Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:6.3.4.6 (urease)
 7,490 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine the prevalence and significance of Helicobacter pylori (H. pylori) infection, biopsies of the antral mucosa were obtained from 139 patients and 43 asymptomatic volunteers. The specimens were examined by hematoxylin-eosin staining and the ureas test. The detection rate of H. pylori by histologic examination was 91.3% in patients with duodenal ulcer, 75.0% in those with combined duodenal and gastric ulcer, 63.6% in those with gastric ulcer, 22.9% in those with gastric carcinoma, 36.4% in those with gastric adenoma, 14.3% in those with gastric hyperplastic polyp, and 51.7% in those with gastritis, and the respective percentages detected by the urease test were 91.3%, 75.0%, 54.5%, 28.6%, 27.3%, 14.3%, and 44.8%. H. pylori was also detected in 10/43 (23.3%) asymptomatic healthy volunteers by histology and the urease test. The prevalence of H. pylori was significantly higher in the patients than in the asymptomatic healthy volunteers (p < 0.05). H. pylori was detected in 62.9% of patients with endoscopic erosive gastritis and in 97.9% of those with histologically proven chronic active gastritis. The urease test was positive in 77/82 patients who were histologically positive for the organism (sensitivity: 93.9%), and it was negative in 98/100 patients who were negative by histology (specificity: 98.0%). Thus, there was over 90% agreement between the urease test and histology. Our investigations showed that H. pylori was closely related to peptic ulcers and antral gastritis, and that the urease test provides a simple, rapid and accurate diagnosis of H. pylori infection.
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PMID:Helicobacter pylori infection and gastroduodenal disease: a comparison of endoscopic findings, histology, and urease test data. 129 70

To determine the incidence and significance of the detection of Helicobacter pylori in an Arab population, 116 patients with dyspepsia were studied. 89 percent of these patients had H. pylori detected by culture or/and histological definition of Campylobacter-like organisms. By the modified rapid urease test (RUT) 80% of the patients had H. pylori (sensitivity of 91%, specificity of 75%). Irrespective of the endoscopic diagnosis, the presence of H. pylori was associated with histologic evidence of gastritis. A heavy growth of H. pylori on culture was associated with active gastritis. There was no difference in the incidence rates of H. pylori with regard to various diagnoses by endoscopy. It is suggested that H. pylori may be hyperendemic among Arab patients with dyspepsia. Its presence is associated with varying severity of gastritis with or without additional endoscopically recognised findings.
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PMID:Helicobacter pylori and dyspepsia in an Arab population. 129 38

Helicobacter pylori has been demonstrated as an etiologic agent of human gastritis and peptic ulcer formation. However, there is no straightforward basis to distinguish different isolates. We used the polymerase chain reaction (PCR) to amplify the urease structural subunit genes, ureA and ureB, which, when digested with appropriate restriction endonucleases, allow the differentiation of patterns on agarose gels. PCR amplification was possible with DNA rapidly extracted from H. pylori by alkaline lysis and phenol-chloroform. The 2.4-kb PCR products amplified from 22 clinical isolates and subjected to HaeII restriction endonuclease digestion produced 10 distinct patterns on agarose gels, with two patterns being shared between five and six strains. PCR amplification of the urease genes may enable the differentiation of closely related H. pylori strains by restriction digest analysis of PCR-amplified ureA and ureB genes.
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PMID:Use of polymerase chain reaction-amplified Helicobacter pylori urease structural genes for differentiation of isolates. 131 51

30 patients with non ulcer dyspepsia (NUD) were evaluated to find out if there was a relationship with Helicobacter pylori (HP) infection. Gastric biopsies from the antrum were taken and two of them sent to pathology to be stained with H&E and Warthin-Starry. The other three were sent to Microbiology, for urease-test, culture and frotis with Gram stain. To diagnose HP was necessary to get it at least in two of the performed test. This was possible in 20 (66.66%). Chronic active gastritis was observed in 15/20 (75%) and in the 3/10 HP negative patients none had histological alteration shown. Normal aspect of gastric mucosa did not predict Helicobacter pylori infection. The presence of the bacteria could not be correlated to any kind of symptoms and always was associated with chronic gastritis.
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PMID:[Nonulcerative dyspepsia associated with Helicobacter pylori]. 134 Aug 9

Helicobacter pylori has been shown to be the cause of chronic active gastritis and the evidence that it is involved in the development of peptic ulcer disease and gastric cancer is compelling. Narrow host range, tissue specificity, and chronic inflammation are hallmarks of infection. The study of virulence determinants has just begun but it seems likely that urease, adhesins, cytotoxins, and mediators of inflammation will prove to be important.
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PMID:Helicobacter pylori and gastroduodenal disease: pathogenesis and host-parasite interaction. 134 68

A transferable solid phase enzyme immunoassay (TSP-EIA) and an immunoblot technique were evaluated for the detection of IgG antibodies against Helicobacter pylori. Using the biopsy urease test as reference method, the sensitivity and specificity of the EIA were 96% and 100%, respectively. Immunoblot analysis was carried out by testing sera from patients with a positive urease test who suffered from type B gastritis, gastric and duodenal ulcers, and a negative control group. The immunoblotted Helicobacter pylori proteins showed reproducible immunoreactive bands at molecular weights of 130, 93, 75 and 67 kDa. The molecular weight protein fractions of Helicobacter pylori of 180 kDa and higher were found to be of minor immunological significance. Proteins of less than 60 kDa exhibited wide serum-specific variations in reactivity after immunostaining. No correlation between specific immunoblot patterns and clinical signs induced by Helicobacter pylori infection was observed.
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PMID:Serodiagnosis of Helicobacter pylori infections by detection of immunoglobulin G antibodies using an immunoblot technique and enzyme immunoassay. 139 65

A prospective case control study was conducted in 50 patients with non-ulcer dyspepsia (NUD) and 10 age and sex matched controls to determine the prevalence of Helicobacter pylori in patients with NUD and to correlate symptoms, histology and presence of H pylori in gastric biopsies. Endoscopic biopsies from antrum and fundus were subjected to urease test and histological examination. On histology, H pylori was identified in 27 (54%) NUD patients and in one of 10 controls. Urease test was positive in 31 (62%) antral and 21 (42%) fundal biopsies in patients with NUD and in only one (10%) of 10 antral biopsies in the control group. On histology, gastritis was present in the antrum in 46 (92%) NUD patients and in the fundus in 40 (80%) cases; of these, 27 (54%) and 15 (30%) had H pylori in antral and fundal biopsies respectively. The severity of antral gastritis correlated with the density of H pylori (p < 0.05).
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PMID:A study of Helicobacter pylori in north Indian subjects with non-ulcer dyspepsia. 150 55

The studies were aimed at the assessment of the coexistence of non-ulcer dyspepsia with chronic gastritis and Campylobacter pylori infection, and of the effect of therapy with De-Nol on the course of such disease. The studies involved 50 patients with non-ulcer dyspepsia. Prior to and after the treatment with De-Nol samples of the mucosa collected from the antrum and corpus of the stomach have been examined histologically with urease test indicating C. pylori infection. Chronic gastritis of the antral mucosa membrane and/or mucosa of the corpus of the stomach has been found in 36 patients, and normal mucosa in 14 patients. Therapy with De-Nol produced statistically significant improvement. Totally histological improvement has been noted in 77.1% of patients with inflammation of the antral mucous membrane and in 64.3% of patients with inflammation of the corporeal gastric mucosa. Campylobacter pylori has been eradicated in all patients with chronic gastritis. De Nol eliminates or significantly lowers an inflammation in the antrum and/or corpus of the stomach. Its action is related to the eradication of Campylobacter pylori infection.
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PMID:[Inflammatory changes in the gastric mucosa of patients with idiopathic non-ulcer dyspepsia and the effect of colloid bismuth treatment on the course of inflammation]. 143 91

Hp now appears to be more than a simple commensal organism in patients with gastritis or peptic ulcer disease. Microbiologic, serologic, and epidemiologic studies all confirm that Hp has an important role in children with abdominal pain. Hp is found in the gastric mucosa of children with histologically proven gastritis or peptic ulcer. The organism can be transmitted from human to human with evidence of colonization, appearance of gastritis, and serum antibody response. Antimicrobial therapy directed at Hp eradicates colonization and resolves symptoms. Hp antibodies appear more frequently in familial clusters and the frequency of antibody positivity increases with age. Children are more likely to have symptomatic disease associated with elevated antibody titers. Recurrence of disease is associated with reappearance of the organism. At the present time, colonization can be detected only by gastric biopsy; however, it may be possible eventually to diagnose or follow infections by obtaining serum antibody titers or urea breath-testing. The natural history of Hp infection is unclear. Although it can cause an acute gastritis, it generally is found in association with chronic gastritis. The increase in seropositivity with age may mean that slow changes evolve over decades or that age cohorts have been infected differentially. How does antral colonization with Hp cause duodenal ulceration? The organism is not found in the duodenum and most patients with gastritis do not develop ulcers. This may be related to changes in acid production and mucosal protection associated with Hp colonization, but few studies have been done. What factors initiate Hp infection? Both volunteers who became colonized first suppressed acid secretion with H2-antagonists. Hypochlorhydria also seems to follow Hp infection in these same studies. The role of diet and drugs, or other environmental and genetic factors, in initiating infection is largely unexplored. An effective means of therapy needs to be developed. Although Hp appears sensitive in vitro to many compounds, it is difficult to eradicate in vivo, especially with monotherapy. Single-drug therapy suppresses the organism, but recurrence rates are high. It is difficult to deliver effective doses of drugs to the mucous niche the organism has selected and concerns about long-term therapy and its side effects persist. Current data suggest no ready solution to the initial case presentation. A child with primary gastritis or duodenal ulcer should be treated first with standard antacid and H2-receptor antagonist therapy. If endoscopy is performed, biopsies of normal-appearing areas of gastric antrum should be stained for Hp and a biopsy urease test should be performed.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Helicobacter pylori, gastritis, and ulcers in pediatrics. 144 15

A spiral shaped bacterium was seen in smears and histological sections (stained by carbolfuchsin) of gastric, ileal and caecal mucosa as well as in stool smears from mice. A significant correlation between the presence of the spiral bacterium and the occurrence of gastritis was observed but the ileal and caecal mucosa seemed unaffected. The bacterium was Gram negative and grew on BHM and Skirrow's medium, under microaerophilic conditions, at 37 degrees C. Its major biochemical characteristics included positive catalase and oxidase reactions and a rapidly positive urease test. There were 2 or 3 spiral turns per cell and a tuft of up to 12 sheathed flagella on each pointed end. Entwined, braided periplasmic fibrils covered the surface of the cell. This spiral bacterium seemed to be part of the normal intestinal flora but was associated with gastritis.
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PMID:Spiral bacterium associated with gastric, ileal and caecal mucosa of mice. 144 7


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