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 variation in the healing and the relapse rates of peptic ulcer disease has led to the search for other factors in the pathogensis of peptic ulcer disease. Helicobacter pylori is believed to be responsible for these different patterns of healing. The results of a study to detect Helicobacter pylori in Sri Lankan patients having duodenal ulcer, gastric ulcer, gastritis and non-ulcer dyspepsia are presented in this paper. The method employed was the urease test which detects the urease enzyme of H. pylori in gastric mucosal biopsies taken during upper gastrointestinal endoscopy. There is a high incidence in those with gastritis and duodenitis.
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PMID:Helicobacter pylori and peptic ulcer disease in Sri Lanka. 158 90

The study using the urease test on mucous biopsies from the antral gastric part and from the duodenum of patients with chronic opisthorchiasis with endoscopic evidence of antral gastritis and gastroduodenitis, and from noninvaded patients with gastritis and duodenitis, some of them with the gastric or duodenal ulcers showed that the test was positive. The test was negative in both groups of patients when the mucosa of the gastric body was examined as well as in those without gastroduodenal pathology. It is supposed that in the both groups of patients gastroduodenal pathology was provoked by the colonization of the gastric and duodenal mucosa by gastric campylobacteria.
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PMID:[The pathogenesis of stomach and duodenal involvement in chronic opisthorchiasis. 1. The urease test]. 175 56

The inflammatory lesions associated with Helicobacter pylori gastritis and duodenitis contain large numbers of mononuclear cells. The close proximity of H. pylori to gastric mucosa suggests that the organism interacts with mononuclear cells, thereby modulating the inflammatory response. To investigate the role of monocytes/macrophages in this response, we examined the effect of whole H. pylori bacteria, H. pylori surface proteins, and H. pylori lipopolysaccharide (LPS) on purified human monocytes. Whole H. pylori and the extracted LPS induced expression of the monocyte surface antigen HLA-DR and interleukin-2 receptors, production of the inflammatory cytokines interleukin 1 and tumor necrosis factor (peptide and messenger RNA), and secretion of the reactive oxygen intermediate superoxide anion. Since H. pylori in vivo does not invade mucosal tissue, we determined whether soluble constituents of the bacteria could activate monocytes. Soluble H. pylori surface proteins, which are enriched for urease and do not contain LPS, stimulated phenotypic, transcriptional, and functional changes consistent with highly activated monocytes. These findings indicate that H. pylori is capable of activating human monocytes by an LPS-independent as well as an LPS-dependent mechanism. H. pylori activation of resident lamina propria macrophages and monocytes trafficking through the mucosa, leading to the secretion of increased amounts of inflammatory cytokines and reactive oxygen intermediates, could play an important role in mediating the inflammatory response associated with H. pylori gastritis and duodenitis.
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PMID:Soluble surface proteins from Helicobacter pylori activate monocytes/macrophages by lipopolysaccharide-independent mechanism. 184 39

Helicobacter pylori seeks gastric mucosa, whether found in the stomach, duodenum, or Barrett's esophagus. Definitive diagnosis can be secured by appropriate stains of mucosal biopsies and culture, but the rapid urease test, breath isotope studies, and serologic testing are also useful. The frequency of colonization increases with advancing age, but infection occurs earlier in underdeveloped countries. Although the reservoir is uncertain, water or food transmission seems likely. There is sufficient evidence to assign an etiologic role to the bacteria in the causation of type B antral gastritis. H. pylori is found in areas of gastric metaplasia within the duodenum and is associated with duodenitis. Although acute infection leads to hypochlorhydria, chronic colonization has little effect on acid secretion. Studies have thus far failed to establish a convincing relationship between H. pylori and nonulcer dyspepsia, although the bacteria may play a role in selected patients. H. pylori is found in association with most idiopathic gastric and duodenal ulcers, but it is unclear as to whether the bacteria plays a causative or permissive role. The organism has a predilection for intercellular spaces and the mucous layer, thus affording relative isolation from luminally active antibiotics. Monotherapy with bismuth preparations transiently eliminates the bacteria, but recolonization is rapid, probably due to regrowth of sequestered organisms. A combination of metronidazole, bismuth, and tetracycline (or amoxicillin) affords the best eradication rate, but the potential side effects of this program should be considered. The present therapy of duodenal ulcer disease is effective and without significant risk. Treatment of H. pylori should be reserved for those patients who relapse on adequate maintenance therapy. If a safe and effective antibiotic becomes available, more frequent testing and earlier treatment intervention may become more attractive. H. pylori is probably an "innocent bystander" for most patients, but the bacteria may sufficiently impair the defenses of the antral and duodenal mucosa to facilitate the development and relapse of ulcer disease in subsets of patients.
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PMID:Helicobacter pylori: aggressor or innocent bystander? 207 88

Twenty three children with coexistent duodenal ulcer and Helicobacter pylori infection were treated with either two weeks of amoxycillin (25 mg/kg/day) in addition to six weeks of cimetidine, or cimetidine alone. Endoscopy with antral and duodenal biopsies for urease test, microaerophilic culture, and histological studies were performed at entry, six weeks, 12 weeks, and at six months. Children with persistent H pylori infection at six weeks were given a further two weeks' course of amoxycillin. H pylori persisted in all children not receiving amoxycillin treatment but cleared in six of the 13 children (46%) treated with amoxycillin. With failure of H pylori clearance at six months, only two out of six (33%) ulcers had healed and 50% of patients had experienced ulcer recurrence. In contrast, when H pylori remained cleared all ulcers healed and no ulcer recurred. Persistent H pylori infection was associated with persistent gastritis and duodenitis despite endoscopic evidence of ulcer healing. Detection and eradication of H pylori deserves particular attention in the routine management of duodenal ulceration in children.
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PMID:Helicobacter pylori and associated duodenal ulcer. 224 31

The authors evaluate clinical experience based on a correlation between the clinical condition and the finding of Campylobacter pylori (CP) in a total of 1027 specimens of the gastric mucosa. They confirmed the high incidence of CP in patients with a fresh duodenal ulcer (g 7%) but also in the inactive stage of duodenal ulcer disease (97.8%) and in patients with a pyloric ulcer (94.4%). An analogous incidence of CP in patients with so-called isolated duodenitis (in the course of the disease no ulcer lesion was ever detected), i.e. in 95.5%, indicates the relationship of this condition with peptic ulcer disease. The authors indicate diagnostic possibilities as regards CP infection by cultivation, rapid urease tests and microscopic examination and they emphasize the practical value of urease tests. Based on their own experience the authors confirm the high eradication effect of bismuth preparations, in particular bismuth subsalicylate and colloid bismuth subcitrate.
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PMID:[Campylobacter pylori, its detection and association with common pathologic conditions of the gastro-duodenum]. 233 15

Endoscopic gastric antral biopsy specimens (133) from 92 dyspeptic patients with endoscopically evident gastritis (34; including one patient with dual pathology) gastric ulcer (13), duodenitis (17; including one patient with dual pathology) duodenal ulcer (29) and 41 subjects of non ulcer dyspepsia (NUD) with endoscopically normal upper gastrointestinal tract were examined for H. pylori by stained smear, various urease tests, culture and histopathology. Crushed tissue smear stained by Gram's method using carbol fuchsin counterstain proved to be the simplest and a reliable technique. Up to 4 h urease broth + ve test correlated well with smear and culture. Positive association of H. pylori with disease was considered when at least two of the above methods were suggestive. Significantly higher positivities were observed in gastritis (61.7%), gastric ulcer (84.6%), duodenitis (58.8%) and duodenal ulcer (82.8%) patients, as compared to NUD subjects (46.3%). Severe histopathological lesions were frequently associated with multiple bacteriological test positives.
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PMID:Evaluation of different methods for detection of Helicobacter pylori in patients with gastric disease. 234 21

From August 1987 through July 1988, we evaluated antral biopsy specimens for Campylobacter pylori (CP) in 212 patients undergoing upper endoscopy. For those patients who had multiple endoscopies, the first endoscopy in which a urease test, histology, and culture were done was used to determine CP status. A patient was regarded as CP-positive if the culture was positive or if both a urease test and the histology were positive. Blacks had an increased CP positivity (61.2%) compared to whites (31.5%). Among non-ulcer patients, CP positivity was 52% in black patients and 18% in white patients. Age and gender were unrelated to CP positivity among controls and those without ulcers. There was increased CP positivity in patients with duodenal ulcers (85%), compared with those without ulcers (37%), and a trend toward increased positivity in those with gastric ulcer (53%) and duodenitis (50%). There was no increased CP positivity in patients with gastroesophageal reflux disease (28%), gastritis (29%), non-ulcer dyspepsia (43%), or the control patients with no gastroduodenal mucosal abnormalities (40%). CP-negative DU patients were older (average 71 yr) than CP-positive DU patients (43 yr), and female DU patients had a lower CP positivity (71%) than males (94%).
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PMID:Prevalence of Campylobacter pylori in patients undergoing upper endoscopy. 272 34

The relationship between the presence of Campylobacter pylori and esophagitis was studied in patients undergoing paired biopsies of distal esophagus and gastric antrum during esophagogastroduodenoscopy. Biopsy specimens were examined for urease activity and for the presence of C pylori by culture and by histologic examination of hematoxylin-eosin- and Warthin-Starry-stained sections. Sixty-two patients were entered into the study. All esophageal biopsy specimens, regardless of histologic findings, were negative for the presence of C pylori by urease test, culture, and histologic examination. Of 35 patients with normal esophageal biopsy specimens, 11 (31%) had antral specimens that were positive for C pylori, while 11 (41%) of the 27 patients with esophagitis had antral specimens that were positive for the organism. Campylobacter pylori was detected in 14 (70%) of 20 patients with chronic gastritis, in 8 (67%) of 12 patients with endoscopically documented duodenal ulcers and erosions, but in only 3 (33%) of 9 patients with endoscopically defined duodenitis. We conclude that histologic esophagitis is not associated with increased prevalence of either gastric or esophageal C pylori. The well-described association of chronic gastritis and duodenal ulcers with C pylori was present in our study population.
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PMID:Prevalence of Campylobacter pylori in esophagitis, gastritis, and duodenal disease. 233 Nov 97

There is now substantial evidence that Campylobacter pylori (Cp) is able to colonize the gastroduodenal mucosa and is responsible for active chronic gastritis, its role in duodenitis, gastric ulceration and duodenal ulceration is still under debate. Cp has a lot of characteristics which are prerequisites for a pathogen: the typical S-shape, the corkscrew-like movement and the powerful urease and protease enzymes. These features allow a rapid movement through the mucous layer to permit access to the apical membranes of the surface mucous cells. There they adhere directly to the membranes and induce several ultrastructural alterations: degeneration of microvilli, depletion of mucous granules and an increase in sialic-acid rich glycoproteins in the apical part of the cytoplasma. Cp weakens the tight-junction complex and is found between the cells and sometimes intracellularly. Cp is phagocytized by invading polymorphonuclear leukocytes and causes an intense inflammatory response. These observations clearly demonstrate pathological alterations which in the cellular level induced by Cp with the result of a disrupted mucosal barrier of the stomach and the duodenum.
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PMID:Pathogenetic implications of ultrastructural findings in Campylobacter pylori related gastroduodenal disease. 316 31


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