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)

Helicobacter pylori is the most common bacterial pathogen world-wide and has been identified in all countries. As long-term infection with H. pylori could potentially lead to duodenal or gastric ulcer disease, asymptomatic chronic gastritis, chronic dyspepsia, or gastric malignancy, including both adenocarcinoma and B-cell lymphoma, a large number of different treatment regimens aimed at eradicating H. pylori has been evaluated and reported. Despite numerous H. pylori treatment studies the optimum regimen for its eradication remains unclear. A treatment regimen, which is effective, safe and inexpensive could be used widespread and reduce the risks of the long-term complications of infection. In this study we compared the efficacy, side effects and cost-effectiveness of 12 different therapy regimens for H. pylori eradication by using meta-analysis methodology. 486 patients (256 male, 230 female; mean age 40.8 years) with H. pylori associated duodenal ulcer (n = 140), gastritis (n = 254), gastroduodenitis (n = 92) were treated with 12 different therapy-regimens. Endoscopy was performed at baseline and 6 weeks after discontinuation of eradication therapy. H. pylori status was assessed by urease test and histology. The therapy with a H2-receptor antagonist is less effective than the triple therapies with omeprazole or lansoprazole. Bismuth-based triple therapies have a mean overall eradication rate of 68%, but are limited by frequent side effects causing poor drug compliance.
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PMID:[Meta-analysis of determining the pathogen eradicating efficacy of various therapeutic regimens in Helicobacter pylori infection]. 1002 50

The non-invasive urea breath test can demonstrate the presence of Helicobacter pylori infection with the same accuracy as invasive methods (histology, rapid urease test, culture), but with less distress and inconvenience to the patient. It is evident that this test can and should substitute invasive methods in patients with uncomplicated duodenal ulcer, in those with non-ulcer dyspepsia and in all who have gastrointestinal disorders that do not require endoscopic examination. The urea breath test has a primary role for determining the success of eradication therapy. It is ideal for short- and long-term follow-up, particularly in the case of duodenal ulcer, which is strictly related to the presence of Helicobacter pylori. In serious disease, when endoscopic examination is mandatory, such as complicated ulcer or mucose associated lymphoid tissue lymphoma, the urea breath test can still improve the diagnostic accuracy of Helicobacter pylori infection as it does not imply sampling error, to which biopsy is subject.
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PMID:Diagnosis of Helicobacter pylori infection: non-invasive diagnostic tests. 1007 63

Omeprazole combined with 2 antimicrobials has been suggested as a first-line option for Helicobacter pylori eradication in recent years. However, controversy exists regarding the efficacy of this protocol. This open-label, prospective clinical study investigated the efficacy of omeprazole-based triple therapy for H pylori eradication in 518 patients with H pylori-positive functional dyspepsia with or without duodenal ulcer. Amoxicillin, macrolides (clarithromycin or roxithromycin), and nitroimidazoles (metronidazole, ornidazole, or tinidazole) were the antibiotics used in the study. Nonulcer patients were randomly assigned to 1 of 8 different treatment protocols and duodenal ulcer patients were randomly assigned to 1 of 4 different treatment protocols consisting of omeprazole (20 mg once daily for nonulcer patients, 20 mg twice daily for ulcer patients for 14 days) with a combination of 2 of the above antimicrobials (for 10 days). H pylori infection was assessed by histologic findings and a rapid urease test before therapy and 4 weeks after therapy ended. Four hundred fifty-nine patients completed their regimens; 327 had functional dyspepsia (180 men, 147 women; median age, 39 years; range, 18 to 70 years) and 132 had ulcers (81 men, 51 women; median age, 40 years; range, 18 to 70 years). Eradication of H pylori was achieved in 58.8% (270 of 459) of all patients, 58.1% (190 of 327) of nonulcer dyspeptic patients, and 60.6% (80 of 132) of duodenal ulcer patients. The eradication rate varied from 47.2% to 69.4% in different treatment protocols. There were no statistically significant differences in eradication rates in any treatment group. All drugs were generally well tolerated in all groups, and no patient discontinued treatment because of side effects. Therapy with omeprazole and 2 antimicrobials for H pylori had limited efficacy in a Turkish population. The reason for these results, which conflict with those of other studies, is not clear. Further investigations of regimens for the eradication of H pylori in our population are necessary.
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PMID:Efficacy of omeprazole plus two antimicrobials for the eradication of Helicobacter pylori in a Turkish population. 1111 61

Sera of 223 dyspeptic patients with endoscopic findings of nonulcer dyspepsia (72%), gastric ulcer (15%) and duodenal ulcer (13%) were tested for antibodies against Helicobacter pylori with an enzyme immunoassay and an immunoblot technique using lysates of Helicobacter pylori cells as antigen source. One hundred and fifty-one (68%) sera were found to be positive for Helicobacter pylori IgG with both methods; 5% of the positive results in the enzyme immunoassay were false-positive due to cross-reactions mainly of proteins with a molecular mass of 43-66 kDa. Since cross-reactivity not only reduces the diagnostic value of the immunoassay but also complicates evaluation of the immunoblot results, an attempt was made to overcome these problems by using specific purified recombinant proteins instead of the crude cell preparations as antigens. Of the commonly recognised immunogens of Helicobacter pylori, antibodies against a cell surface protein of 26 kDa, the small urease subunit (29 kDa) and the cytotoxin-associated protein (130 kDa) were identified as highly sensitive serological markers for inclusion in a recombinant antigen mixture for Helicobacter pylori screening. Only the cytotoxin-associated protein was confirmed to be an indicator immunogen for ulcerogenic strains. To assess the reliability of recombinant fragments of this protein in serological screening, the reactivity of antibody to purified fragments of the cytotoxin-associated protein was compared with that to the natural protein. A C-terminal recombinant fragment of 58 kDa showed results identical to those obtained with the natural protein and was thus considered to be an appropriate component of an antigen mixture for serological detection of Helicobacter pylori.
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PMID:Immune response to natural and recombinant antigens of Helicobacter pylori in patients with dyspeptic complaints. 1053 85

Age-specific prevalence of IgA and IgG antibodies in 714 subjects without gastrointestinal complaints aged 6 months to 90 yr was measured by an enzyme linked immunoassay using an acid-glycine extract of H. pylori as the antigen. The urease test and histology were used for the diagnosis of H. pylori infection in 83 subjects with a clinical diagnosis of dyspepsia, and these results were compared with measurement of IgG, IgA and IgM antibodies. The age specific prevalence of IgG and IgA antibodies respectively was 57 and 43 per cent for subjects aged 6 months to 4 yr and showed an increase with age to a maximum of 90 per cent for IgG in subjects > 60 yr of age and to 87 per cent for IgA in subjects between 51 and 60 yr. In symptomatic patients, there was a high degree of correlation between severity of H. pylori infection on histopathological examination and IgG (P < 0.02) levels. The use of IgG and IgA estimation could have identified H. pylori infection without endoscopy in 50 of the 83 patients. Serology for IgG and IgA antibodies against H. pylori may play a major role in decreasing the need for endoscopy, but cut-off values must be determined for each assay based on the prevalence of antibodies in the population.
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PMID:Use of serology, the urease test & histology in diagnosis of Helicobacter pylori infection in symptomatic & asymptomatic Indians. 1061 9

We have previously cloned 10 Helicobacter pylori antigen genes from a Chilean strain including: cytotoxin VacA, a truncated region of CagA (called A17), a species-specific protein (Ag26), urease subunits (UreA, UreB), a flagellin, (FlaB), heat shock proteins (HspA and HspB), an adhesin (HpaA) and a lipoprotein (Lpp20). Immunogenicity of these antigens was tested by immunoblot with sera of Chilean infected patients, revealing that HpaA, A17, HspB and VacA were more frequently recognized (86%, 82%, 68% and 68%, respectively). According to the clinical condition, it was determined that Lpp20 was preferentially recognized by sera from non-ulcer dyspepsia patients (80%), A17 and VacA by patients with duodenal ulcer (92% and 83% respectively), and HspB by patients with duodenal ulcer (83%) and gastric cancer (90%). An ELISA was developed with a purified mixture of A17 and VacA antigens to test the different groups of patients. It was found that sera from duodenal ulcer patients showed higher values than those from non-ulcer dyspepsia patients, but this difference was not significant (p<0.2). Moreover, sera from gastric cancer patients showed values lower than those from non-ulcer dyspepsia patients (p<0.019). These results indicate that, in the Chilean population, antibodies raised against VacA and A 7 are not markers either for duodenal ulcer or for gastric cancer.
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PMID:Serological response to Helicobacter pylori recombinant antigens in Chilean infected patients with duodenal ulcer, non-ulcer dyspepsia and gastric cancer. 1066 Jan 36

Free radicals (FRs) play an important role in the pathogenesis of gastroduodenal mucosal inflammation, peptic ulcer disease, and probably even gastric cancer. Various micronutrients protect the gastric mucosa by scavenging FRs. Only limited data is available regarding the concentration of micronutrients in the gastric mucosa in patients with gastritis and peptic ulcer disease. Our aim was to analyze micronutrient antioxidant concentrations in the antral mucosa in patients with gastritis and gastric ulcer and to determine the influence of Helicobacter pylori infection on gastric mucosal antioxidants in patients with gastritis and gastric ulcer. Patients who underwent upper endoscopy for evaluation of dyspepsia were included in the study. Ascorbic acid, alpha-tocopherol, alpha-carotene, beta-carotene, total carotenoids, lutein, cryptoxanthin, and lycopene levels were measured in the sera and antral mucosal biopsies in these patients. The diagnosis of H. pylori was confirmed by histology, urease test (CLO) and serology. Patients with negative endoscopic findings and normal histology and no H. pylori infection served as controls. In patients with gastritis, alpha-tocopherol levels were reduced in serum and mucosa irrespective of H. pylori status, whereas carotenoids and ascorbic acid levels were similar to controls. However, in patients with gastric ulcer, serum and mucosal levels of all micronutrient antioxidants were markedly decreased compared with both controls and patients with gastritis. The degree of depletion of antioxidants was similar in patients with either H. pylori-induced or nonsteroidal antiinflammatory drug (NSAID)-induced ulcers. Patients with gastric ulcer have very low gastric antioxidant concentrations compared to patients with gastritis and normal mucosa. This depletion in antioxidants seems to be a nonspecific response and was not related to H. pylori infection.
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PMID:Micronutrient antioxidants in gastric mucosa and serum in patients with gastritis and gastric ulcer: does Helicobacter pylori infection affect the mucosal levels? 1115 82

The etiology of chronic urticaria is largely unknown. The role of Helicobacter pylori infection, which is the most important cause of gastritis and peptic ulcer, is not clear in the pathophysiology of chronic urticaria. In this study, we aimed to define the impact of H. pylori on chronic urticaria. Thirty-eight patients who had chronic urticaria of unknown origin and dyspepsia were included in the study. In all patients, standard laboratory tests for detection of urticaria etiology were performed. Mean urticaria symptom scores of patients were carried out. All patients underwent upper gastrointestinal endoscopy. The presence of H. pylori was investigated using urease testing and histopathology. Duodenal fluid aspirated during upper endoscopy was examined for the presence of Giardia lamblia. H. pylori infection was detected in 29 patients. After successful eradication of H. pylori infection, the mean symptom score of patients did not change significantly (2.6 +/- 0.6 vs., 2.4 +/- 0.8). Only one patient had a total disappearance of urticaria symptoms. Out of 38 patients, only one had G. lamblia infection. The results of our study suggest that there is no association between H. pylori infection and chronic urticaria.
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PMID:Impact of Helicobacter pylori and Giardia lamblia infections on chronic urticaria. 1087 97

Factors influencing Helicobacter pylori infection recurrence still have not been fully clarified. The aim of this study was to determine whether, after eradication of H. pylori, any clinical or histologic features could yield information on infection relapse. We enrolled in the study 72 patients successfully treated for H. pylori infection by either dual (n = 49) or triple (n = 23) therapy. H. pylori eradication was defined as a negative bacterial finding by rapid urease test and histologic assessment at least 4 weeks after cessation of therapy. Upon eradication, gastritis grading was performed and patients were asked to return for an endoscopic control 6-8 months later. The recurrence of H. pylori infection was observed in 12 of 72 (16.7%) patients. The infection recurrence rate resulted significantly higher in nonulcer dyspepsia patients (p = 0.01 ) and in women (p = 0.03), whereas infection relapse did not differ between patients treated with dual or triple therapy. There was a strong (p = 0.0001 ) relationship between the persistence of chronic active gastritis after H. pylori eradication and recurrence of infection, whereas gastritis grade and metaplasia were not related to recurrence. In conclusion, this study found that H. pylori infection recurrence after successful dual or triple therapy is fairly high and that gastroduodenal disease, gender, and gastritis activity seem to affect infection relapse.
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PMID:Clinical and histologic predictors of Helicobacter pylori infection recurrence. 1091 74

Recognition of Helicobacter pylori (Hp) as the major cause of peptic ulcer disease has profoundly changed treatment and prognosis of this disease. The diagnostic tests are invasive (i.e. via the endoscopy) or non-invasive. The invasive tests are: urease test, histology, culture and PCR. Non invasive tests are: breath test, serology and Hp-antigens in faeces. The performance of the tests are almost similar. Sensitivities and specificities usually are > 90%, however the sensitivities and specificities of serological tests may be lower. Choice of diagnostic test depends on the clinical situation, sensitivity and specificity of test and the prevalence of Hp. Patients who should be examined for Hp: 1. The peptic ulcer patient who has used ASA/NSAID (urease test). 2. MALT-lymphoma, (histology). 3: The young (< 45 years) dyspeptic patient with no alarm symptoms and not taking NSAID/ASA (breath test). 4. Recurrence of upper dyspepsia after former eradication of Hp in peptic ulcer patients (if malignancy is not suspected breath test is first choice). 5. Verification of Hp eradication is necessary only in patients with MALT-lymphoma (histology) or patients with complicated peptic ulcer. Breath test will be the first choice in patients with complicated peptic ulcer when endoscopy is not performed. When endoscopy is performed, the urease test is the first choice. Diagnosis of Hp status not indicated: 1. There is no documentation that Hp eradication is of benefit in patients with non organic dyspepsia. Therefore, there is no indication for diagnosis of Hp. 2. Although there is some association between Hp positivity and chronic active gastritis and carcinoma of the stomach, there is at present no indication for diagnosis of Hp, as treatment of the infection has not proved effective in reversing atrophy or dysplasia. 3. The relationship between Hp and ASA/NSAIDs in peptic ulcer disease is far from clear. There is no indication for diagnosis and treatment of the infection prior to treatment with these medications. 4. For patients treated with longterm proton pump inhibitors there is no indication for diagnosis and treatment.
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PMID:[Diagnosis of Helicobacter pylori infections--how, when and in whom?]. 1101 47


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