Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013395 (dyspepsia)
 4,879 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dyspepsia is a digestive syndrome distinct from (although frequently overlapping with) gastro-oesophageal reflux disease (GORD) and irritable bowel syndrome (IBS), which is characterised by various combinations of painful and non-painful symptoms arising from the epigastrium. Dyspepsia can be secondary to a variety of diseases, but in most instances it is idiopathic. Helicobacter pylori infection is responsible for the majority of peptic ulcers and of other diseases potentially associated with dyspepsia. Nevertheless, a causal role for H pylori infection in symptom occurrence has not been established. Experimental data indicate that H pylori eradication does not improve symptoms in the majority of dyspeptic patients. It has been proposed recently that H pylori negative patients should be managed according to their clinical presentation. Some reports suggest that taking into consideration the most relevant or "predominant" symptom may help to identify distinct subgroups among dyspeptic patients with different underlying pathophysiological abnormalities and different responses to treatment. Well designed and conducted prospective studies are needed to verify whether treatment of H pylori negative dyspeptic patients based on the predominant symptom actually is a cost effective approach.
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PMID:How should Helicobacter pylori negative patients be managed? 1045 34

This study determines the prevalence of Helicobacter pylori infection in a group of immigrants from East Africa with dyspepsia symptoms. Costs of treatment (including financial costs, adverse effects of treatment, and complexity of care) are compared for empiric treatment and treatment guided by serologic testing. Of the symptomatic patients, 93% had H. pylori antibodies. Empiric treatment of all patients with dyspepsia could reduce the cost of care by approximately half, with minimal risk to uninfected patients.
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PMID:Helicobacter pylori in immigrants from East Africa. 1049 Dec 48

Chronic ingestion of NSAIDs increases the risk for gastrointestinal complications, which range from dyspepsia to gastrointestinal bleeding, obstruction, and perforation. Among patients using NSAIDs, 0.1 to 2.0% per year suffer serious gastrointestinal complications. Patients who require analgesic therapy should be carefully assessed for the lowest possible dosage and shortest duration of NSAID use and for the potential of treatment with a non-NSAID pain reliever. These patients should also be assessed for factors that increase their risk of gastrointestinal complications, including increased age, concomitant anticoagulant or corticosteroid use, and past history of NSAID-associated gastrointestinal complications. The exact association between Helicobacter pylori infection and NSAID-related ulcer disease is unclear, and the routine testing and treatment of all NSAID using patients for H. pylori infection is not recommended at this time. NSAID-using patients who suffer from dyspepsia should have NSAIDs discontinued, the dosage changed, or be changed to a different class of NSAID. If NSAIDs cannot be discontinued, then an antisecretory agent should be initiated. Misoprostol prevents NSAID-associated gastrointestinal complications. Proton pump inhibitors are the most effective at healing NSAID-associated ulcers among patients who cannot discontinue NSAID therapy.
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PMID:Review article: nonsteroidal anti-inflammatory drug-associated gastrointestinal complications--guidelines for prevention and treatment. 1054 41

Epidemiological and pathophysiological studies, as well as clinical trials, attempting to identify a relationship between Helicobacter pylori infection and non-ulcer dyspepsia (NUD), or a subset of NUD, have produced inconsistent and confusing results. While it is possible that H. pylori eradication may be beneficial for symptom relief in a small proportion of patients, routine H. pylori testing and treatment in documented NUD is not currently widely accepted. Despite the lack of convincing evidence, the European Helicobacter pylori Study Group, an Asian Pacific Consensus Meeting, the American Digestive Health Foundation and the American Gastroenterology Association have all recommended considering H. pylori eradication in patients with NUD on a patient-by-patient basis. Recently, large prospective, randomised, double-blind, controlled clinical trials applying highly effective antimicrobial therapy have been conducted with 12 months follow-up. Although these well-designed studies have reached differing conclusions, the results have been largely negative. H. pylori eradication therapy in NUD will fail to relieve symptoms in most patients in the long term.
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PMID:Helicobacter pylori eradication in patients with non-ulcer dyspepsia. 1059 59

There is evidence that Helicobacter pylori infection up-regulates the expression of HLA class II molecules by gastric epithelial cells (GEC). In this study we evaluated whether GEC are capable of expression of costimulatory molecules in H. pylori gastritis. The expression of FasL by GEC, before and after eradication of H. pylori, was also studied. Thirty patients (23 men) aged 27-81 years (53.67 +/- 13.99 years (mean +/- s.d.)) with dyspepsia were studied. Upper gastrointestinal endoscopy was performed and six biopsies were obtained (antrum, n = 3; corpus, n = 3) for Campylobacter-Like Organisms (CLO) test and histology; 23 (16 men) were H. pylori+ and seven (all men) were H. pylori- by both methods and served as controls. Helicobacter pylori eradication therapy was given to H. pylori+ patients and all patients were re-endoscoped after 116 +/- 9 days. Formalin-fixed paraffin-embedded tissue sections were stained by the ABC immunoalkaline phosphatase method. In H. pylori gastritis HLA-DR was expressed and correlated with disease activity (P < 0.01). No HLA-DR was observed in controls. In H. pylori-eradicated patients significant decrease of HLA-DR was found (antrum, P < 0. 001). ICAM-1 was expressed by GEC in 80% of H. pylori+ patients; ICAM-1 expression did not correlate with gastritis parameters and decreased significantly after eradication (antrum, P < 0.01). B7-1 and B7-2 were expressed on H. pylori+ samples and their expression decreased after eradication, albeit not significantly. Weak epithelial expression of both B7 molecules was observed in all the controls. FasL was steadily expressed by GEC in both H. pylori+ and H. pylori- patients and remained almost unchanged after eradication. These findings suggest that GEC may acquire antigen-presenting cell properties in H. pylori infection through de novo expression of HLA-DR and costimulatory molecules. This seems to be attenuated after eradication and resolution of mucosal inflammation. The same cells exhibit the capacity to control the inflammatory process, probably by inducing apoptotic cell death to Fas-bearing infiltrating lymphocytes.
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PMID:Expression of HLA-DR, costimulatory molecules B7-1, B7-2, intercellular adhesion molecule-1 (ICAM-1) and Fas ligand (FasL) on gastric epithelial cells in Helicobacter pylori gastritis; influence of H. pylori eradication. 1069 18

Proton pump inhibitor (PPI)- based triple therapy has been a recent trend for treatment of Helicobacter pylori infection, with the PPI-amoxicillin-clarithromycin (PPI/AC) regimen being one of the most popular. We have reported the effectiveness of PPI/AC regimens in the Japanese population and have demonstrated that the effectiveness of 40 mg rabeprazole, a recently developed PPI, is similar to that of 40 mg of omeprazole and 60 mg of lansoprazole when used in combination with amoxicillin and clarithromycin. In this study, we focused on whether 20 mg of rabeprazole is effective in our patient population by comparing that dosage with 40 mg of rabeprazole and 60 mg of lansoprazole. In all, 308 H. pylori-infected patients [236 men and 72 women; age (mean +/- SEM) 49.3+/-0.6 years] with peptic ulcer disease (N = 270) or nonulcer dyspepsia (N = 38) were randomly assigned to one of three different PPI/AC regimens for seven days: LAC (N = 104), consisting of lansoprazole 30 mg twice a day, amoxicillin 500 mg three times a day, and clarithromycin 200 mg twice a day; RAC (N = 104), consisting of rabeprazole 20 mg twice a day, amoxicillin 500 mg three times a day, and clarithromycin 200 mg twice a day; and the R1/2AC regimen (N = 100), which included rabeprazole 10 mg twice a day, amoxicillin 500 mg three times a day, and clarithromycin 200 mg twice a day. Cure of the infection was determined by the [13C]urea breath test one month after completion of the treatment. Intention-to-treat based and per-protocol based cure rates for the LAC, RAC, and R1/2AC regimens were 82.7 (95% CI, 74-89) and 88.7% (81-94), 85.6 (77-92) and 89.8% (82-95), and 87.0 (79-93) and 89.7% (82-95), respectively. Although adverse effects were reported by 20.3% of the patients, these affected compliance in only five patients in the RAC and LAC regimens and none in the R1/2AC group. Overall complete compliance was achieved in 94.7% of interviewed patients. In conclusion, the effectiveness of the PPI/AC regimen with 20 mg of rabeprazole is comparable with and even safer than that of 40 mg of rabeprazole and 60 mg of lansoprazole in our patient population.
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PMID:Efficacy of reduced dosage of rabeprazole in PPI/AC therapy for Helicobacter pylori infection: comparison of 20 and 40 mg rabeprazole with 60 mg lansoprazole. 1069 17

A number of commercial ELISA kits are now available for detection of Helicobacter pylori infection. Generally, whereas the manufacturers have claimed high sensitivity and specificity, independent studies have often failed to confirm the results. The aim of this study was to independently evaluate the pylori DTect ELISA, a commercial kit for detection of H. pylori infection, in Australian patients with dyspepsia and reflux symptoms. Two hundred and nine consecutive patients (102 males and 107 females, mean age 52.8 years) who were referred for endoscopy due to upper gastrointestinal symptoms, but had not received anti-H. pylori therapy were enrolled. A 10 mL blood sample was obtained from each subject and used to evaluate the kit. The absorbance index (AI) was calculated from the mean of two readings of optical density (OD) of each serum sample. Eight biopsies from the gastric antrum (x3), body (x2), fundus (x2), and incisura (x1) were obtained from each patient for CLO-testing (x1), culture (x3), and histological examination (x4) for H. pylori. Overall, 84 (40.2%) patients were infected with H. pylori as determined by the biopsy-based "gold standard." The AIs ranged from 0 to 1.86; 0.12 to 1.86 in H. pylori positive patients and 0 to 1.49 in negative patients. The pylori DTect ELISA obtained an accuracy of 94 to 95% under AI ranges between 0.20 to 0.40, with the highest accuracy being 95% under AIs of 0.25 and 0.35. An AI of 0.25 was recommended as the best cut-off AI, with a sensitivity of 96.4%, specificity of 93.6%, positive predictive value of 91% and negative predictive value of 97.5%. It is concluded that the pylori DTect ELISA is accurate for detecting H. pylori infection in patients with dyspepsia and reflux symptoms in Australia, when an AI of 0.25 is taken as the cut-off value.
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PMID:High sensitivity and specificity of a laboratory-based serological test, pylori DTect ELISA, for detection of Helicobacter pylori infection. 1070 45

Three groups of children aged 4 to 14 years who complained of having dyspepsia were examined. Group 1 included 31 children without tuberculous infection; Group 2 comprised 30 newly tuberculosis-infected children; Group 3 consisted of 35 children who had an over one-year history of the infection. Esophagoduodenoscopy and biopsy indicated that the incidence of Helicobacter infection and gastritis was higher in children with tuberculous infection than in those without it and it was directly related to the duration of infection. The specific features of chronic gastritis in the infected children were the totality of gastric mucous lesion with more profound antral changes, the predominance of progressive gastritis, as appeared as neutrophilic infiltration, gastric mucous contamination with Helicobacter and Candida, and metaplasia.
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PMID:[Gastroduodenal mucosal morphological changes in tuberculosis-infected children]. 1071 60

The purpose of the study was to assess risk factors for intestinal metaplasia arising from H. pylori-related chronic gastritis in a subset of the population referred to endoscopic examinations due to dyspeptic complaints. We aimed specifically to establish whether H. pylori itself may be responsible for the occurrence of intestinal metaplasia and to which extent the metaplasia may be associated with life style factors such as cigarette smoking, alcohol consumption or dietary habits. The study was carried out in a sample of 1290 outpatients referred for the first time to gastroenterologic outpatient clinics in 6 university centers in Poland. The study methods covered standardized health interviews, endoscopy and histology of gastric antral specimens taken at endoscopy. The interviews performed by trained interviewers sought information on tobacco and alcohol intake, diet, socioeconomic status, and other variables. In non-ulcer dyspepsia subjects there was 54.9% H. pylori related gastritis and 25.1% of non-H. pylori-related gastritis. The corresponding rates in the group of ulcer dyspepsia were 67.5% and 20.5%. The increased risk of chronic gastritis in antrum was associated with Helicobacter pylori infection (OR = 2.28; 95% CI:1.93-2.69), and with gastric peptic ulcer (OR = 1.88; 95% CI:1.20-2.94). In the non-ulcer dyspepsia the prevalence of metaplasia was 11.1% and in ulcer dyspepsia 19.7%. The risk of intestinal metaplasia within antrum depended greatly upon the presence of gastric peptic ulcer (OR = 3.85; 95% CI:2.35-6.32) and increased with age (OR = 1.05; 95% CI:1.04-1.07), smoking cigarettes currently or in the past (OR = 1.42; 95% CI:1.10-1.84), higher frequency of drinking vodka (OR = 1.32, 95% CI:1.01-1.75) and antral chronic gastritis (OR = 1.31; 95% CI:1.00-1.70), however, it was inversely related to daily consumption of fresh fruits or vegetables (OR = 0.59; 95% CI:0.38-0.93). The results of the study suggest that there is no sufficient evidence supporting the hypothesis about an association between H. pylori gastritis and intestinal metaplasia, however, the transition of gastritis to metaplasia depends greatly on life style factors such as cigarette smoking or vodka drinking and is impeded by daily consumption of fresh fruits or vegetables.
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PMID:Effect of Helicobacter pylori infection, smoking and dietary habits on the occurrence of antrum intestinal metaplasia. Clinico-epidemiological study in Poland. 1072 Dec 69

The interest of gastroenterologists in the relationship between Helicobacter pylori and gastrointestinal motility emerges from the observation that Helicobacter pylori may be involved in the pathogenesis of functional dyspepsia and that a relatively large percentage of patients with dyspepsia may show impaired gastrointestinal motility. A number of studies have been published on the interaction between Helicobacter pylori infection and gastrointestinal motility with controversial results, and, therefore, there are no definite conclusions, as yet, as to whether Helicobacter pylori is able, at all, or in which degree, to influence the motility of the upper gastrointestinal tract. Motility of the upper gastrointestinal tract has been studied in Helicobacter pylori positive and negative individuals by means of manometry, scintigraphy, radio-opaque markers or by other, recently developed, procedures such as breath tests, ultrasonography, and barostat. The vast majority of studies do not support the hypothesis that Helicobacter pylori may influence gastrointestinal motility. Nearly all these studies are, however, affected by methodological problems related to the small numbers of patients, different methodological approaches, and to the well-known difficulties in studying both gastrointestinal motility and functional dyspepsia.
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PMID:Relationship of Helicobacter pylori infection with gastrointestinal motility. 1073 May 63


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