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)

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

The investigations on the presence of Helicobacter pylori in gastric mucosa biopsy specimens have evidenced another morphologically distinct spiral bacterium, Helicobacter heilmanii, which is associated with histopathological lesions of antral gastritis. The authors found 18 cases of such infection in a number of 1508 children with dyspeptic manifestations examined endoscopically. While H. pylori-associated infection was detected in 48.7% of the cases, H. heilmanii-associated gastritis had a much lower prevalence, 1.1%. The diagnosis was made by microscopic examination of the gram fuchsin-stained smear from a biopsy fragment, the urease test being more commonly erratic or late positive. In 10 cases, the endoscopic examination of gastric mucosa revealed nodularity of antral mucosa, in one of these cases a ulcer lesion at the level of the great curvature being also associated. Histopathological changers of active chronic gastritis have been found but in 4 out of children, the examined fragments of gastric mucosa being collected in most cases from the fundic area: in the child with gastric ulceration the histopathological lesions were of antral acute gastritis. Clinical, bacteriological, endoscopic and histological cure of H. heilmanii gastritis is possible by therapy with bismuth compounds alone.
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PMID:[Helicobacter heilmanii gastritis: the bacteriological, endoscopic and histopathological considerations in 18 cases of infection in children]. 945 52

Anacardic acids and (E)-2-hexenal characterized from the cashew Anacardium occidentale L. (Anacardiaceae) apple have been found to exhibit antibacterial activity against the Gram-negative bacterium Helicobacter pylori, which is now considered to cause acute gastritis. The same antibacterial compounds have also been found to inhibit urease (EC 3.5.1.5).
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PMID:Anti-Helicobacter pylori agents from the cashew apple. 1056 28

We describe the case of a young female referred to our unit because of acute upper abdominal symptoms. Upper gastrointestinal endoscopy showed a gastric picture resembling lymphoma or acute non-steroidal anti-inflammatory drug gastropathy (deep, large and irregular ulcers), but the clinical history and the histological examination of gastric biopsies were consistent only with acute gastritis Helicobacter pylori-correlated. The patient was treated with omeprazole and antibiotics with complete recovery. As the patient's cat had suffered from an acute gastrointestinal distress two weeks earlier, a case of zoonosis was hypothesized and an upper gastrointestinal endoscopy was performed also on the cat. Unfortunately, we were not able to detect Helicobacter pylori in the cat gastric mucosa, but only urease-producing spiral microorganisms. Possible sources of infection and pathogenetic mechanisms of the severe gastritis are discussed.
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PMID:Severe acute gastritis associated with Helicobacter pylori infection. 1097 53

Hp diagnostic is made by invasive methods using gastric biopsy of antrum, for culture and histological study. Non invasive are serology and urea breath test. 152 Hp from 19 children's with acute gastritis (46. 1%); 9 Hp from an adult. There had ampicillin resistance, 27. 4%, claritromicin 21. 8%, metronidazol 58. 4% and tetracycline 31. 5%, the 21 % susceptible to four anti-microbial. RAPD-PCR with 4 primers gave 44 profiles, related with clinical profile. In 7 children, there were two profiles RAPD. Three were similar but different each other. AFLP 23 adults 151 Hp; cagA and vacA genotypes gave unique patterns for each patient. The genes cagA, babA and oipA, secuencing and compared with reported Hp (Genbank); gave high polymorfism. Everything indicates that there are colonization with multiple Hp strains in Mexicans. In 645 sera from 352 children: 36.9% with Hp, the 46. 9% gave him/her anti-shits and 16. 2% antibodies to urease. Adults 293 (89. 1%) with Hp, 78. 9% gave anti-CagA and 59% antibodies to urease. The expression of IL-8 was bigger in infected children that in not infected and more significant in peptic ulcer. Genomic library Cag-PAI revealed 90% (Hp) positive, they had the complete PAI, 2 were incomplete and three negatives. PCR -LiPA LiPA (LineProbe Assay) is suggestive for genotyping assays.
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PMID:[Microbiologic, serologic diagnosis, and genotypification of Helicobacter pylori isolated from biopsies in children and adult people. Molecular detection of the cag pathogenicity island of Helicobacter pylori]. 1757 80