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.