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 diagnosis of Helicobacter pylori infection represents a fundamental step for a correct clinical approach to the patient with gastritis, peptic ulcer or gastric adenocarcinoma or lymphoma. Upper gastrointestinal endoscopy has first to be made in order to obtain gastric juice and mucosal biopsies, where Hp can be found. Two different procedures are recommended to diagnose Hp infection (e.g. urease test and histology or culture). The identification of specific DNA sequences with the polymerase chain reaction represents a sensitive and specific method to diagnose Hp infection. Serum anti Hp antibodies, pepsinogen A and C determination is recommended at diagnosis and during the follow-up to assess the success of therapy.
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PMID:[The role of the laboratory in the diagnosis and monitoring of Helicobacter pylori infection]. 876 55

Many animal models of Helicobacter infection have been described, including infection in rhesus monkeys, ferrets, gnotobiotic piglets, and mice. These animal models utilize a combination of detection methods, including culture, urease testing, and histopathology, all of which may be unreliable, insensitive, or labor-intensive. Development of new animal models of Helicobacter pylori requires new methods of detection with increased sensitivity and specificity. We have developed sensitive and specific PCR primers based on the 16S ribosomal gene sequence of H. pylori. The primers detected single-copy 16S DNA representing 0.2 cell of pure H. pylori (2 cells in the presence of mouse stomach mucosal DNA) and did not cross-react with closely related bacteria. We were able to detect colonization by H. pylori in conventional, euthymic, outbred mice up to 4 weeks postinoculation with a high percentage of isolates tested. One isolate of H. pylori was detected by PCR in 100% of the mice at 6 months and 60% of the mice 1 year after inoculation. Approximately 10(3) to 10(4) H. pylori cells per stomach were detected by utilizing this PCR methodology semiquantitatively. These primers and PCR methodology have facilitated detection of H. pylori colonization in conventional, euthymic mice, colonization which may not have been detectable by other methods.
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PMID:PCR detection of colonization by Helicobacter pylori in conventional, euthymic mice based on the 16S ribosomal gene sequence. 877 May 6

The aim of this study was to investigate the consequence of Helicobacter pylori eradication on gastric mucosa and antral G and D-cells. Forty children, aged 5-17 years with Helicobacter pylori infection were assessed. Helicobacter pylori was detected by a urease test and identified by serological and microbiological methods. Twenty children were again assessed after the therapy (the combination of colloid bismuth subcitrate, amoxycillin and metronidazole). Gastroscopic examination was performed and at least six bioptic specimens were taken from the antrum, body and fundus. Tissue samples, processed with the paraffin method and stained with hematoxyllin and eosin, were assessed. Monoclonal antiserum Gastrin PAP kit 516 and somatostatin PAP kit 512 (DAKO) in the peroxidase-antiperoxidase technique (PAP) have been used to detect G and D-cells. Helicobacter pylori in the gastric mucosa was demonstrated with the Giemsa method. The results show the coincidence of Helicobacter pylori infection and the count of antral G and D-cells and active chronic gastritis in children. After the treatment Helicobacter pylori was eradicated in 70% of children. In 34% of these cases the eradication was followed by a diminution of activity of gastric antral mucosa inflammation and in 20% of these children the resolution of the inflammatory infiltration in the gastric mucosa was seen. A decrease of the antral G and D-cells count and also a diminution of G/D index in these cases were observed.
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PMID:Morphological and immunohistochemical examinations of the dynamic changes of gastric mucosa associated with the treatment of helicobacter pylori infection in children. 877 26

Groups of squirrel monkeys (Saimiri spp.), predetermined to be free of Helicobacter infections in the gastric mucosa, were immunized orally with 0.5-4.5 mg of Helicobacter pylori recombinant urease (rUrease) and 25-500 micrograms of Escherichia coli heat-labile enterotoxin (LT) adjuvant. Oral immunization with rUrease resulted in a markedly elevated serum immunoglobulin G (IgG) antibody response with peak levels at 45 days after immunization. No significant gastric inflammation or cytotoxicity was evident in rUrease immunized monkeys as determined by light and electron microscopy. Twenty-five micrograms of LT was a sufficient and safe adjuvant dosage, whereas higher dosages resulted in diarrhea and lethargy. Animals developed a serum IgG antibody response to LT that did not impede the production of anti-rUrease antibody levels. The results of this investigation indicate that rUrease is immunogenic in a nonhuman primate.
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PMID:Immunogenicity and safety of recombinant Helicobacter pylori urease in a nonhuman primate. 879 6

We aimed to determine the frequency of portal hypertensive gastropathy (PHG) in children with extrahepatic portal venous obstruction (EHPVO) and to find out the role of esophageal variceal obliteration by endoscopic injection sclerotherapy (EIS) and Helicobacter pylori (H. pylori) infection in the pathogenesis of PHG. Twenty consecutive children were studied before EIS and 20 after esophageal varices obliteration. Diagnosis of PHG was established by endoscopic assessment. Helicobacter pylori infection was diagnosed by rapid urease test, H. pylori culture, smear, and histopathologic examination of antral biopsy specimens. Portal hypertensive gastropathy was characterized and graded by endoscopy according to previously established criteria. In the pre-EIS group, eight (40%) had PHG (mild in all) compared with 16 (80%; mild in eight, severe in eight) in the post-EIS group (p < 0.05). Portal hypertensive gastropathy was more extensive in the post-EIS group. There was no significant difference between frequency of gastric varices and H. pylori infection in the pre-EIS and post-EIS groups. We conclude that PHG is common in children with EHPVO; its frequency, extent, and severity increase after esophageal variceal obliteration by EIS, and H. pylori infection does not play any role in its development.
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PMID:Portal hypertensive gastropathy in children with extrahepatic portal venous obstruction: role of variceal obliteration by endoscopic sclerotherapy and Helicobacter pylori infection. 881 18

In cirrhosis, Helicobacter pylori infection may be implicated, together with portal hypertension, bile reflux and alcohol abuse, in damage to gastric mucosa. Aim of this study was to define the influence of non-alcoholic liver disease on the incidence of Helicobacter pylori infection and on the diagnostic accuracy of specific serology. Enrolled in the study were 232 individuals, 105 also had cirrhosis. Infection by Helicobacter pylori, diagnosed by a positive concordance of quick urease test and histology, was detected in 97 (48 with cirrhosis) out of 184 patients. Severe gastritis was more frequent in patients with Helicobacter pylori infection than in patients without. Cirrhosis did not significantly affect the prevalence of Helicobacter pylori infection or the histological features of gastritis. Specific anti-Helicobacter pylori IgG and IgA assay (Bio-Rad GAP test) was used for serological diagnosis. Anti-Helicobacter pylori IgG showed a high sensitivity (85% in cirrhotics, 89% in non-cirrhotics) and low specificity being more evident in cirrhotics (38% vs 56% non-cirrhotics). Serum specific IgA showed low sensitivity (approximately 25% in both groups) and specificity of 79% in cirrhotics vs 84% in non-cirrhotics. In conclusion, non-alcoholic cirrhosis does not affect the incidence of Helicobacter pylori infection and the histological features of chronic gastritis but does decrease diagnostic efficiency of serological tests for Helicobacter pylori.
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PMID:Cirrhosis negatively affects the efficiency of serologic diagnosis of Helicobacter pylori infection. 889 48

The aim of this study was to investigate the prevalence of Helicobacter pylori infection-associated chronic gastritis in an unselected Spanish population. Between November 1990 and May 1991, consecutive patients referred for upper gastrointestinal endoscopy due to severe upper abdominal complaints were studied. Only patients with chronic gastritis were included. Four biopsy specimens were taken (two for histologic examination, one for a rapid urease test, and one for culture of H. pylori). A total of 3094 patients from 17 Spanish Autonomic Communities 1817 men (58.7%) and 1277 women (41.3%) were studied by endoscopy. The mean age of the patients overall was 51.4 years. Of these 3094 patients, 1642 had symptomatic chronic gastritis. The prevalence of H. pylori infection in chronic gastritis patients in Spain was 85% (pooled data of the three methods above), and there was at a close correlation between severity of gastritis and H. pylori infection.
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PMID:Prevalence of Helicobacter pylori infection-associated histologic chronic gastritis in the Spanish population. 895 8

Helicobacter pylori infection is associated with peptic ulcer disease and chronic gastritis, and eradication of the microorganism markedly reduces the recurrence of peptic ulcer. However, a major problem is the choice of a treatment that is effective, has high eradication rate, and is well tolerated by patients. We evaluated the eradication of H. pylori infection in patients with chronic gastritis (CG), duodenal ulcer (DU), and gastric ulcer (GU) after two dual therapies (omeprazole with either amoxycillin or clarithromycin). Of 450 patients initially included in the study, 207 had CG, 187 DU and 56 GU, and all presented with H. pylori infection. Diagnosis was made from endoscope examination, biopsy samples, rapid urease test and 13C-urea breath test (UBT). H. pylori infection was considered to be present when two of the tests had positive results. All patients were randomized to one of two regimens: (A) omeprazole (20 mg b.i.d.) plus amoxycillin (750 mg t.i.d.) or (B) omeprazole (40 mg b.i.d.) plus clarithromycin (500 mg t.i.d.). The duration of each of the regimens was 2 weeks. Fifty-eight patients who showed H. pylori infection after the first treatment (27 with CG, 24 with DU, and 7 with GU) were allocated to a second therapy. H. pylori eradication was assessed by UBT, 6 weeks after the end of the therapies; positive values were those higher than 5 delta units. A second consecutive dual therapy of omeprazole plus an antibiotic (amoxycillin or clarithromycin) not used in the first therapy improved on the eradication rates obtained with the first regimen. The overall eradication rates were also higher, but no significant differences were found between amoxycillin and clarithromycin. The best results were obtained in those patients with GU.
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PMID:Significant increase in eradication rates of Helicobacter pylori infection with two consecutive dual therapies (omeprazole and amoxycillin or omeprazole and clarithromycin). A randomized study in 450 Spanish patients. 895 19

The initial steps have been taken towards the development of a vaccine against the human gastroduodenal pathogen, Helicobacter pylori. Proof of principle was achieved when mice were protected against challenge with living Helicobacter felis, a close relative of the human pathogen, following oral immunization with H. felis sonicate and the mucosal adjuvant, cholera toxin. Similar results with H. pylori antigen have allowed development of possible human vaccines. Recombinant urease protein has been proposed as a major vaccine candidate, together with the heat-labile toxin of Escherichia coli as the adjuvant. Probably the most significant finding in the early vaccine studies was that immunization of already infected mice resulted in a cure of Helicobacter infection. The possibility of a therapeutic vaccine makes commercial development more attractive, as large populations could be immunized without the potential for development of drug-resistant strains that currently restricts widespread antibiotic use. For advanced societies with powerful economies yet a high prevalence of H. pylori, such as Japan, vaccine development should become a high national health priority.
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PMID:Vaccination against Helicobacter pylori. 895 25

Eight commercial enzyme-linked immunosorbent assays (ELISAs) were used to test sera taken from 102 patients in whom Helicobacter pylori infection status had been determined by means of biopsy culture, PCR, histology, and urease production and by 13C urea breath test. By those means, 61 patients had been found to be infected. Assays were compared by receiver operating characteristic analysis. Sensitivities ranged from 86 to 98%; specificities ranged from 83 to 98%. In a group consisting of the assays by Bio-Whittaker, Meddens Biotech, Orion (Pyloriset EIA G, new version), and Enteric Products, Inc. (HM Cap), differences in performance were not statistically significant. Sensitivities in this group ranged from 93 to 98%; specificities ranged from 95 to 98%. Assays from this group may be useful in addition to biopsy-based methods in diagnosing H. pylori infection.
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PMID:Evaluation of eight enzyme immunoassays for detection of immunoglobulin G against Helicobacter pylori. 896 30


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