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)

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

The relationship of Helicobacter felis, an organism that is observed in the stomachs of dogs, to gastric disease in dogs is unclear. The objective of this study was to determine if Helicobacter felis infection alters gastric morphology and gastric secretory function in dogs. Five specific-pathogen-free (SPF), Helicobacter-free Beagle dogs were examined before and for 26 weeks after inoculation with H. felis (ATCC 49179). Three SPF uninfected dogs served as controls. All five dogs became colonized by H. felis as determined by urease activity, histopathology, polymerase chain reaction, and transmission electron microscopic examination of serial gastric biopsies. The degree of colonization ranged from < 1 organism/400 x field to > 10 organisms/400 x field. The fundus, body, and cardia were most heavily colonized. Evaluation of gastric biopsies showed mild gastric inflammation and lymphoid follicles in both infected and uninfected dogs. There was no correlation between the number of organisms observed and the degree of gastric inflammation or number of lymphoid follicles. The gastric secretory axis, assessed by fasting and meal-stimulated plasma gastrin, mucosal gastrin and somatostatin immunoreactivity, fasting gastric pH, and pentagastrin-stimulated gastric acid secretion, was similar in both infected and uninfected dogs. Fasting gastric pH was not a reliable indicator of gastric secretory function. These findings suggest that H. felis may not be a gastric pathogen in dogs. However, the density of colonization and limited duration of infection should be considered when interpreting these findings.
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PMID:Helicobacter felis infection in dogs: effect on gastric structure and function. 1033 32

The relationship of Helicobacter felis, a bacterium observed in the stomachs of cats, to gastric disease is unclear. The objective of this study was to determine if H. felis infection alters gastric histopathology, proinflammatory cytokine expression, and secretory function and evokes a humoral immune response in cats. Five specific-pathogen-free (SPF) Helicobacter-free cats were studied before and for 1 year after oral inoculation with H. felis (ATCC 49179). Four SPF H. felis-uninfected cats served as controls. The stomachs of all five H. felis-inoculated cats became colonized, as determined by urease activity, histopathology, PCR, culture, and transmission electron microscopy of serial gastric biopsies at 0, 3, 5, 8, and 12 months. Uninoculated cats remained Helicobacter free. Lymphoid follicular hyperplasia, atrophy, and fibrosis were observed primarily in the pylorus of infected cats. Mild mononuclear inflammation was detected in both infected and uninfected cats, but was more extensive in infected cats, with pangastric inflammation, eosinophilic infiltrates, and cardia gastritis observed only in infected cats. No upregulation of antral mucosal interleukin 1alpha (IL-1alpha), IL-1beta, or tumor necrosis factor alpha was detected by reverse transcription-PCR in any cat. The gastric secretory axes, assessed by fasting plasma gastrin, antral mucosal gastrin and somatostatin immunoreactivity, and pentagastrin-stimulated gastric acid secretion, were similar in both infected and uninfected cats. Gradual seroconversion (immunoglobulin G) was observed in four of five infected cats, with enzyme-linked immunosorbent assay values reaching 4x to 12x baseline 12 months postinfection. These findings indicate that H. felis infection in cats induces lymphoid follicular hyperplasia, mild gastritis, and seroconversion, but is associated with normal gastric secretory function.
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PMID:Helicobacter felis infection is associated with lymphoid follicular hyperplasia and mild gastritis but normal gastric secretory function in cats. 1063 46

The discovery of the spiral bacterium Helicobacter pylori and its causative role in gastric disease in humans has brought a dramatic change to gastroenterology. Although spiral bacteria have been known for more than a century to infect the stomachs of dogs and cats, recent research has been conducted mainly in the wake of interest in H. pylori. H. pylori has not been found in dogs and only very rarely in cats and zoonotic risk is minimal. A variety of other Helicobacter spp. can infect the stomach of pets; however, their pathogenic role is far from clear, and they have a small but real zoonotic potential. The prevalence of gastric Helicobacter spp. in dogs and cats is high, irrespective of clinical signs, and as in human medicine, mode of transmission is unclear. The relationship of Helicobacter spp. to gastric inflammation in cats and dogs is unresolved, with inflammation, glandular degeneration, and lymphoid follicle hyperplasia accompanying infection in some but not all subjects. Circulating anti-Helicobacter immunoglobulin G antibodies have been detected in 80% of dogs with naturally acquired infection and most dogs and cats with experimental infection. The gastric secretory axis is similar in infected and uninfected cats and dogs and no relationship of infection to gastrointestinal ulcers has been found. Differences in the pathogenicity of Helicobacter spp. are apparent, because infection with H pylori is associated with a more severe gastritis than infection with other Helicobacter spp. in both cats and dogs. Rapid urease test, histopathology, and touch cytology are all highly accurate invasive diagnostic tests for gastric Helicobacter-like organisms in dogs and cats, whereas culture and polymerase chain reaction are the only means to identify them to the species level. Urea breath and blood tests or serology can be used to diagnose Helicobacter spp. noninvasively in dogs and cats. Most therapeutic studies in pets have not shown long-term eradication of Helicobacter spp. Whether this is due to reinfection or recrudescence has not been established.
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PMID:Helicobacter infection in dogs and cats: facts and fiction. 1077 82

The Working Party Report on the Management of Helicobacter pylori serves as a clinical practice guideline for Malaysian doctors. H. pylori is not uncommon in the Malaysian population. Marked racial differences and the consistently low prevalence rates amongst Malays are noted. The working party recommends that if endoscopy is to be performed, a rapid urease test should be used for diagnosis. Where suspicion of the infection is strong and the urease test is negative, histology should be performed on gastric biopsies. Culture should be used to monitor resistance patterns to antibiotics and regional laboratories should assume this responsibility. The urea breath tests are highly accurate tests for diagnosis of H. pylori but is as yet not widely available in Malaysia. The working party strongly recommends that all peptic ulcer patients infected with H. pylori whether active, in remission and complicated ulcers should be treated for the infection. Patients with low-grade gastric mucosal lymphoid tissue lymphoma should also be treated for H. pylori infection. It is considered advisable that patients on long term nonsteroidal antinflammatory drug (NSAID) treatment with a history of peptic ulcers or dyspepsia and patients following resection of early gastric cancer or those with a family history of gastric cancer should also be tested and treated for H. pylori. The working party recommends, as first line treatment a 7-day combination therapy of a proton pump inhibitor, clarithromycin and metronidazole or amoxicillin. High metronidazole resistance rates locally may adversely affect regimens containing the antibiotic. It should also be noted that regimens that yield lower eradication rates may result in higher long term expenditure.
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PMID:Management of Helicobacter pylori infection--a Working Party Report of the Malaysian Society of Gastroenterology and Hepatology. 1096 73

The principal aims of this study were to evaluate the humoral immune response (IgG) of cats with gastric Helicobacter spp. infection, and to determine the prevalence of different types of Helicobacter spp. in the stomachs of cats. The Helicobacter infection status of 45 cats (12 healthy spay/neuter cats, 9 sick cats, 24 colony cats) was determined by evaluating endoscopic gastric biopsies for urease activity, presence of Helicobacter-like organisms (HLO) on histopathology, and genus and species-specific PCR. Serum samples were evaluated with a kinetic enzyme linked immunosorbent assay (ELISA) utilizing the high molecular cell-associated protein (HM-CAP) fraction of H. felis ATCC 49179.Seventeen of 45 cats were infected with Helicobacter spp.: "H. heilmannii" 9/17, H. felis 4/17, mixed "H. heilmannii" and H. felis 3/17, unclassified-Helicobacter spp. 7/17. H. pylori was not detected in any cat. Kinetic ELISA results were significantly higher for infected cats, than for uninfected cats. Cats infected with different Helicobacter spp. showed similar distribution of OD/min values. There were no effects of age or clinical signs on the results of kinetic ELISA. No correlation between colonization density and seroconversion was observed. There were statistically significant, but weak correlations between the degree of seroconversion and the degree of inflammation, and the number of lymphoid follicles. Infected cats had more severe inflammation in the pylorus and fundus than uninfected cats. Infected sick cats had a higher degree of pyloric, but not fundic inflammation, than healthy infected cats and uninfected sick cats. The results indicate that naturally acquired infection with gastric Helicobacter spp. is associated with seroconversion (IgG) in cats. The similar ELISA values in cats infected with a variety of Helicobacter spp. suggests substantial antigenic homology between different Helicobacter spp. The higher degree of inflammation in infected than uninfected cats, supports a role for Helicobacter as a cause of gastritis in cats.
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PMID:Helicobacter spp. infection in cats: evaluation of the humoral immune response and prevalence of gastric Helicobacter spp. 1124 Jan 3

Detailed histopathological evaluation of the gastric mucosa of Helicobacter-infected cats is complicated by the difficulty of recognizing Helicobacter organisms on hematoxylin and eosin (HE)-stained sections and the ability of multiple Helicobacter species to infect cats. In this study, the presence and localization of different species of Helicobacter in the stomachs of cats was investigated using silver staining and immunohistochemistry. Five groups containing 5 cats each were established (group 1: urease negative and Helicobacter free; groups 2, 3, 4, and 5: urease positive and infected with Helicobacter heilmannii, unclassified Helicobacter spp., Helicobacter felis, and Helicobacter pylori, respectively). Gastric samples were evaluated by HE and silver staining and by immunohistochemistry with 3 different anti-Helicobacter primary antibodies. Helicobacter were detected by Steiner stain in all infected cats at the mucosal surface, in the lumen of gastric glands, and in the cytoplasm of parietal cells. In silver-stained sections, H. pylori was easily differentiated from H. felis, H. heilmannii, and unclassified Helicobacter spp., which were larger and more tightly coiled. No organisms were seen in uninfected cats. Helicobacter antigen paralleled the distribution of organisms observed in Steiner-stained sections for 2 of the 3 primary antibodies tested. The antisera were not able to discriminate between the different Helicobacter species examined. A small amount of Helicobacter antigen was present in the lamina propria of 3 H. pylori-, 3 H. felis-, and 1 H. heilmannii-infected cat. Minimal mononuclear inflammation was present in uninfected cats and in those infected with unclassified Helicobacter spp. and H. heilmannii cats. In H. felis-infected cats, lymphoid follicular hyperplasia with mild pangastric mononuclear inflammation and eosinophilic infiltrates were present. The H. pylori-infected cats had severe lymphoid follicular hyperplasia and mild to moderate mononuclear inflammation accompanied by the presence of neutrophils and eosinophils. These findings indicate that Steiner staining and immunohistochemistry are useful for detecting Helicobacter infections, particularly when different Helicobacter species can be present. Monoclonal antibodies specific for the different Helicobacter species could be important diagnostic aids. There appear to be differences in the severity of gastritis in cats infected with different Helicobacter species.
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PMID:Histological and immunohistochemical detection of different Helicobacter species in the gastric mucosa of cats. 1124 59

Chronic, idiopathic diffuse colitis is a well recognised clinical and pathological entity in captive rhesus monkeys. Six rhesus monkeys were diagnosed with clinically debilitating, chronic diarrhoea. Histologically, colonic tissues were characterised as chronic, moderate to severe colitis and typhlitis, with diffuse mononuclear inflammation of lamina propria, reactive lymphoid hyperplasia and multifocal micro-abscesses. Colonic tissues were cultured for Salmonella spp. and Shigella spp.; all results were negative. Samples were negative for Clostridium difficile A and B toxins, and special stains of colonic tissue for acid-fast bacteria were also negative. The six diarrhoeic monkeys tested gave negative results for serum IgG antibodies to herpes B virus, STLV, SRV and SIV. Colonic tissue from the six diarrhoeic and two clinically normal monkeys with histologically confirmed colitis from the same colony were also subjected to micro-aerobic culture. Micro-aerobic cultures from all eight monkeys incubated at 37 degrees C and 42 degrees C revealed pinpoint or spreading colonies on antibiotic-containing media. Bacteria were identified as gram-negative, oxidase positive and urease negative. Of the nine strains characterised biochemically, two separate biotypes (corresponding to different species by 16S rRNA analysis) were identified. One biotype (type 1), from non-diarrhoeic monkeys and the second biotype (type 2) from diarrhoeic animals with subclinical chronic colonic inflammation, differed by catalase activity, ability to reduce nitrate to nitrite and sensitivity to cephalothin. Complete 16S rRNA analysis of five of the nine strains characterised biochemically indicated that the organisms isolated were two novel Helicobacter spp. By electron microscopy, these novel helicobacters had spiral morphology with bipolar sheathed flagella. This is the first report describing the isolation of novel Helicobacter spp. from inflamed colons of rhesus monkeys. Studies are needed to determine whether these novel Helicobacter spp. play a causal role in the initiation and progression of chronic colitis in macaques. Further microbiological and histological analysis of this chronic idiopathic colitis syndrome in macaques may prove useful in understanding the aetiology and pathogenesis of inflammatory bowel disease in man.
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PMID:Novel Helicobacter species isolated from rhesus monkeys with chronic idiopathic colitis. 1133 49

Tonsillar tissue is a component of mucosa-associated lymphoid tissue (MALT), which has evolved to protect vulnerable mucosal surfaces. Helicobacter pylori, implicated as an aetiological factor in duodenal ulcers and gastritis, induces the appearance of lymphoid aggregates (MALT) in the stomach. This organism is cytotoxic via a nitric oxide synthase cascade. The possibility that tonsillar tissue processes Helicobacter pylori or that Helicobacter pylori can colonize the palatine tonsils is explored. The study design was that of a prospective study. We determined if Helicobacter pylori (i) forms part of the normal microenvironment of the tonsil, (ii) plays a role in the pathogenesis of tonsillitis and (iii) is associated with increased expression of inducible nitric oxide synthase (iNOS) in macrophages of the tonsil. Serology for Helicobacter pylori was performed on 50 patients undergoing tonsillectomy. Tonsillar specimens were monitored for urease activity by CLO test (a sealed plastic slide holding an agar gel, which contains urea and detects the urease enzyme of Helicobacter pylori), and immunocytochemically probed for Helicobacter pylori and iNOS expression. The mean age of this patient group was 17.2 years (3-36 years). Fourteen (28%) were sero-positive for Helicobacter pylori but no evidence of this pathogen was found in any tonsillar specimen. The number of macrophages staining for iNOS, per field, under a magnification of x40, was increased in sero-positive patients (13.3 +/- 1.3 versus 9.9 +/- 0.7; P = 0.01). Helicobacter pylori does not appear to colonize the tonsil. We believe that Helicobacter pylori primes the tonsils by inducing macrophage iNOS expression. The higher expression in sero-positive patients is a reflection of a pro-inflammatory reaction to Helicobacter pylori that is both local and systemic.
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PMID:Helicobacter pylori and tonsillectomy. 1184 33

The discovery of Helicobacter pylori (H. pylori) has revolutionised the pathophysiological and clinical approach to gastric and duodenal ulcer. Since the first paper identifying H. pylori was published only 19-20 years ago, it has been found out that this bacterium causes probably the commonest human infection. Like other revolutions in history, the original directions of the H. pylori story have changed in response to conflicting ideologies, observation, and practices. It is known that once H. pylori is acquired, colonisation continues for life unless the organism is eliminated by antimicrobial treatment or by the usually late-in-life development of the atrophic gastritis. If any recent achievement in the world of medicine is to be called revolutionary, then it is the discovery of the role of this spiral bacterium in the etiopathogenesis of gastritis, gastric ulcer, duodenal ulcer, gastric adenocarcinomas and gastric mucosa-associated lymphoid type (MALT) B-cell lymphomas. Essentially everyone who carries the organism in the gastric mucous layer has evidence of tissue reaction (termed chronic active gastritis), but most colonised persons remain asymptomatic for life. In the absence of treatment, the presence of H. pylori can be determined with a high degree of confidence by endoscopy (with culture, histologic examination, or urease testing of gastric biopsy specimens), by serologic testing, or by urea breath tests. After successful treatment, specific antibody levels decrease so slowly that serologic testing cannot be used to document success for at least 6 months. In most patients, elimination of H. pylori changes the natural history of peptic ulcer disease and of gastric MALT lymphomas. It is now recommended that these patients have to be treated to eliminate H. pylori because the benefits seem to substantially outweigh the risks and costs. Currently, enthusiasts, drug companies, and the lay press are putting pressure on physicians to eliminate H. pylori from all patients, symptomatic or not, in whom it is detected. There is little evidence that this is appropriate, and management will continue to change as new knowledge emerges and socioeconomic environments change in ways that are relevant to H. pylori and clinical medicine.
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PMID:[Is the only good Helicobacter a dead Helicobacter?]. 1205 16


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