Diagnostic methods for detecting forms and strains of Helicobacter pylori isolated from biopsy specimens of gastric mucosa in 28 patients with duodenal ulcers and evaluation of its eradication were compared. Biopsy specimens from all patients were tested for the presence of H. pylori by the urease test, histological method, and PCR with species-specific primers before and after treatment. H. pylori infection was detected in all patients before treatment, the mean titer of serum IgG being 36.7+/-16.6 U/ml. Biopsy specimens positive for H. pylori in PCR were subjected to restriction analysis of specific PCR-amplified genes or their fragments. The fingerprint analysis gave electrophoregrams of restriction products amplified fragment of flaA gene of H. pylori in 7 patients. Differences in restriction maps indicate the presence of 5 H. pylori strains in the studied samples.

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It is shown that in patients with ulcer disease endogenous biosynthesis of prostaglandins E and F2~ in gastric and duodenal mucosa is suppressed. In patients treated with Venter (sucralfat), ulcer healing is accompanied by enhanced prostaglandin production in both scar tissue and unaffected areas. Stimulation of prostaglandin E and F2, " synthesis in the gastroduodenal mucosa followed by activation of their cytoprotective effect in the gastrointestinal system is a key mechanism underlying the effect of Venter.