The investigations of 43 duodenal ulcer cases in the patients whose ulcers failed to cicatrize after a 8-week treatment with almagel and vicalin or cimetidine monotherapy revealed the role of the hereditary load, smoking intensity, initial ulcer dimensions, the presence of antral erosions and a pronounced periulcerous duodenitis in the phenomenon of slow healing duodenal ulcer. There was no statistical difference between the values of the basal and pentagastrin-stimulated levels of hydrochloric acid secretion in the morning, partial alkaline gastric secretion, gastrinemia, the rate of evacuation of the gastric contents into the duodenum, the outcome of pancreatic bicarbonates in the sample with exogenic secretin in those whose ulcers cicatrized after a 6-week therapy and those who failed to be cured after being exposed to the same therapy during 8 weeks. The production of hydrochloric acid in the evening and the incidence of manifest duodenal reflux were significantly higher in the patients with slowly healing ulcer. They also had a decreased sensitivity to the intraduodenal inflow of the hydrochloric acid that resulted in the increase of endogenic secretin (stimulating the production of pancreatic bicarbonates and their transport into the duodenum). In case the combination treatment with almagel and vicalin failed, the therapy with gastrocepin or sucralfate was employed. A supplementary course of sucralfate helped to reach a complete healing of noncomplicated ulcers even in the patients in whom the preceding cimetidine treatment failed.