Evaluation of the polymerase chain reaction for detecting the urease C gene of Helicobacter pylori in gastric biopsy samples and dental plaque.

A polymerase chain reaction (PCR) assay with oligonucleotide primers homologous to a portion of the urease C gene of Helicobacter pylori was evaluated for specificity with pure DNA and biopsy material. The assay was used to test for the presence of the organism in dental plaque. The species specificity of detection was confirmed by ensuring that the primers did not amplify DNA extracts from H. cinaedi, H. felis, H. fennelliae, H. mustelae and H. nemestrinae. Sixty-two gastric biopsy samples collected from 14 patients (antrum, body and duodenal sites) were cultured and PCR was performed on the samples after culture. Primer sites were conserved in genomically diverse strains. Samples prepared by single-step heat lysis of bacterial cells and biopsy material did not inhibit PCR. The overall specificity was 96% irrespective of genotype. H. pylori was not cultured from dental plaque (15 patients), neither was H. pylori DNA detected by PCR in either urea breath test-positive or -negative individuals. The results showed that primer pair sequences within the urease C gene are conserved in most strains and provide an accurate basis for detecting H. pylori. As the PCR assay was not inhibited and did not yield false positive results with crude extracts from organisms or in the presence of biopsy material, its value as a diagnostic test was confirmed.

The effect of fasting on 24-hour intragastric acidity and plasma gastrin concentration.

Nine healthy subjects underwent two 24-h studies, either when fed six standard meals by mouth or when fasting. There was no significant difference in the median integrated 24-h intragastric acidity when fed or when fasting, 805 or 801 mmol.h/L, respectively. However, the median integrated 24-h plasma gastrin concentration was significantly higher when fed than when fasting, 284 pmol.h/L and 114 pmol.h/L, respectively (p less than 0.01). There appears to be a normal circadian rhythm for intragastric acidity: feeding appears to cause an acute decrease of intragastric acidity and to release gastrin, which in turn causes a compensatory rise of intragastric acidity. The results of this study suggest that the need to reinstate "normal" intragastric acidity is the drive to food-induced gastric acid secretion.

[Histamine 2 receptor antagonists in the treatment of gastric ulcer]. / Los antagonistas de los receptores de histamina dos en el tratamiento de la úlcera gastrica

Eight patients with a clinical, radiology and endoscopic diagnosis of benign peptic ulcer were studied in a prospective fashion using Cimetidine (H2-Receptor antagonist). With this outgoing form of therapy the need for antiacid diminished greatly and pain totally disappeared. We discuss the possible etiological pathways of gastric ulcer and finally propose the simultaneous use of H2-Receptor antagonist and colesteramine with the goal of eliminating the two predominant factors that cause the lesion.

Relief of duodenal ulcer sysmptons by oral metiamide.

Thirty patients with symptoms of duodenal ulceration were treated for five to eight weeks in a double-blind trial with either metiamide 1 g daily by mouth or a placebo. In the 15 patients receiving metiamide there were significant reductions in nocturnal pain and antacid consumption. Daytime pain was diminished. The results suggest that histamine H2-receptor antagonists are likely to be useful in the medical management of the symptoms of duodenal ulceration.