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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Samples of gastric juice were aspirated every 15 minutes from 54 normal subjects and 31 patients with chronic gastric ulcers during a maximal histamine infusion test. The known tendency of patients with gastric ulcers to secrete a less acid gastric juice than that of normal subjects was confirmed. However, the hypo-acidity was related to the extent by which the total ionic concentration was less than the isotonic value of 328 mEq/l. On the assumption that such hypo-acidity was produced by the neutralisation of hydrogen ions by bicarbonate ions refluxing into the stomach from the duodenum, the data were corrected and resulted in a normal estimate of the hydrogen ion concentration in the gastric ulcer group. Independent corrections, according to the sodium content of refluxed duodenal juice, yielded similar results for the volume of gastric juice aspirated. It is concluded that while back-diffusion can explain the hypo-acidity of gastric juice in patients with gastric ulcers, duodenal reflux can explain both the hypo-acidity and the hypotonicity, and is therefore more likely to be the correct explanation.
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PMID:Hypo-acidity of gastric juice in chronic gastric ulceration caused by neutralisation. 0 97

CD-3400 developed by Nippon Chemiphar Co. Ltd., is a new antihypertensive agent belonging to the class of rauwolfa alkaloids. Influence of the agent on gastric mucosa, healing process of acetic acid-induced gastric ulcer and gastric juice in rats was investigated and compared with effects of reserpine and rescinnamine. CD-3400-induced gastric lesions were fewer in number than those produced with reserpine and rescinnamine in fasted rats. After a three day treatment of CD-3400 to fed rats, however, there were few gastric lesions, while reserpine- and rescinnamine-induced gastric lesions were aggravated to a greater extent that when a single administration was given to fasted rats. Influence of CD-3400, reserpine and rescinnamine on the healing process of acetic acid-induced ulcer was insignificant, but treatment with high doses of reserpine and rescinnamine resulted in death. Pretreatment with CD-3400 and reserpine produced a decrease in gastric acid and K+, and an increase in Na+. Repeated administration of reserpine for 5 days resulted in a decrease of both gastric volume and acid, while such was not seen with CD-3400. Treatment with anticholinergic agents such as atropine sulfate and atropine methylbromide inhibited CD-3400- and reserpine-induced gastric lesions. From these results, it would appear that cholinergic factors play a role in the pathogenesis of CD-3400-induced gastric lesions, as in the case with reserpine, and that the responses of these lesions to reserpine and CD-3400 correlate with changes of ionic fluxes in gastric juice.
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PMID:[Findings in the gastric mucosa and gastric secretion in rats treated with methyl O-(4-hydroxy-3-methoxycinnamoyl)reserpate (CD-3400) and reserpine derivatives]. 1 71

A study was made of the treatment received by 135 gastric ulcer patients within one month and within six months of diagnosis. The treatment was divided into three types. Effective measures included surgery and those measures that have been shown favourably to influence the initial healing rate of chronic gastric ulcer (i.e. hospital admission and carbenoxolone sodium). Ineffective measures included those that have been shown convincingly not to accelerate ulcer healing--diet, antacids, sedatives and no treatmen at all. Anticholinergic drugs were included in the third group where the evidence is conflicting. The patient's therapeutic status was assessed one month and six months after diagnosis. Within six months of diagnosis only 32% of patients received treatment that clinical trials have shown favourably to influence the course of gastric ulcer and approximately half received treatment that has never been shown favourably to influence the course of gastric ulcer. The social class of the patients and whether they were seen by a consultant physicians or family doctor made no difference to the form of therapy received.
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PMID:Treatment of chronic gastric ulcer a study of the treatment recived by 135 gastric ulcer patients in a western community. 26 84

Fifty-four outpatients with endoscopically diagnosed benign gastric ulcer were allocated at random to treatment with either cimetidine 800 mg daily for six weeks or carbenoxolone sodium 300 mg daily for one week then 150 mg daily for five weeks. Ulcers were reassessed by endoscopy at the end of the trial. The endoscopist was unaware of the treatment and did not take part in the clinical care of the patients. Twenty-one of the 27 patients (78%) given cimetidine and 14 of the 27 (52%) given carbenoxolone had healed ulcers. Symptomatic response occurred earlier with cimetidine but was not significantly better. Unwanted effects were more common in the carbenoxolone group: 12 patients developed hypokalaemia, four of whom needed oral potassium supplements. The results suggest that histamine H2-receptor blockade is at least as effective as carbenoxolone sodium for benign gastric ulcer and produces fewer side effects.
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PMID:Controlled comparison of cimetidine and carbenoxolone sodium in gastric ulcer. 37 54

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

Because of intolerance to oral steroids, a patient with Chronic Active Hepatitis and an active gastric ulcer was treated with rectal steroids in addition to azathioprine and carbenoxolone sodium. The liver function tests showed a marked improvement with this therapy, and the gastric ulcer healed. The possible advantages of steroid administration by suppositories are discussed.
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PMID:The use of steroid suppositories in the treatment of chronic active hepatitis complicated by peptic ulceration. 42 7

Neither basal nor peak acid output changed significantly after treatment for four weeks with carbenoxolone sodium as Biogastrone tablets in patients with gastric ulcer or Duogastrone capsules in patients with duodenal ulcer.
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PMID:Effect of carbenoxolone sodium on human gastric acid secretion. 60 92

Reflux of duodenal contents into the stomach has been implicated in the disruption of mucosal defence and the subsequent occurrence of gastric ulcer. The change produced in the rheological properties following the addition of bile salts and phospholipids to mucus samples was used to assess resultant structural changes. Sodium deoxycholate, sodium taurodeoxycholate, sodium glycocholate, and lysophosphatidylcholine decreased both viscosity and elasticity, indicating that structural breakdown had occurred, whereas phosphatidylcholine could not be shown to have any effect. It is therefore suggested that some of the ulcerogenic activity of naturally occurring surfactants may be associated with their ability directly to reduce mucus consistency.
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PMID:Direct effect of bile salts and phospholipids on the physical properties of mucus. 63 25

The absorption of carbenoxolone sodium has been studied in 15 patients with gastric ulcer and eight patients with duodenal ulcer treated for four weeks. Blood levels of carbenoxolone showed a log distribution, varied markedly between patients, and were significantly higher after Biogastrone tablets (300 mg/day) than after Duogastrone capsules (200 mg/day). Serum carbenoxolone levels were similar in patients taking Biogastrone tablets before or after meals, and in patients taking Biogastrone tablets or Duogastrone capsules with or without antacids following chronic administration. Serum carbenoxolone levels were similar in patients whose gastric ulcers had or had not healed after four weeks' treatment. Serum carbenoxolone was significantly higher in patients who developed oedema, and was significantly correlated with age and with fall in plasma potassium. Carbenoxolone may exert its metabolic effects systemically, but its ulcer-healing effects topically; additional studies are needed to test this hypothesis.
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PMID:Serum carbenoxolone in patients with gastric and duodenal ulcer: Absorption, efficacy and side-effects. 64 39

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


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