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. Etiopathogenetic heterogeneity is suggested in the group with complicated ulcer.

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