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)

Antacids prove ready if only temporary relief of the symptoms of ulcers. Physicians have been able to increase the rate of healing of gastric ulcers by advising patients to stop smoking and then either admit them to hospital for bed-rest, or use carbenoxolone sodium as an outpatient therapy. The early trials of some other drugs have shown increase in rate of healing of gastric ulcer, but there is no medical treatment which will prevent the high recurrence rate of benign gastric ulcer. The limited data indicate that adequate medical reduction in acid secretion and enhancement of mucosal resistance may benefit patients with duodenal ulcer.
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PMID:Medical treatment of gastric and duodenal ulcer. 79 9

The authors present the results of treatment with acetazolamide of gastroduodenal ulcer (356 gastric ulcer, 1.250 duodenal ulcers--859 with craters--, 24 pyloric stenosi with functional components, and 42 postgastrectomy peptic ulcers). The acetazolamide was administed in daily dosis of 25-30 mg/kg of body weight, sodium and potassium salts were added, and the liquid intake was increased (approx. 2 1 daily). A control was kept of the clinical, secretory, radiological, enzymological, and hydrolectrolytical modification. A decrease is observed of the in the carbonic anhidrase of the gastric mucosa and of the gastric secretion. There is also an increase in the gastric protection factors and a disappearance of ulcer pain. There are no significant hydroelectrolytic modifications of the blood. From a radiogical point of view, the crater of the postoperative gastric, pyloric and peptic ulcer disappears after 2 weeks of treatment, and in duodenal ulcers in 89% of the cases in 3 weeks. The method is the same time a quick, simple, an efficient therapeutic test for the differentiation of the gastric craters. The drug is well tolerated. Nevertheless a clinical, secretory and radiological control of the patients is necessary taking into account the counter-indication for the administration of acetazolamide.
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PMID:[Carbonic anhydrase inhibitors in the treatment of gastro-duodenal ulcer]. 82 86

We report a case of gastrocolic fistula resulting from a benign gastric ulcer, diagnosed by barium meal and endoscopy. The fistula healed with conservative management and treatment with carbenoxolone sodium. To our knowledge this is the first reported case of successful conservative treatment of a benign gastrocolic fistula using carbenoxolone.
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PMID:Benign gastrocolic fistula healing with conservative management. 85 67

Recognising the inhibitory activity of acetazolamide upon acid gastric secretion and its favorable effects in the treatment of gastric ulcer which we have described (see reference) - we applied the therapeutical testing by acetazolamide in the differentiation of benign from malignant niches of the stomach. Acetazolamide was administered orally at doses of 25-30 mg per kilogram body weight in a long term trial, together with 3 gr sodium bicarbonate, 1 gr potassium bicarbonate, 1.5 gr magnesium oxide per day and an increased quantity of liquids, to 741 patients with radiologically demonstrated ulcer craters. The fundamental criterion was the size of the niche as established by radiologic examination. In all gastric ulcers the size of the niche was considerably reduced after 7-9 days of treatment with acetazolamide; the niche disappeared in 2-3 weeks. This favorable result was obtained without diet and rest. In 38 cases in which there was no significant radiologic change of the niche after 7-9 days of treatment with acetazolamide - the malignancy of the niche was confirmed. The simplicity and the effectiveness of this rapid therapeutic test, makes it useful in the differentiation of benign from a malignant ulcer craters.
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PMID:Therapeutic testing by acetazolamide in the differentiation of a benign from a malignant niche. 88 70

Effects of carbenoxolone Na on acute or chronic types of gastric lesions or ulcer models produced in rats, guinea pigs, or dogs were studied. Carbenoxolone Na, given either orally or intraperitoneally, produced a significant inhibition of stress-induced gastric lesions in intact or in pylorus-ligated rats. Acetylsalicylic acid (ASA)-induced or serotonin-induced gastric lesions in rats were also inhibited significantly by pretreatment with the drug. However, carbenoxolone Na did not affect the development of Shay ulceration in rats even though the peptic activity in gastric juices was markedly reduced by the drug. Histamine-induced gastric lesions in guinea pigs were not prevented by pretreatment with carbenoxolone Na. Although carbenoxolone Na, given for 10-20 days, did not promote the healing of stress-induced gastric lesions and acetic acid gastric jlcers in rats, it significantly accelerated the healing of chronic gastric ulcer produced in dogs by 3 weeks' treatment. Carbenoxolone Na prevented the acid back-diffusion caused by ASA without any influence on Na+ efflux in pylorus-ligated rats.
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PMID:Effects of carbenoxolone Na on acute and chronic gastric ulcer models in experimental animals. 98 16

To investigate both the cause and reversibility of pyloric sphincter dysfunction in patients with gastric ulcer, pyloric sphincter pressures were measured in 10 normal subjects and 13 patients with gastric ulcer before and during gastric acidification. Fasting serum gastrin concentration was significantly higher in patients with gastric ulcer than in normal subjects. Compared to normals, patients with gastric ulcer had significantly lower pyloric pressures in response to intraduodenal amino acids and sodium oleate. However, during gastric acidification, these same patients demonstrated normal pyloric responses to these stimuli. Serum gastrin concentrations did not change during gastric acidification. These studies show that: (1) in patients with gastric ulcer the pyloric sphincter does not respond normally to intraduodenal stimulation; (2) fasting serum gastrin concentration is elevated in patients with gastric ulcer; and (3) in these patients, pyloric sphincter dysfunction can be reversed by gastric acidification. The mechanism of pyloric dysfunction in patients with gastric ulcer remains unknown.
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PMID:Reversibility of pyloric sphincter dysfunction in gastric ulcer. 115 75

Administration of 2-DG accompanied by simultaneous neutralization of gastric contents with sodium bicarbonate resulted in a rise in serum gastrin in 4 patients without gastric disease, 4 with duodenal ulcer and 4 with gastric ulcer. The rise in gastrin equals that observed on stimulation with meat extract. Patients with gastric ulcers display a low PAO and a small rise in gastrin compared with normals and patients with duodenal ulcers. This finding correlates well with the chronic atrophic changes of the antral mucosa in patients with gastric ulcer.
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PMID:[Behavior of serum gastrin under vagus stimulation with 2-deoxy-D-glucose with special reference to acid secretion and the mucosal histology]. 125 25

When 17 macrocyclic lactone antibiotics were examined for their abilities to inhibit gastric H+,K(+)-ATPase, copiamycin A was found to have the strongest and relatively specific activity with IC50s of 15.7 micrograms/ml and greater than 100 micrograms/ml against the hog gastric H+,K(+)-ATPase and the dog kidney Na+,K(+)-ATPase, respectively. Furthermore, this antibiotic inhibited the histamine-induced gastric acid secretion in the isolated gastric mucosal membrane of guinea pigs and the gastric ulcer formation in pylorus-ligated rats.
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PMID:Inhibitory effects of copiamycin A, a macrocyclic lactone antibiotic, on gastric H+,K(+)-ATPase, acid secretion and ulcer formation. 164 41

The distribution of (+)-(1R,4aS,10aR)-1,2,3,4,4a,9,10,10a-octahydro-1,4a- dimethyl-7-(1-methylethyl)-6-sulfo-1-phenanthrenecarboxylic acid 6-sodium salt pentahydrate (TA-2711) in stomach was studied after oral administration of 14C-TA-2711 (100 mg/kg) to rats. At 6 h after dosing, most of the radioactivity was found in the lower intestine, caecum and large intestine. However, the radioactivity in the stomach was higher than that in the upper and middle small intestine. The concentration of the radioactivity in the glandular stomach was about 1.5 mg eq. TA-2711/g at 30 min after administration. Thereafter, it decreased gradually to about 60 micrograms eq. TA-2711/g at 6 h after dosing. In the radioluminograms of 6 and 24 h after dosing, most of the radioactivity was observed on the surface of gastric mucosa. After administration to rats with gastric ulcer induced by acetic acid, higher radioactivity was observed in the ulcerated tissues of the stomach than in the nonulcerated control tissues. In the stomach damaged by ethanol, the concentrations of radioactivity in lesion parts were also higher than those in non-lesion parts. In the microautoradiograms of gastric mucosa damaged by ethanol, the developed silver grains were densely distributed in necrotic tissues.
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PMID:Metabolic fate of a new anti-ulcer drug (+)-(1R,4aS,10aR)-1,2,3,4,4a,9,10,10a- octahydro-1,4a-dimethyl-7-(1-methylethyl)-6-sulfo-1- phenanthrenecarboxylic acid 6-sodium salt pentahydrate (TA-2711). II. Distribution in the rat stomach. 177 9

We examined the healing promoting effects of azuletil sodium on acetic acid and clamping cortisone-induced gastric ulcer in rats. For the experiments on clamping-cortisone gastric ulcer, we used not only conventional rats in conventional conditions but also specific pathogen free (SPF) rats on SPF environment in order to prevent infection. The following results were obtained. 1) In acetic acid ulcer, azuletil sodium (AZE) (greater than or equal to 90 mg/kg/day, p.o.) significantly decreased ulcer index. As estimated on the basis of stage analysis (Ulcer, Healing, Scar), AZE (greater than or equal to 30 mg/kg/day, p.o.) significantly promoted the healing of ulcers. 2) In clamping cortisone ulcer (conventional), AZE (100 mg/kg/day, p.o.) significantly promoted the regeneration of blood vessels. 3) In clamping cortisone ulcer (SPF), AZE at greater than or equal to 30 mg/kg/day and 100 mg/kg/day significantly increased the healing index and mucosal regeneration index, respectively. 4) In clamping cortisone ulcer (SPF), the infection that was observed in the conventional test was not seen at all and the acceleration of healing was observed. Furthermore, the extent of adhesion was also reduced, and the standard errors of various healing indices were smaller. From these results, it is concluded that AZE accelerated the healing of experimentally-induced gastric ulcers in rats.
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PMID:[Healing promoting effect of azuletil sodium (KT1-32) on experimental chronic gastric ulcers and acceleration of healing in SPF environment]. 182 59


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