Acid secretory changes and early relapse following duodenal ulcer healing with ranitidine or sucralfate
Article Abstract:
Physiologists have always been impressed with the abilities of the parietal cells lining the stomach. These cells manage to secrete large amounts of very strong hydrochloric acid into the stomach. In some cases, the normal protective mechanisms of the stomach and the duodenum fail, and an ulcer may result from the action of this acid. Many types of effective treatment are available for stomach and duodenal ulcers; unfortunately, the relapse rate is extremely high and most ulcer sufferers can expect to experience a recurrence. Some anti-ulcer drugs, such as ranitidine, work by decreasing the secretion of stomach acid. However, there is some evidence of a 'rebound' effect. That is, once the medication is halted, the parietal cells, which secrete the stomach acid, rebound and secrete more stomach acid than they did prior to treatment. To determine the relation between stomach acid secretion and the likelihood of a quick relapse, several studies of acid secretion were conducted with duodenal ulcer patients treated with ranitidine or sucralfate. In contrast with ranitidine, sucralfate does not decrease acid secretion during treatment, but rather appears to provide a protective barrier for the ulcer. When measurements made prior to treatment were compared with those made after the ulcers had healed, it was found that the amount of acid secretion varied for each patient, but was reduced on average. However, it was noted that stomach acid secretion at night actually rose after treatment with ranitidine and fell after treatment with sucralfate. While the actual amount of change was different for individual patients, it was found that those with increased acid secretion were more likely to suffer an early ulcer relapse, compared with patients in whom stomach acid secretion decreased after treatment. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Medicine
Subject: Health care industry
ISSN: 0002-9343
Year: 1991
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Sucrose octasulfate stimulates gastric somatostatin release
Article Abstract:
Sucralfate promotes the healing of peptic ulcers in both experimental animals and people. There are many theories attempting to explain the success of sucralfate in the treatment of ulcers, but none appears to be entirely satisfactory. Many of the explanations offered for the therapeutic effectiveness of sucralfate focus on the physiochemical properties of the substance and how they might provide an effective barrier between stomach acid and the living cells lining the organ. It is certain that sucralfate does not directly effect the release of stomach acid. However, it is possible that the medication does influence a host of other physiological processes. Somatostatin is a hormone that is suspected of playing important roles in stomach physiology, including the regulation of acid secretion and perhaps blood flow within the stomach. A study was therefore conducted to determine if sucralfate has any effect on the secretion of somatostatin by stomach cells. The response of isolated stomach cells in tissue culture to sucralfate was measured, as was the response of stomachs of laboratory rats. Using an antibody test to measure the amount of somatostatin, it was found that both the isolated cells and the stomachs increased secretion of somatostatin in response to sucralfate treatment. In the case of the rat stomachs, the increase was 60 percent above normal. Previous studies have demonstrated that somatostatin increases the production of stomach mucus. Furthermore, somatostatin has been shown to prevent the experimental induction of ulcers in some laboratory studies. Therefore, it seems reasonable to suggest that the stimulation of somatostatin by sucralfate may account for at least some of the beneficial effects of sucralfate on peptic ulcers. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Medicine
Subject: Health care industry
ISSN: 0002-9343
Year: 1991
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