Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In seven elderly patients with benign gastric ulcer, numerous spores and mycelia of Candida were found in the inflammatory exudate and in the base of the ulcer. All patients were treated with cimetidine and antacids. In five patients the ulcer failed to heal. Cimetidine was replaced with mycostatin and after four weeks of treatment, the ulcers healed completely in four patients. It is assumed that in the elderly, due to the weakening of the host defense mechanisms, Candida may invade the base of the ulcer and disturb the normal process of healing.
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PMID:Candidal infection of benign gastric ulcers in aged patients. 723 43

Measurements were made of the amounts of histamine extracted from patients with peptic ulcer disease and control subjects suffering from various gastrointestinal diseases. Patients with duodenal ulcer, gastric ulcer, or recurrent duodenal ulcer after proximal gastric vagotomy often had less gastric mucosal histamine than did normal controls. Cimetidine therapy increased the amounts of the histamine to above control levels, presumably by suppression of output. It is concluded that endogenous amounts of histamine reflect the pathogenic states in the gastric mucosa of patients with peptic ulcer diseases. Cimetidine, as does vagotomy, increases the amount of gastric mucosal histamine. These findings suggest that the increase in mucosal histamine with cimetidine is not due to activation of histamine methyl transferase, but rather to suppression of histamine output into the gastric juice.
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PMID:Effect of cimetidine on the amounts of histamine in the gastric mucosa of patients with gastric or duodenal ulcers. 730 46

The relationship between histopathological alterations and G-cell population in the stomach was studied in l4 resected stomachs from patients with chronic peptic ulcer disease (6 with duodenal ulcer and 8 with gastric ulcer). G-cells were identified by indirect immunoperoxidase method. When atrophy was graded three steps (0, 1, 2), the average grade of DU and GU was 0.23 and 0.89, respectively. There was a significant correlation (r=0.871, p less than 0.005) between atropic grade and G-cell population in each stomach. The mean occupation rate with intestinal metaplasia was 0.9% in DU and 35.8% in GU. There was no correlation between total pyloric area and G-cell population, however residual pyloric area excluding intestinal metaplasia correlated significantly with G-cell population (r=0.557, p less than 0.05). There was a significant difference in the mean G-cell population which were 26.5 millions in DU and 8.9 millions in GU. The mean integrated gastrin response to Cimetidine-OXO test meal were 559+/-236 pg/ml in DU and 216+/-124 pg/ml in GU, and there was significant correlation (r=0.889, p less than 0.005) between G-cell population and integrated gastrin response. The average age of both groups, however, was 27.7 in DU and 52.8 in GU, so that these differences of G-cell population and functional G-cell mass in both groups might originate in the histopathological alterations accompanying with the aging.
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PMID:G-cell population and serum gastrin response to cimetidine-OXO test meal in relation to histopathological alterations in resected stomachs from patients with peptic ulcer disease. 738 Jan 65

Antacids reduce gastric acidity by neutralization, diminish peptic activity by increasing luminal pH above that optimal for proteolysis and provide thereby the rational for their use in ulcer disease. In clinical trials antacids fastened ulcer healing in patients with duodenal ulcer but not with gastric ulcer when compared to placebo. Furthermore, the prophylactic use of antacid medication can significantly reduce the frequency of acute bleeding when gastric content is titrated to a pH greater 3.5 on an hourly basis. Cimetidine does not adequately protect seriously ill patients from acute upper gastrointestinal tract bleeding. Antacids are better for this purpose. So far the efficacy of an antacid therapy has not been proven in controlled trials in patients with chronic ulcer disease, in patients with recurring ulcers following gastric surgery and in patients bleeding from acute or chronic gastroduodenal lesions.
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PMID:[Complicated ulcer; prevention and therapy of upper gastrointestinal bleeding; indications for antacid therapy]. 741 51

Since the introduction of cimetidine the number of patients operated upon for peptic ulcer has decreased in most departments of surgery. This is mainly due to a change in attitude towards the indication for surgery in chronic uncomplicated duodenal ulcer. The classic surgical indications of perforation, hemorrhage, and pyloric obstruction remain unchanged, but the criterion of intractability as an indication for elective surgery needs to be redefined. For chronic recurrent uncomplicated duodenal ulcer in the otherwise fit and healthy subject, prolonged treatment with cimetidine is not a suitable alterative to surgery. Proximal gastric vagotomy is the method of choice for elective operation in chronic duodenal ulcer. In gastric ulcer the situation is complicated by the risk of failure to diagnose malignancy and erroneous conservative treatment of cancer taken for benign ulcer disease. Follow-up by repeated endoscopies and biopsies is a sine qua non for conservative management of gastric ulcer. The results of surgical treatment of gastric ulcer are satisfactory. Postsurgical symptoms and recurrent ulcer are less frequent after resection for gastric ulcer than after operations for duodenal ulcer. Resection is still considered the method of choice. The results of prospective studies do not at present support the treatment of gastric ulcer by vagotomy rather than by gastric resection. Reoperation for postoperative recurrent ulcer carries a higher risk than the primary intervention. On the other hand, recurrent ulcer responds quite favorably to cimetidine treatment. Cimetidine may serve as an initial therapeutic approach to obtain healing of the ulcer and postpone corrective surgery to a later, elective date.
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PMID:[Surgical treatment of ulcers]. 742 75

The effects of three typical antisecretory agents: cimetidine, atropine and prostaglandin E2 were compared on an acute rat gastric ulcer model which consisted of perfusing the stomach continuously, at a high intraluminal pressure (120 mm H2O), with a simulated gastric juice (0.1 M HCl plus 600 mg pepsin/l). As the acid and pepsin are given exogenously the inhibitory action of the antisecretory drugs is obviated in this model. Cimetidine and atropine failed to reduce gastric erosions, whereas prostaglandin E2 markedly reduced the severity of the mucosal lesions with respect to control values. Long-term treatment with cimetidine also failed to increase the resistance of the gastric mucosa to the digestive action of the artificial gastric juice. These findings indicate that only prostaglandin E2 is cytoprotective and do not support the view that anticholinergics or histamine H2-receptor antagonists have a cytoprotective role on the cells of the gastric mucosa.
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PMID:Effects of cimetidine, atropine and prostaglandin E2 on rat mucosal erosions produced by intragastric distension. 744 34

The healing of acetic acid-induced gastric ulcer in rats and the effects of cimetidine and calcitonin were investigated with reference to the enzyme activity of both prolylhydroxylase and collagenase as related to histological findings. The rats were observed by endoscopy on the 3rd day after the subserosal injection of acetic acid; rats with ulcers were divided into three groups: non-treated, and cimetidine- and calcitonin-treated. The latter two groups were treated for 7 days. Prolylhydroxylase activity in active ulcers in the non-treated group was slightly higher on the 3rd day and significantly higher on the 10th day than the activity in control rats that had received subserosal injections of physiological saline solution on the respective days. In non-treated rats, the healed ulcer on the 10th day showed lower prolylhydroxylase activity than that in the active ulcer on the same day. Cimetidine did not affect prolylhydroxylase activity, but, with calcitonin, there was higher prolylhydroxylase activity in the healed than in the active ulcer, although the difference was not significant. Interstitial collagenase showed the highest activity on the 3rd day and decreased on the 10th day in non-treated rats. Collagenase activity was higher in the cimetidine-treated group, than that in the non-treated group, and numerous peroxidase-positive granulocytes were seen in the mucosa and submucosa. Calcitonin did not affect collagenase activity. The participation of both enzymes is indispensable in the healing process and the effects of anti-ulcer agents on these enzymes must be considered.
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PMID:Wound healing of acetic acid-induced gastric ulcer in rats and the effects of cimetidine and calcitonin, with special reference to prolylhydroxylase and collagenase enzyme activity. 764 95

Gastric ulcer is relatively infrequent, and clinical trails are often based on small-sized samples. The aim of this study was to define the "gold standard" therapy of active gastric ulcer. We included all single- or double-blind clinical trials on the short-term treatment of gastric ulcer. All the articles published over the period 1977-1994 were reviewed. Meta-analysis was done with both fixed and random effect models; results were shown using Galbraith's radial plot. Forty-eight papers comprising 52 studies were evaluated. Cimetidine, ranitidine, and famotidine proved significantly better than placebo [odds ratio (OR) and 95% confidence interval (CI 95%) at four to six weeks were: 2.67 (2.03-3.52), 3.94 (2.28-6.80), 1.76 (1.08-2.88), respectively]. Cimetidine and ranitidine had results comparable with the newer H2 blockers [OR (CI 95%) at four weeks: 1.16 (0.91-1.47), 1.11 (0.80-1.55), respectively]. H2 blockers were proved comparable with either sucralfate [OR (CI 95%) at eight weeks: 0.81 (0.37-1.79)] or bismuth [OR (CI 95%) at four to six weeks: 0.67 (0.37-1.20)]. Omeprazole is more effective than H2 blockers [OR (CI 95%) at four weeks: 2.00 (1.57-2.55)]. It is concluded that H2 blockers are preferred to either a placebo or sucralfate for short-term gastric ulcer treatment; the newer H2 blockers do not have significant advantages over the older types; omeprazole can be regarded as the "gold standard" for active gastric ulcer treatment.
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PMID:Short-term treatment of gastric ulcer. A meta-analytical evaluation of blind trials. 865 42

Lafutidine is a new type antiulcer agent with antisecretory and gastroprotective activities. We investigated the effect of lafutidine on indomethacin-induced antral ulcer in refed rats. Subcutaneous indomethacin injection resulted in the formation of gastric antral ulcer. Lafutidine (1-10 mg/kg, p.o.) reduced the area of ulcer in a dose-dependent manner when administered immediately after the indomethacin injection. Capsaicin at 3 mg/kg, p.o. and 16,16-dimethyl prostaglandin E2 at 3 microg/kg, p.o. also reduced the ulcer area. Chemical deafferentation of capsaicin-sensitive neurons or N(G)-nitro-L-arginine treatment aggravated the ulcer formation and abolished the preventive effect of lafutidine and capsaicin. After the induction of gastric ulcer, lafutidine given twice daily for 2.5 days reduced the area of ulcer in a dose-dependent manner with a significant effect at 10 mg/kg, p.o., as compared with that of the control group. In chemically-deafferentated rats, lafutidine did not show any healing effect. Cimetidine (30 mg/kg, p.o.) and famotidine (1 mg/kg, p.o.) had no significant effect on indomethacin-induced antral ulcer. These results may suggest that lafutidine, unlike cimetidine and famotidine, can prevent the indomethacin-induced antral ulcer formation and accelerate the healing of the ulcer in refed rats through mechanisms involving the capsaicin-sensitive afferent neurons and nitric oxide.
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PMID:Antiulcer effect of lafutidine on indomethacin-induced gastric antral ulcers in refed rats. 1046 68

In this study, we compared the effects of cimetidine and omeprazole on the healing of acetic acid-induced gastric ulcers in 8-, 48-, and 96-week-old rats. The repeated oral administration of cimetidine or omeprazole for 14 consecutive days markedly accelerated the ulcer healing in 8- and 48-week-old rats. However, both drugs were ineffective in 96-week-old rats. The basal gastric acid secretion of 8-, 48-, and 96-week-old rats decreased with aging. A single oral administration of cimetidine or omeprazole strongly decreased basal gastric acid secretion in the three different ages of rats. Cimetidine and omeprazole produced a potent and sustained serum gastrin-elevating action in 8- and 48-week-old rats. However, the gastrin-elevating actions of both drugs in 96-week-old rats were much weaker than in the 8- and 48-week-old rats. These results indicate that cimetidine and omeprazole have potent gastric ulcer healing actions in 8- and 48-week-old rats, as well as potent serum gastrin-elevating actions, but both drugs are ineffective in 96-week-old rats, which have lost their gastrin-elevating actions.
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PMID:Influence of aging on gastric ulcer healing activities of cimetidine and omeprazole. 1206 82


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