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)

A double-blind 4-week trial of sodium oxyferriscorbone versus placebo (distilled water) was conducted in 46 outpatients with endoscopically confirmed gastric ulcer. Ulcer healing occurred in 15 of 20 patients receiving sodium oxyferriscorbone (75%) and in 7 of 20 patients receiving placebo (35%). Patients receiving sodium oxyferriscorbone experienced less pain and required less antacid than those receiving placebo (P less than 0.05). Side effects were reported in 12 patients, 7 while receiving sodium oxyferriscorbone and 5 while receiving placebo. Six patients did not complete the study due to ulcer complications. Routine laboratory tests revealed no persistent abnormalities that could be related to the treatment. Five placebo-treated patients that were therapeutic failures were switched to sodium oxyferriscorbone and healing was observed within 3 weeks. It is concluded that sodium oxyferriscorbone is effective in enhancing healing of gastric ulcers.
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PMID:Randomized double-masked trial of sodium oxyferriscorbone for the treatment of gastric ulcers. 38 61

The observations upon the therapeutic effect of Caved S preparation are reported, being a combination of deglycyrrhizinated liquorice, alkalizing substances and vagolytic drugs. The clinical trial of the medicine reveals it to be with a quick effect on the subjective complaints good tolerance and no manifested disturbances on water and electrolyte balance. It is suitable for the treatment of patients with gastric and duodenal ulcers. Ulcer niche roentgenologically is healed in 37,5% of the patients with gastric ulcer and in 33% in the patients with duodenal ulcer. Endoscopically, the niche is healed in 25% of the patients with gastric ulcer and in 28,5%--with duodenal ulcer. The medicine is with no effect in cases of gastric callous ulcer, as well as with pyloric stenosis.
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PMID:[Clinical trial of the preparation Caved S in treating peptic ulcer]. 77 69

Carbenoxolone sodium has been shown to accelerate the rate of healing of both gastric and duodenal ulcers, but its overall value in duodenal ulcer is probably less because of the high rate of natural remission of duodenal ulcers. Further studies are required to decide whether it should be used prophylactically to delay ulcer recurrence. Carbenoxolone may act by affecting both the proliferative activity of gastric epithelium and the differentiation of the epithelial cells to produce mucus (as well as favourably altering the physicochemical properties of mucus and by reducing peptic activity), factors which may be relevant ot the prevention of acute gastric ulcers. Some studies suggest that carbenoxolone adds to the effect of hospitalisation and bed rest on ulcer healing. Whether bed rest confers additional benefit to the drug's ulcer healing effect in outpatients is also uncertain. There is no evidence that accelerated healing by carbenoxolone is associated with improved overall prognosis. Carbenoxolone is of greatest benefit in accelerating the healing of gastric ulcers in patients for whom hospitalisation is not possible or desirable, but it should only be used in the ambulatory patient when careful and regular observation of serum electrolytes (particularly potassium), blood pressure and weight is possible and when it is known that the patient will attend regular follow-up. Patient must be educated in the proper use of the drug. If severe mineralocorticoid-like toxic effects such as sodium and water retention and hypokalaemia appear, as they do in a variable proportion of patients but most frequently in those receiving excessive doses, carbenoxolone should be stopped and the complication treated; they respond to thiazide diuretics and potassium supplements, and probably to amiloride given in conjunction with a low dose of a thiazide diuretic. Treatment with carbenoxolone can continue with concurrent diuretic therapy in patients with less severe side-effects. Optimum therapeutic effect in gastric ulcer with the least side-effects is achieved with a dosage of 100mg carbenoxolone tablets 3 times daily for the first week followed by 50mg 3 times daily thereafter, best taken before meals. A lower dosage is desirable in the elderly and in those with liver, cardiac or renal disease. Barium meal or preferably endoscopic examinations should be performed regularly and therapy continued until the ulcer is healed. Dosage for duodenal ulcer is 50mg 4 times daily, in special positioned-release capsules. These are best taken about 20 minutes before meals.
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PMID:Carbenoxolone: a review of its pharmacological properties and therapeutic efficacy in peptic ulcer disease. 78 88

Studies of water soluble proteins of mucous and cancer tissue of the stomach were conducted by a method of electrophoresis in a polyacrylamid block. Under study were 18 postresection specimens (12--gastric cancer, 5--gastric ulcer, 1--duodenal ulcer). 5--7 prealbumin fractions were found in normal mucosa and that with histological changes typical for superficial and, sometimes, moderately pronounced atrophic gastritis. Gastric mucous membrane in marked atrophic, gastritis and of cancerous tissue were characterized by disappearance of the first 2,3, 4 prealbumin fractions or reduction of their peaks.
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PMID:[Pre-albumins of cancerous tissue of the stomach]. 113 8

The gastric acid secretion in response to graded antral distension was determined in healthy subjects and in peptic ulcer patients with water perfusion or alkaline buffer perfusion of the stomach, giving an intragastric pH of 1.8-3.0 and 6.2-8.3 respectively. Intragastric neutralization increased the basal acid secretion in healthy subjects and gastric ulcer patients but did not change the basal acid secretion in duodenal ulcer patients. Distension of the antrum produced the same secretory effect with and without intragastric neutralization: no increased acid response in healthy subjects, a slight acid response in patients with a quiescent duodenal ulcer or a gastric ulcer, and a more pronounced acid response in patients with an active ulcer, amounting to about 30% of the peak acid response to pentagastrin. The results show that: a) the peptic ulcer patients - and particularly patients with an active duodenal ulcer - are more sensitive to the acid secretory effect of antral distension than healthy subjects; b) increasing the intragastric pH above 20 does not enhance the acid response to antral distension; c) the acid secretory effect of antral distension is markedly less in man than the effect observed in the dog.
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PMID:The effect of intragastric neutralization on the gastric acid response to antral distension in man. 117 56

Pyloric sphincter pressure was assessed with water-perfused polyvinyl tubes. Smoking one cigarette significantly decreased the basal pyloric pressure, whereas 10 mg of metoclopramide as an intravenous bolus increased the pyloric pressure in normal subjects and in patients with gastric ulcer with low basal pressure. Duodenal acidification with 0.1 N HCl significantly increased pyloric pressure. Atropine 15 mug per kg, subcutaneously prevented the rise of pyloric pressure in response to acid infusion into the duodenum.
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PMID:Manometric studies on the human pyloric sphincter. Effect of cigarette smoking, metoclopramide, and atropine. 125 34

This study presents an observation of the anti-inflammatory effect of Aconitum carmichaeli decoction on water-immersion stress induced gastric ulcer in mice and 0.6 mol/L HCl induced gastric ulcer in rats. The observation showed that the decoction was resistant to the castor oil induced and Cassia angustifolia leaf induced experimental diarrhea in mice, and also had marked analgesic action. It is thus suggested that Aconitum carmichaeli is useful clinically as a spleen-stomach warming and analgesic agent in traditional Chinese medicine.
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PMID:[Pharmacological study on spleen-stomach warming and analgesic actions of Aconitum carmichaeli Debx]. 141 55

The preventive effects of hydroxychalcone derivatives on ulcer formation induced by severe necrotizing agents such as 60% ethanol in 150 mM HCl (HCl-ethanol) and 0.2 N NaOH in rats were examined. Among the compounds tested, 2',4'-dihydroxychalcone gave the strongest activity in both experimental models and protected the gastric mucosa from the insult of either necrotizing agent at oral doses ranging from 1 to 10 mg/kg, as evidenced by a dose-related reduction in the ulcer index. The mucosal protective activity of 2',4'-dihydroxychalcone was not affected by pretreatment with indomethacin (5 mg/kg, s.c.). To investigate the detailed mechanism of the mucosal protective action of 2',4'-dihydroxychalcone, its inhibitory effects on the decrease in the hexosamine content from the gastric mucus induced by HCl-ethanol were studied by using it in combination with a dye, Alcian blue. As a result, 2',4'-dihydroxychalcone at an oral dose of 10 mg/kg inhibited the decrease in the dye-recovery from the gastric mucus induced by HCl-ethanol. PGE2 at an oral dose of 0.1 mg/kg exhibited a similar action. These results established that 2',4'-dihydroxychalcone is a potent cytoprotective agent similar to PGE2 effectively preventing gastric ulcer formation induced by strong necrotizing agents and seems to suggest that this compound protects the stomach against its own peptic secretions by reinforcement of gastric resistances. In fact, 2',4'-dihydroxychalcone prevented ulcer formation induced by water-immersion stress in rats and also showed a marked enhancement of the healing of acetic acid-induced gastric ulcers in rats.
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PMID:Gastric cytoprotective anti-ulcerogenic actions of hydroxychalcones in rats. 147 Jun 60

The effects of a weakly acidic polysaccharide fraction, GL-4, from the leaves of Panax ginseng C. A. Meyer on various experimental gastric ulcer models in mice and rats have been studied. Oral administration of GL-4 at doses of 50 to 200 mg/kg inhibited the formation of the gastric lesions induced by necrotizing agents such as HCl/ethanol and ethanol in a dose-dependent manner. This protective effect was observed not only upon oral but also upon subcutaneous administration of GL-4 (50-100 mg/kg). GL-4 also inhibited the formation of gastric ulcers which were induced by water immersion stress, indomethacin, or pylorus-ligation. The contents of prostaglandin E2 in the gastric juice from rats were not influenced by oral administration of GL-4. The protective action of GL-4 against HCl/ethanol-induced gastric lesions was not abolished by pretreatment with indomethacin. When GL-4 (100 mg/kg, p.o.) was administered into pylorus-ligated rats, both gastric acidity and pepsin activity in the gastric juice decreased significantly.
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PMID:Anti-ulcer activity and mode of action of the polysaccharide fraction from the leaves of Panax ginseng. 147 Jun 67

Nicotine is known to influence locomotor activity. The alkaloid also intensifies gastric ulcer formation in stressed rats. The effects of nicotine on locomotor activity in relation to gastric lesions induced by restraint at 4 degrees C for 2 h (stress) were, therefore, studied. Ten-day treatment with nicotine 25 or 50 micrograms/ml drinking water potentiated stress-evoked ulceration and mast cell degranulation. These same doses of nicotine increased vertical motor activity; only the higher dose of the alkaloid enhanced horizontal movements. Phenobarbitone (12.5, 25, or 50 mg/kg, SC) dose dependently reduced vertical activity, as well as stress-induced gastric ulceration and mucosal mast cell degranulation. The drug also lessened the potentiating effects of nicotine on motor activity and stress-evoked gastric lesion formation. It is concluded that the ability of chronic nicotine treatment to intensify stress-induced gastric ulceration most likely owes part of its action to a mechanism evoking increased activity, which possibly reflects an influence on the CNS, as well as to enhancement of mast cell degranulation in the stomach glandular mucosa.
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PMID:Effects of nicotine on activity and stress-induced gastric ulcers in rats. 147 87


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