysis before second‐line eradication to increase the accuracy of clarithromycin‐susceptibility testing and to improve eradication efficacy.
Colorectal carcinoma and inflammatory bowel disease
Authors: Eaden J. 
Published: December 2004

SummaryThe risk of colorectal cancer for any patient with ulcerative colitis is estimated to be 2% after 10 years, 8% after 20 years and 18% after 30 years of disease. The relative risk of colorectal cancer in Crohn's colitis is approximately 5.6 and should raise the same concerns as in ulcerative colitis. Risk factors for colorectal cancer include disease duration, early onset, extensive disease, primary sclerosing cholangitis and a family history of sporadic colorectal cancer. All patients should have a review colonoscopy 8–10 years after diagnosis to establish the extent of the disease. Surveillance should begin 8–10 years after disease onset for pancolitis and 15–20 years after disease onset for left‐sided disease. Regular surveillance is recommended, with a screening interval every 3 years in the second decade of disease and annually by the fourth decade. Random biopsies should be taken at regular intervals with attention paid to dysplasia‐associated lesions or masses, irregular plaques, villiform elevations, ulcers and strictures. Dysplasia is recognized as a premalignant condition, but the likelihood of progression to cancer is difficult to predict. High‐grade dysplasia, confirmed by two expert gastrointestinal pathologists, is a strong indication for colectomy, as is low‐grade dysplasia, although the diagnosis of low‐grade dysplasia is unreliable. Surveillance programmes indicate that the overall 5‐year survival rate is higher in surveyed patients, although patients still present with Dukes C cancers or disseminated malignancy. Surveillance has huge socioeconomic implications. As surveillance is not 100% effective, alternative ways of reducing the cancer risk with chemopreventive agents, such as aminosalicylates, are being considered.
Aminosalicylates in inflammatory bowel disease
Authors: Hanauer S. B. 
Published: December 2004

SummaryAminosalicylate therapy for ulcerative colitis remains a foundational strategy for the induction and maintenance of remission for mild to moderate disease. Although it seems clear that topical mesalazine (mesalamine) is the most efficacious approach to distal ulcerative colitis, recent trials with orally delivered azo conjugates suggest that there may be an advantage over pH‐released mesalazine as a first‐line approach to active disease. No such comparisons are available for azo products and the prolonged‐release formulation, Pentasa. However, recent meta‐analyses have demonstrated that, although there is little difference in systemic exposure between marketed products, luminal concentrations may vary. In maintenance therapy, aminosalicylates remain the standard approach after aminosalicylate‐induced remission. A number of gaps remain in the evidence base with regard to the optimal dosing of oral mesalazine as a maintenance agent, whether oral mesalazine can maintain remissions after rectal mesalazine induction, and the dose–response and efficacy of aminosalicylates after steroid‐ or ciclosporin‐induced remissions. Although aminosalicylates have been advocated for several decades in Crohn's disease, a number of controversies have evolved since the original trials with sulfasalazine in active Crohn's disease. The original trials demonstrated benefits for sulfasalazine in colonic involvement, but controlled trial evidence for the role of sulfasalazine as maintenance therapy has not been as firmly established. In addition, although oral mesalazine has been demonstrated in controlled trials to be superior to placebo in mild to moderate disease, it is less efficacious than corticosteroids at inducing remissions. The maintenance benefits of mesalazine appear to be limited to patients ‘induced into remission’ with mesalazine and in some post‐operative settings.
Antibiotics and probiotics in inflammatory bowel disease
Authors: Kruis W. 
Published: December 2004

SummaryTreatment with antibiotics in inflammatory bowel disease has a long tradition and is widely used. The indications for antibiotic therapy are wide ranging, from specific situations such as abscesses or fistulae, to patients with severe disease (as an unspecific ‘protective’ measure), and to address the hypothesis that the enteric flora as a whole, or specific microorganisms such as mycobacteria, are involved in the pathogenesis of inflammatory bowel disease. The best‐studied single antibiotic compound is metronidazole. However, overall, the scientific basis for the use of antibiotics is limited, which may reflect a lack of interest from sponsors within the pharmaceutical industry. Despite this weak evidence base, antibiotics are a globally established therapeutic tool in inflammatory bowel disease. Growing evidence from human and animal studies points towards a pivotal pathogenetic role of intestinal bacteria in inflammatory bowel disease. In view of these experimental findings, clinical trials have been undertaken to elucidate the therapeutic effects of probiotics in inflammatory bowel disease. Probiotics are viable nonpathogenic microorganisms which confer health benefits to the host by improving the microbial balance of the indigenous microflora. So far, of the many candidates, one specific strain (Escherichia coli Nissle 1917) and a mixture of eight different bacteria have demonstrated convincing therapeutic efficacy in controlled studies. Maintenance therapy in ulcerative colitis and prevention therapy, as well as the treatment of pouchitis, have emerged as areas in which probiotic therapy offers a valid therapeutic alternative to current treatments. Further investigations may detect additional clinically effective probiotics and other clinical indications.
Bone disease in inflammatory bowel disease
Authors: Schulte C. M. S. 
Published: December 2004

SummaryInflammatory bowel disease (IBD) is associated with an increased incidence of osteoporosis. Osteoporosis with osteoporotic pain syndromes, fragility fractures and osteonecrosis accounts for significant morbidity and impacts negatively on the quality of life. It is generally agreed that there is a need to increase awareness for inflammatory bowel disease‐associated osteoporosis. However, the best ways in which to identify at‐risk patients, the epidemiology of fractures and an evidence‐based rational prevention strategy remain to be established. The overall prevalence of IBD‐associated osteoporosis is 15%, with higher rates seen in older and underweight subjects. The incidence of fractures is about 1 per 100 patient years, with fracture rates dramatically increasing with age. While old age is a significant risk factor, disease type (Crohn's disease or ulcerative colitis) is not related to osteoporosis risk. Corticosteroid use is a major variable influencing IBD‐associated bone loss; however, it is difficult to separate the effects of corticosteroids from those of disease activity. The recommendations in inflammatory bowel disease are similar to those for postmenopausal osteoporosis, with emphasis on lifestyle modification, vitamin D (400–800 IE daily) and calcium (1000–1500 mg daily) supplementation and hormone replacement therapy (oestrogens/selective oestrogen receptor modulators in women, testosterone in hypogonadal men). Bisphosphonates have been approved for patients with osteoporosis (T‐score < 2.5), osteoporotic fragility fractures and patients receiving continuous steroid medication. Data on the recently Food and Drug Administration‐approved osteoanabolic substance parathyroid hormone and on osteoprotegerin are promising in terms of both steroid‐induced and inflammation‐mediated osteoporosis, the key elements of inflammatory bowel disease‐associated bone disease.
Exploration of the genetic aetiology of inflammatory bowel disease — implications for diagnosis and therapy
Authors: Schreiber S. , Hanpe J. , Nikolaus S. , Foelsch U.R. 
Published: December 2004

SummaryGenomic technologies offer new approaches to the investigation of the aetiology and pathophysiology of inflammatory bowel disease. An important field relevant to inflammatory bowel disease therapy is the pharmacogenetic investigation of gene variations that may predict responses to certain medications in order to target these therapeutic interventions more precisely. To date, only about 12 000 of the estimated 30 000–50 000 human genes have been characterized. Therefore, the use of techniques for a global analysis of gene expression may allow the identification of new pathways or molecules in the therapeutic mechanisms of drugs. Recently, NOD2 has been identified as the first disease gene in inflammatory bowel disease. DLGS and OCTN‐1 have been named as further disease genes. Although the detection of disease‐associated variants has greatly advanced our understanding of the primary events that lead to the development of inflammatory bowel disease in a subgroup of patients with Crohn's disease, the implications of the findings for diagnostic and therapeutic algorithms are less clear. However, it appears that there is a clear association between certain subphenotypes of Crohn's disease and the disease‐associated variants in the NOD2 gene. It can be anticipated that genomic findings will profoundly influence the future therapy of inflammatory bowel disease.
Systemic and topical steroids in inflammatory bowel disease
Authors: Schölmerich J. 
Published: December 2004

SummarySteroids are still widely used in the treatment of inflammatory bowel diseases. Pharmacological studies have shown that there is no major abnormality in the pharmacokinetics of steroids in these disorders. Foam preparations with rectal application decrease the bioavailability to low levels, eliminating systemic complications. For oral use, ‘nonsystemic’ steroids have been developed. In ulcerative colitis, steroids are rarely needed as 5‐aminosalicylates are effective in the majority of patients. This is true for rectal application in distal colitis, as well as in more extensive disease. In Crohn's disease, steroids are more often used; however, in population‐based studies, less than 50% of patients have been treated with steroids, as there are alternative treatments available for the large group of patients with mild to moderate activity. For those patients needing steroid treatment, budesonide seems to be a good choice in active disease, but has not shown convincing effects in the maintenance of remission over longer periods of time. There is no place for long‐term steroid treatment in ulcerative colitis and very little in Crohn's disease — immunosuppression with azathioprine or related drugs is certainly the better alternative.
Gut flora and inflammatory bowel disease
Authors: Marteau P. , Lepage P. , Mangin I. , Suau A. , Doré J. , Pochart P. , Seksik P. 
Published: December 2004

SummaryThe pathogenesis of inflammatory bowel disease involves interactions between the host susceptibility, mucosal immunity and intestinal microflora. There is therefore great interest in the changes in the endogenous flora in inflammatory bowel disease patients and in the establishment of potential genetic variations in host responses to endogenous bacteria. In this review, we summarize the modifications in the various regional ecosystems in the gastrointestinal tract during inflammatory bowel disease (luminal bacteria in faeces or inside the gastrointestinal tract, bacteria in mucus and bacteria directly attached to the mucosa). Results were obtained following a ‘candidate microorganism strategy’ and, as is occurring increasingly frequently, following a ‘full description strategy’, which has progressed largely due to the development of culture‐independent techniques. The possibility of modifying the ecosystem using prebiotics or probiotics offers hope for new treatment developments, particularly in the prevention of relapse.
Daily use of non‐steroidal anti‐inflammatory drugs is less frequent in patients with Barrett's oesophagus who develop an oesophageal adenocarcinoma
Authors: Tsibouris P. , Hendrickse M. T. , Isaacs P. E. T. 
Published: December 2004

SummaryBackground : Non‐steroidal anti‐inflammatory drugs use may protect against development of oesophageal adenocarcinoma.Aim : To define the consequences of non‐steroidal anti‐inflammatory drugs use in patients with Barrett's oesophagus.Methods : Records of all Barrett's oesophagus/oesophageal adenocarcinoma patients examined in Blackpool‐Wyre‐Fylde area were reviewed. All surviving patients completed validated questionnaires.Results : Use of non‐steroidal anti‐inflammatory drugs of any type and at any frequency was more prevalent in Barrett's oesophagus patients [147 (38%) Barrett's oesophagus vs. 30 (26%) oesophageal adenocarcinoma, P = 0.02]. Daily use of non‐steroidal anti‐inflammatory drugs was more prevalent in Barrett's oesophagus patients [88 (23%) Barrett's oesophagus vs. 14 (12%) oesophageal adenocarcinoma, P = 0.02], due to more prevalent consumption of non‐aspirin non‐steroidal anti‐inflammatory drugs [48 (13%) Barrett's oesophagus vs. four (4%) oesophageal adenocarcinoma, P =0.009]. There was no difference between the two groups in usage of either daily low‐dose aspirin or of occasional non‐steroidal anti‐inflammatory drugs. In logistic regression analysis any use of non‐steroidal anti‐inflammatory drugs [odds ratio (OR) = 0571 (95% CI: 0.359–0.909), P = 0.018] and daily use of non‐aspirin non‐steroidal anti‐inflammatory drugs [OR = 0.297 (95% CI: 0.097–0.911), P = 0.034] were significant protective factors. Non‐steroidal anti‐inflammatory drugs use did not affect the survival of oesophageal adenocarcinoma patients. Oesophageal adenocarcinoma and Barrett's oesophagus consuming non‐steroidal anti‐inflammatory drugs did not differ in upper gastrointestinal bleeding [26 (15%) non‐steroidal anti‐inflammatory drugs consumers vs. 29 (9%) non‐consumers, P = 0.08], oesophageal ulcers [31 (18%) non‐steroidal anti‐inflammatory drug consumers vs. 49 (15%) non‐consumers, P = 0.43] or stricturing [19 (11%) non‐steroidal anti‐inflammatory drug consumers vs. 41 (13%) non‐consumers, P = 0.58].Conclusions : (i) Daily use of non‐steroidal anti‐inflammatory drugs is more prevalent in Barrett's oesophagus than oesophageal adenocarcinoma patients, because of a more prevalent use of non‐aspirin non‐steroidal anti‐inflammatory drugs. (ii) Use of non‐steroidal anti‐inflammatory drugs in Barrett's oesophagus patients is safe if acid suppression is adequate.
Differential effects of two types of antidepressants, amitriptyline and fluoxetine, on anorectal motility and visceral perception
Authors: Siproudhis L. , Dinasquet M. , Sébille V. , Reymann J. M. , Bellissant E. 
Published: December 2004

SummaryBackground : Although antidepressants are used for functional gastrointestinal disorders, the mechanisms of their effects on gut are incompletely understood.Aim : To assess the effects of two types of antidepressants (tricyclic, serotoninergic) on anorectal motility and visceral perception.Methods : A placebo‐controlled, randomized, double‐blind, crossover study was performed in 12 healthy male volunteers who received a single oral dose of amitriptyline (80 mg), fluoxetine (40 mg) or placebo. Drug effects were assessed using phasic isobaric distensions of the rectum with an electronic barostat (11 levels from 1 to 51 mmHg) 4 h after drug intake. Maximal rectal volume and pressure, mean and residual pressures at upper anal canal, mean pressure at lower anal canal, defecation sensation (5‐level scale) and visceral perception (visual analogue scale) were recorded at each level of distending pressure.Results : Ten subjects completed the study. Compared with placebo, neither amitriptyline nor fluoxetine modified rectal compliance or visceral perception. Compared with placebo, antidepressants significantly reduced mean and residual pressures at upper anal canal (−18%, P = 0.0019, and −27%, P = 0.0002, respectively, for amitriptyline; −26%, P = 0.0001, and −33%, P = 0.0001, respectively, for fluoxetine) whereas only amitriptyline significantly reduced mean pressure at lower anal canal (−16%, P = 0.0008).Conclusion : Both antidepressants similarly relaxed the internal anal sphincter, probably through a non‐specific mechanism, without modifying visceral perception. Only amitriptyline relaxed the external anal sphincter.
Rapid improvement of bone metabolism after infliximab treatment in Crohn's disease
Authors: Franchimont N. , Putzeys V. , Collette J. , Vermeire S. , Rutgeerts P. , De Vos M. , Van Gossum A. , Franchimont D. , Fiasse R. , Pelckmans P. , Malaise M. , Belaiche J. , Louis E. 
Published: December 2004

SummaryBackground : Crohn's disease is associated with low bone mineral density and altered bone metabolism.Aim : To assess the evolution of bone metabolism in Crohn's disease patients treated with infliximab.Methods : We studied 71 Crohn's disease patients treated for the first time with infliximab for refractory Crohn's disease. Biochemical markers of bone formation (type‐I procollagen N‐terminal propeptide, bone‐specific alkaline phosphatase, osteocalcin) and of bone resorption (C‐telopeptide of type‐I collagen) were measured in the serum before and 8 weeks after infliximab therapy and compared with values in a matched healthy control group.Results : Eight weeks after treatment with infliximab, a normalization of bone markers was observed with a median increase in formation markers of 14–51% according to marker and a lower but significant decrease in resorption marker (median 11%). A clinically relevant increase in bone formation markers was present in 30–61% of patients according to the marker. A clinically relevant decrease in C‐telopeptide of type‐I collagen was present in 38% of patients. No association was found with any tested demographic or clinical parameter.Conclusion : Infliximab therapy in Crohn's disease may rapidly influence bone metabolism by acting either on bone formation or bone resorption. This improvement seems to be independent of clinical response to infliximab.
Esomeprazole 20 mg on‐demand is more acceptable to patients than continuous lansoprazole 15 mg in the long‐term maintenance of endoscopy‐negative gastro‐oesophageal reflux patients: the COMMAND Study
Authors: Tsai H. H. , Chapman R. , Shepherd A. , McKeith D. , Anderson M. , Vearer D. , Duggan S. , Rosen J. P. 
Published: December 2004

SummaryBackground : Symptom relief, through adherence to appropriate maintenance therapy, is the sole objective of treatment for patients with endoscopy‐negative gastro‐oesophageal reflux disease.Aim : To compare the efficacy of ‘on‐demand’ treatment with esomeprazole 20 mg vs. continuous treatment with lansoprazole 15 mg daily in patients with endoscopy‐negative gastro‐oesophageal reflux disease.Methods : Endoscopy‐negative gastro‐oesophageal reflux disease patients who achieved complete resolution of heartburn after short‐term (2–4 weeks) treatment with esomeprazole 20 mg (n = 774) were randomized to receive either esomeprazole 20 mg on‐demand (n =311) or lansoprazole 15 mg continuous daily treatment (n = 311) for 6 months.Results : Significantly more patients were willing to continue taking esomeprazole on‐demand than lansoprazole continuous therapy after 6 months (93% vs. 88%; P = 0.02). This superior outcome was achieved despite patients on esomeprazole requiring medication only 38% as often as those on lansoprazole, leading to direct cost savings of more than one‐third (36%). Furthermore, patients receiving esomeprazole 20 mg on‐demand were more satisfied with their treatment after 1 month compared with patients taking lansoprazole 15 mg continuously.Conclusions : In patients with endoscopy‐negative gastro‐oesophageal reflux disease, esomeprazole 20 mg on‐demand is more acceptable to patients and is an economically more effective treatment than lansoprazole 15 mg continuously.
Review article: tegaserod — the global experience
Authors: Chey W. D. 
Published: December 2004

SummaryStudies from the Western hemisphere have established the efficacy and safety of tegaserod in women with irritable bowel syndrome and constipation. This review summarizes the results of recent studies from around the world that confirm the efficacy and safety of tegaserod, and expand our understanding of the role of this drug in the treatment of patients with irritable bowel syndrome.
Review article: the overlap between functional dyspepsia and irritable bowel syndrome — a tale of one or two disorders?
Authors: Cremonini F. , Talley N. J. 
Published: December 2004

SummaryFunctional dyspepsia and irritable bowel syndrome are currently considered to be two separate nosological entities. However, the overlap of symptoms and the evidence of a number of common pathophysiological characteristics suggest that functional dyspepsia and irritable bowel syndrome may be different presentations of the same disorder. In this review, we critically appraise points in common, as well as differences, in the epidemiology, pathophysiology and response to treatment of functional dyspepsia and irritable bowel syndrome. Population‐based studies and large case series show that one‐ to two‐thirds of subjects with irritable bowel syndrome have symptoms that overlap with functional dyspepsia. Symptom analyses have generally failed to support functional dyspepsia and irritable bowel syndrome as separate entities. An exaggerated motor response to meals, delayed gastric emptying and abnormal small bowel and colonic transit can all be found in subsets of functional dyspepsia and irritable bowel syndrome, and are not exclusive to either condition. Visceral hypersensitivity is a common feature to both entities and seems unlikely to be site or disease specific. There is good evidence for the post‐infectious development of irritable bowel syndrome, and this may also apply in functional dyspepsia. Psychiatric comorbidities are similar in functional dyspepsia and irritable bowel syndrome. Several common drug classes (prokinetics, visceral analgesics, psychoactive agents) may similarly improve both functional dyspepsia and irritable bowel syndrome symptoms. The evidence available suggests that at least subsets of functional dyspepsia and irritable bowel syndrome represent different manifestations of a single entity. The identification of common pathophysiological targets for therapy should be pursued in future research.