The authors investigate the relevance of ulcer clinical variants (recent ulcer, of 10 years history and 2-3 annual exacerbations, chronic ulcer with aggravations and incomplete remissions) to production of endogenic PGE by gastric mucosa and to blood PGE level. It is shown that with ulcer progression PGE synthesis activization is replaced by its inhibition. A reverse relationship appeared between gastric juice and blood PGE and duration of ulcer.
View Article and Find Full Text PDFKlin Med (Mosk)
April 1995
The author shows that persistent contamination of the mucosa in ulcer patients noticeable even after ulcer healing with Helicobacter pylori leads to disordered coordination of energetic processes in immunocompetent cells. The reserve pathway becomes more active than basic pathway of oxidation, this combining with lymphocyte sensitization to the mucosal tissue. An unfavourable prognostic implication is given to a 1.
View Article and Find Full Text PDFPGE levels were measured in duodenal ulcer patients treated by H2-blockers of histamine receptors of hyperbaric oxygenation (HBO). Histadyl is shown to cause a marked decrease in gastric juice PGE concentrations in contrast to HBO that raised PGE levels close to normal values. It is thought necessary to administer long-term maintenance therapy after cicatrisation of the ulcer lesion with the drugs improving local microcirculation and stimulating bicarbonates production in gastric mucosa, synthetic prostaglandins analogues, in particular.
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