Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.30.2 (endonuclease)
 18,621 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine whether omeprazole eradicates Helicobacter pylori infection of the gastric antrum, six adolescents and one adult with H. pylori colonization of the antrum were entered into a clinical, open trial of medical therapy. Histologic evidence of antral gastritis and three complementary methods to document H. pylori colonization of the stomach (silver stain, urease testing, and culture of antrum) were obtained before and after an 8-week course of omeprazole. In vitro susceptibility to omeprazole and restriction endonuclease analysis were performed on H. pylori isolates obtained from patients before and after omeprazole therapy. Each of the seven patients treated with omeprazole had continued active inflammation in the antrum and one or more features indicative of persisting H. pylori colonization. Minimum inhibitory concentrations and DNA fingerprints of H. pylori isolated after therapy were identical to those of the pre-treatment bacterial isolates in each of the four subjects examined. We conclude that omeprazole therapy alone did not eradicate H. pylori infection of the human antrum. Continued bacterial colonization was not related to either acquired bacterial resistance to the drug or reinfection of the stomach with a different H. pylori strain.
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PMID:Omeprazole therapy for Helicobacter pylori infection. 147 17

The aim of this study was to identify the natural reservoir and route of transmission of Helicobacter pylori infection. Two hundred eight (208) dyspeptic patients (114 males, 94 females; peak age of cohort, 50-59.9) were recruited. Specimens were collected from saliva, supra- and subgingival dental plaque, tongue scrapings, and oropharyngeal swabs. At subsequent endoscopy, gastric antral biopsy was performed for the rapid urease test (RUT), microbiological culture, and, in some patients, histology. Gastric juice samples were aspirated, and in 50 patients duodenal aspirate was collected. Polymerase chain reaction (PCR) with primers targeted to the 16S rRNA sequence of H. pylori was also employed for each of the specimens. In those patients where H. pylori was detected from multiple sites (dental plaque, gastric juice, gastric biopsy, and duodenal aspirate), restriction endonuclease digestion with Hae III was performed to determine if they were epidemiologically linked. The results indicated that 15/208 patients (7%) tested positively for H. pylori by PCR in dental plaque; only 2 samples were positive by culture. In none of the other oral sites sampled was H. pylori detected by any test used in the study. Gastric juice and gastric biopsy specimens from 36/ 208 patients (17%) and 114/208 patients (55%), respectively, were positive by PCR. Duodenal aspirate from 6/50 patients (12%) also tested positively by PCR. All specimens tested by restriction endonuclease digestion with Hae III (15/15 patients) were positive in both antral biopsy and gastric juice specimens, as well as 5 specimens from the duodenal aspirate. Four of the dental plaque strains had restriction patterns similar to those of the stomach and duodenal sites, providing evidence that these sites were infected with the same strain of H. pylori. In conclusion, the results suggest that H. pylori selects the gastric mucosa as its preferred site. The detection in dental plaque could indicate that the oral cavity may act as a reservoir or sanctuary for the organism. Whether H. pylori is a resident or transient oral microorganism is still unclear, although it is more likely to be transient in nature.
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PMID:Helicobacter pylori: the mouth, stomach, and gut axis. 972 11