Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:6.3.4.6 (urease)
7,490 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gastric colonization of Helicobacter pylori (H. pylori) occurs in a very early age via infected mothers having H. pylori-specific IgG antibodies that would be transplacentally transferred to infants. In addition, H. pylori urease-specific IgG was associated with chronic gastric atrophy and post-immunization gastritis is usually correlated with a strong local IgG response. These findings indicate that H. pylori-specific IgG antibodies, in particular its urease-specific IgG, may induce unfavorable influence on host resistance against H. pylori. Here, we show that we have found a unique H. pylori urease-specific IgG monoclonal antibody (MAb), termed S3, recognizing the conformational structure of the small subunit Ure-A, which enhanced the urease enzymatic activity. Such enhancement of the H. pylori urease activity induced by 1 microg of S3 was almost completely cancelled by simultaneously added the same amount of L2 MAb, which has a strong and specific inhibitory activity against H. pylori urease and recognizes a liner epitope of 8-mer peptide (F8: SIKEDVQF) within its large subunit Ure-B (Infect. Immun. 69: 6597, 2001). Intravenous pre-administration of purified S3 into BALB/c mice showed significant augmentation for gastric colonization with the susceptible strain Sydney Strain-1 (SS-1). To our knowledge, this is the first demonstration that a H. pylori urease-specific IgG MAb induced an augmentation of their gastric colonization in vivo.
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PMID:Augmentation of Helicobacter pylori urease activity by its specific IgG antibody: implications for bacterial colonization enhancement. 1580 82

Results of clinical and instrumental-laboratory study of 17 cases are presented. According to the rapid urease test (CLO) and histological studies, the helicobacter infection was found in 12 (70.6%) cases out of the group of 17 suffering from chronic atrophic gastritis, gastric ulcer adenomatous polyposis. Analyses of Helicobacter pylori dissemination over the gastric mucosa manifested the I (weak) degree (up to 20 microbes within field of vision) prevailing in 8 (66.7%) of 12 cases, while the II (medium) degree (up to 50 microbes within field of vision) and III (high) degree (over 50 microbes within field of vision) occurred only in 4 cases (33.3%). By comparative cytogenetic research of the peripheral blood lymphocytes we found the immunogenetic markers and characteristic features of cytogenetic disturbances in the immunocompetent cells in cases of pre-cancer Helicobacter pylori-associated diseases (chronic atrophic gastritis, gastric ulcer, adenomatous polyposis). Statistical data confirmed an increase in the percentage of cells with chromosomal aberrations, which amounted to 4.25+/-0.51 in the chronic atrophic gastritis cases, 3.5+/-0.46 in the gastric ulcer cases, 5.75+/-0.60 in the adenomatous polyposis cases for 100 analyzed metaphases. Considering the questionable role of Helicobacter pylori as a direct initiator of mutagenesis, the immune disturbances may be caused by the damage of DNA of lymphocytes resulting from the genotoxic effect of some intermediates of inflammation.
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PMID:[Chromosomal instability of peripheral blood lymphocytes in patients with precancer gastric cases]. 1698 Jul 44

Chronic infections are associated with cardiovascular diseases. Helicobacter pylori-induced chronic active gastritis results in atrophic gastritis. In this study, we attempted to determine carotid intima-media thickness in patients with and individuals without H. pylori-induced atrophic gastritis. Oesophagogastroduodenoscopy was performed on 123 patients for various reasons. Helicobacter pylori were considered positive when histological examination and rapid urease test showed H. pylori. Helicobacter pylori-positive cases were divided into two groups, namely atrophic gastritis and non-atrophic gastritis. Of 123 patients, 92 patients had H. pylori-positive non-atrophic gastritis and 31 had H. pylori-positive atrophic gastritis. There was no significant difference in carotid intima-media thickness between the two groups. Carotid intima-media thickness is not associated with H. pylori-induced atrophic gastritis.
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PMID:Helicobacter pylori-associated atrophic gastritis and carotid intima-media thickness: is there a link? 1734 67

This study investigated the influence of urease-positive non-Helicobacter pylori bacteria on the results of a urea breath test (UBT) to evaluate the diagnostic utility of a UBT using film-coated [(13)C]urea tablets. The UBT was performed in 102 patients treated with a proton pump inhibitor and antibiotics for the eradication of H. pylori. Urease-producing bacteria other than H. pylori were isolated and identified from the oral cavity and stomach. In 4/102 patients, the UBT gave false-positive results. These false-positive results were found to be caused by the presence of urease-positive bacteria in the oral cavity and stomach. Five bacterial species with urease activity (Proteus mirabilis, Citrobacter freundii, Klebsiella pneumoniae, Enterobacter cloacae and Staphylococcus aureus) were subsequently isolated from the oral cavity and/or stomach. As there was no correlation between the in vitro urease activity of urease-positive non-H. pylori bacteria and the UBT value, and all of the patients with a false-positive UBT result were suffering from atrophic gastritis, it is possible that the false-positive results in the UBT were a result of colonization of urease-positive bacteria and gastric hypochlorhydric conditions. Thus, for the diagnosis of H. pylori infection using a UBT, the influence of stomach bacteria must be considered when interpreting the results.
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PMID:Urease-positive bacteria in the stomach induce a false-positive reaction in a urea breath test for diagnosis of Helicobacter pylori infection. 1856 38

The Helicobacter pylori (Hp) infection is common. However, only 10-20% of infected individuals require antibacterial treatment. The main indications to such treatment are peptic ulcer disease, atrophic gastritis, dyspeptic symptoms, previous surgical procedure for gastric cancer, family history of gastric cancer and low-grade gastric mucosa-associated lymphoid tissue (MALT) lymphoma. The treatment may also be undertaken at the patient's request. To detect the infection the urease test (when the patient has indications for gastroscopy), the urea breath test or serologic test are most commonly used. A standard treatment of Hp infection consists of a 7-day administration of one of the proton pump inhibitors and 2 out of 3 antibiotics such as amoxicillin, clarithromycin and metronidazole. After failure of the first-line treatment, the recommended second choice treatment is a quadruple treatment regimen consisting of bismuth salts, tetracycline, metronidazole and proton pump inhibitor. European guidelines (Maastricht III) allow the use of the quadruple treatment regimen already as the first choice treatment and therapy prolongation up to 14 days. Ineffectiveness of the second-line treatment is an indication for antimicrobial susceptibility testing. New antibiotics used for Hp eradication are levofloxacin and rifabutin. Eradication treatment should be obligatorily assessed with the use of the urease or breath test only in patients with peptic ulcer bleeding. The current guidelines do not envisage an active search for Hp infection in an asymptomatic population and treating people infected with this bacterium, for gastric cancer prevention.
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PMID:Clinical aspects of Helicobacter pylori infection. 1871 38

In India, the role of host genetic factors is poorly studied for Helicobacter pylori associated diseases. Therefore, we evaluated the association of functionally relevant COX-2 gene polymorphisms (-765 G>C and +8473 T>C) in gastritis and precancerous lesions susceptibility. After upper GI endoscopy, 130 rapid urease test positive patients with non-ulcer dyspepsia, also showed positivity for H. pylori using modified Geimsa staining and anti-CagA IgG serology were included. All patients and 260 asymptomatic controls were genotyped for COX-2 variations using PCR-RFLP. COX-2 -765 (GC+CC) genotypes, -765 C allele, +8473 CC genotype, +8473 (TC+CC) genotypes, +8473 C allele, and variant haplotypes imparted high risk for gastritis (P = 0.036, OR = 1.82; P = 0.007, 1.92; P = 0.025, OR = 2.13; P = 0.017, OR = 1.80; P = 0.017, OR = 1.45; P = 0.010, OR = 2.40; P = 0.023, OR = 1.50 and P = 0.012, OR = 2.20 folds, respectively). In contrast, COX-2 -765 C allele carriers had low risk for lymphocyte (P = 0.020, OR = 0.35), plasma cell infiltrations (P = 0.016, OR = 0.33), and gastric atrophy (GA) development (P = 0.019, OR = 0.35). In conclusion, COX-2 variant allele/genotype/haplotype carriers may be at high risk for gastritis. However, COX-2 -765 C allele carriers may be at low risk for GA development.
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PMID:Role of cyclooxygenase-2 functional gene polymorphisms in Helicobacter pylori induced gastritis and gastric atrophy. 1882 88

We report the case of a patient with gastroesophageal reflux disease who developed gastric atrophy and intestinal metaplasia (IM) while on 20-year treatment with proton pump inhibitors. This is perhaps the first report in human beings. A 74-year-old man, who presented with heartburn, showed abnormally high gastric pH (average 6.57) on 24-hour dual channel pH-metry even after discontinuing acid suppressive drugs for one month. No significant esophageal acid exposure was noted, which may be related to an impairment of the acid secreting capacity of the stomach (percentage time esophageal pH<4 during 24-h period 0.3%). Upper gastrointestinal endoscopy was normal except for the prominent submucosal vessels in the body and fundus suggesting gastric atrophy. Histopathological examination of multiple biopsies from the body and antrum of stomach showed signs of gastric atrophy and IM. Rapid urease test and histopathology of gastric biopsies were negative for Helicobacter pylori. Anti-H.pylori IgG ELISA however, was positive. Patient was asked to stop all anti-secretory drugs and only prokinetics were prescribed following which his symptoms markedly improved. On follow-up, in April 2007, he developed symptoms of peripheral neuropathy; serum vitamin 812 level was low. He responded to parenteral vitamin 812 therapy. 24-h dual channel pH-metry repeated after one and a half years showed persistently high gastric pH (average pH 6.76). The patient remained well after discontinuing proton pump inhibitors and continuing prokinetics and vitamin B12 injections.
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PMID:Gastric atrophy and intestinal metaplasia in a patient on long-term proton pump inhibitor therapy. 1911 12

The expression of growth factors, proteolytic enzymes, fibrogenic factors, and cytokines is altered in the Helicobacter pylori-infected gastric mucosa. Therefore, we aimed to evaluate the association of functional promoter variants of transforming growth factor (TGF)-B1 and matrix metalloproteinase (MMP)-7 genes with gastritis and gastric precancerous lesions. After upper gastrointestinal endoscopy, a total of 130 rapid urease test-positive patients with nonulcer dyspepsia were examined for H. pylori infection using modified Giemsa stain and IgG anti-CagA ELISA. All patients and 200 asymptomatic controls were genotyped for TGF-B1 (-509 C>T) and MMP-7 (-181 A>G) substitutions using PCR-RFLP. The genotype and allele frequencies of TGF-B1 and MMP-7 polymorphisms did not differ between patients and controls (p > 0.05). However, the CagA-positive patients with TGF-B1 -509 T allele had higher risk for gastric atrophy (p = 0.026, odds ratio [OR] = 2.38) and lymphoid follicle development (p = 0.028, OR = 2.29). In addition, CagA-positive patients carrying MMP-7 -181 G allele had risk for lymphoid follicle formation (p = 0.027, OR = 2.30). Thus, the present study revealed significant association of functional MMP-7 and TGF-B1 gene variants toward susceptibility to H. pylori-induced precancerous gastric lesions.
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PMID:Transforming growth factor-B1 and matrix metalloproteinase-7 promoter variants induce risk for Helicobacter pylori-associated gastric precancerous lesions. 1931 20

The main conclusions drawn from the presentations related to Helicobacter pylori at Digestive Diseases Week 2008 are summarized. Several strains of H. pylori frequently infect the same patient, and consequently samples for culture should be obtained from the gastric antrum and body. The test-and-treat strategy in dyspepsia is as effective as empirical antisecretory therapy and is probably cheaper. The benefit of eradication therapy in patients with uninvestigated dyspepsia, although small, seems to be lasting. Eradication in the general population seems to reduce the development of dyspeptic symptoms in the long term and consequently could be cost-effective. The prevalence of H. pylori infection in peptic ulcer is decreasing and the frequency of idiopathic ulcers is increasing. Patients with H. pylori-negative bleeding ulcers have a high probability of hemorrhagic recurrence and should therefore receive maintenance antisecretory therapy. H. pylori eradication reduces the incidence of gastric adenocarcinoma, which could warrant a screening and treatment strategy for this infection in the general population in high risk areas. H. pylori infection should be eradicated in patients undergoing endoscopic mucosal resection for early gastric cancer. To prevent the development of gastric cancer, eradication therapy should be administered early, before gastric atrophy develops. H. pylori-negative and H. pylori-positive gastric lymphomas have an equally favorable prognosis. New diagnostic techniques have been developed: the ultra-rapid urease test, a simpler 14C-urea breath test, and an ELISA method for rapid bacterial susceptibility determination. In patients with gastrointestinal bleeding, the 13C-urea breath test performed immediately after emergency gastroscopy allows early diagnosis of infection. Eradication regimens with double doses of proton pump inhibitors are more effective than those with standard doses. "Sequential" therapy is more effective and cheaper than classical triple-drug therapy, although the superiority of administering therapy sequentially rather than concomitantly has not been established. In penicillin-allergic patients, a combination with levofloxacin and clarithromycin is a promising alternative in rescue therapy. Second-line rescue therapy with levofloxacin is effective and is also simpler and better tolerated than quadruple-drug therapy. The rate of quinolone resistance is increasing as a result of the widespread use of these antibiotics. Third-line treatment with levofloxacin is also a promising alternative. Even after the failure of three previous treatments, a fourth empirical rescue therapy (with levofloxacin or rifabutin) can be effective in more than half of patients. The annual recurrence rate of H. pylori infection is approximately 3% in developed countries and is higher than 10% in developing countries.
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PMID:[Helicobacter pylori-related diseases: dyspepsia, ulcer and gastric cancer]. 1943 62

Chronic gastritis has a high incidence in adults, causing progressive destruction of glandular structures, favoring the development of gastric atrophy. The association of chronic gastritis with intestinal type metaplasia of gastric mucosa has a poor outcome as intestinal metaplasia is regarded as a precancerous lesion. Metaplasia is common in patients with Helicobacter pylori infection and also heavy smokers. The aim of our study was to evaluate the relationship between chronic gastritis and intestinal metaplasia. The study was conducted on a total of 1218 patients, aged between 5 and 90 years, who presented for dyspeptic disorders in the period 2007-2010 and were examined clinically and endoscopically. During the gastroscopic examination, fragments of gastric mucosa were collected for the histopathological study and for highlighting the H. pylori infection. For the histopathological study, the Hematoxylin-Eosin and PAS-Alcian Blue stains were performed, while for the immunohistochemical study the anti-TAG72 and anti-PCNA antibodies were used. A diagnosis of gastritis was established in 615 patients, representing approximately 50.5% of all cases. Most cases with gastritis were found in people of middle age. Gastritis was present in almost all age groups, from teenagers to the elders. Of the 615 cases of gastritis, urease test was positive in 353 patients, representing approximately 57.40% of all patients with gastritis. Histopathological examination identified the presence of intestinal metaplasia in 61.60% of patients with chronic gastritis, mostly complete metaplasia. PCNA immunohistochemistry revealed that cell proliferation processes are intensified in intestinal metaplasia. This study highlights the importance of chronic gastritis, intestinal metaplasia, and H. pylori infection in the etiopathogeny of gastric cancer.
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PMID:Chronic gastritis with intestinal metaplasia: clinico-statistical, histological and immunohistochemical study. 2273 98


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