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

Conservative management of peptic ulcer relies on the use of drugs as an adjuvant to the time-honored measures of avoiding stress, reducing gastric secretion, and regulating the diet. Alkalies neutralize acid and anticholinergic drugs partly inhibit secretion.. Both are widely used but are often inadequate to control symptoms. Carbenoxolone appears to have a more specific effect in promoting healing of gastric ulcers and has now been used for 15 years. Its role in the treatment of gastric ulcer can be critrically examined, particularly in relation to how this influences surgical management. Recently introduced compounds know as histamine H2-receptor antagonists have a profound effect in inhibiting gastric secretion. Early experience in patients with duodenal ulcer indicated the efficacy of these compounds in promoting healing. These potent new drugs are likely to influence strongly the management of patients with duodenal ulcer, and this may affect the indications for surgery.
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PMID:Drugs for peptic ulcer. 1 29

The effect of carbenoxolone on the healing of gastric ulcer and erosions was compared with that of placebo. The series consisted of 20 patients with chronic gastric ulcers and 20 patients with superficial erosions of the stomach. The diagnosis as well as the follow-up of the lesions were based on gastroscopic examinations. The ulcers were measured gastroscopically. A double-blind method was used. Besides carbenoxolone 50 mg or placebo three times daily, all the patients received antacids in fixed dosage for six weeks. Subjective symptoms and cardiovascular side-effects were recorded. Maximal acid output and serum gastrin levels were measured before and after the treatment. No difference was seen between carbenoxolone and placebo groups with regard to the healing rate of the ulcers of disappearance of the erosions. The subjective symptoms subsided significantly faster in the treatment groups than in the control groups. No cardiovascular side-effects were evident during the treatment with carbenoxolone. One patient needed potassium supplements. Carbenoxolone had no effect on the pentagastrin-stimulated gastric acid secretion nor on the serum gastrin values.
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PMID:Double-blind study of carbenoxolone in gastric ulcer and erosions. 35 71

The beneficial antiulcer actions of carbenoxolone may possibly be due to an aldosterone-like component on the gastric mucosa. This suggests that aldosterone and possibly other corticoids may have antiulcer actions. The potential gastric antisecretory and antiulcer actions of aldosterone (ALDO) and desoxycorticosterone acetate (DOCA) were studied in the rat in comparison to the reference standard carbenoxolone. Stress ulcers were induced in fasted rats by the the forced exertion technique. Gastric secretion was evaluated in the five-hour pyloric ligated Shay rat model. The renal mineralocorticoid actions of these drugs were also studied in the adrenalectomized rat. Intragastric administration of carbenoxolone and DOCA, but not ALDO, significantly inhibited gastric ulcer formation in rats. Carbenoxolone given subcutaneously (s.c.) did not inhibit ulcer formation. ALDO exhibited antiulcer actions only when multiple s.c. injections were made. The antiulcer actions of DOCA and ALDO are not mediated via an inhibitory effect on gastric secretion. At all doses tested DOCA and ALDO showed significant renal effect, while carbenoxolone exhibited this effect only at the highest tested dose. These results suggest that the beneficial antiulcerogenic action of carbenoxolone is due to a direct effect on gastric mucosa and is not related to an aldosterone-like component.
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PMID:Gastric antiulcer and antisecretory effects of carbenoxolone, aldosterone and desoxycorticosterone in rats. 54 42

The conventional treatment of peptic ulcer disease with special dietary regimens, antacids or anticholinergics has been found wanting. Recently introduced agents show considerable promise in the benefit they can render. Carbenoxolone accelerates the healing of gastric ulcers by increasing gastric mucosal resistance. Cimetidine, a histamine HI-receptor antagonist, is an effective suppressant of acid secretion and therefore promotes healing of duodenal ulcers. Metoclopramide hastens gastric emptying and increases the tone of the gastroesophageal sphincter, and is valuable in cases of reflux esophagitis and gastric ulcer.
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PMID:Symposium on peptic ulcer disease. 1. Medical treatment of peptic ulcer. 57 7

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

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

3-hydroxy-lup-20(29) en-23-28-dioic acid (HLEDA) at doses of 50-100 mg/kg was found to be an effective anti-ulcer agent in three rat experimental gastric ulcer models: the indomethacin-induced, pyloric ligation-induced, and absolute alcohol-induced ulcers. Its anti-ulcer activities were similar to those of carbenoxolone. HLEDA was shown to increase the hexosamine levels in gastric juice collected from pylorus ligated stomachs. No influence on gastric secretion and peptic activity was observed. Carbenoxolone was found to significantly inhibit the elimination of Na+ and K+ in rat urine. HLEDA had no effect on the elimination of Na+ and K+.
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PMID:[Effect of 3-hydroxy-lup-20(29)en-23-28-dioic acid on rat experimental gastric ulcers]. 215 Mar 56

Carbenoxolone in a dose dependent manner inhibits the activity of the prostaglandin (PG) metabolizing enzymes 15-hydroxy-PG-dehydrogenase and delta 13-PG-reductase in vitro, while this drug in the same dose range does not influence gastric mucosal PG synthesis by a microsomal cell fraction. Using a radioimmunoassay for carbenoxolone determination, we could show that during absorption high levels of the drug are reached within the gastric mucosa of human volunteers and gastric ulcer patients. From the tissue levels reached it seems possible that carbenoxolone inhibits PG inactivating enzymes of gastric mucosa in vivo as it does in vitro. Thus, decreased inactivation cytoprotective PG synthesized within the gastric mucosa, might contribute to the ulcer healing effect of carbenoxolone.
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PMID:Effect of carbenoxolone on prostaglandin synthesizing and metabolizing enzymes and correlation with gastric mucosal carbenoxolone concentrations. 625 13

The influence of oral carbenoxolone sodium (50 mg X 3 daily) on prostaglandin E2 release into gastric juice has been examined in nine peptic ulcer patients (duodenal ulcer, n = 6; prepyloric ulcer, n = 1; gastric ulcer, n = 2) during modified sham feeding and following bolus stimulation of acid secretion by pentagastrin (6 micrograms/kg). Carbenoxolone increased the overall mean of prostaglandin E2 concentrations in gastric juice following modified sham feeding by 32 +/- 9% (mean +/- SEM; P less than 0.02) and decreased the acidity slightly but significantly (P less than 0.05). A marked rise in prostaglandin E2 levels (46 +/- 11%; n = 5; P less than 0.02) was observed in for duodenal ulcer patients and the patient with a prepyloric ulcer responding to therapy (i.e., pain relief and ulcer healing within 4 weeks of treatment). A significant peak (P less than 0.05) related to modified sham feeding was observed only during medication, while a late gradual increase in prostaglandin E2 levels--not associated with vagal stimulation--occurred both in control and carbenoxolone experiments. No significant differences were observed following pentagastrin stimulation. The initial peak in prostaglandin E2 levels observed during medication favours the notion that the mechanism of drug action relies on inhibition of enzymatic degradation while the late increase in prostaglandin E2 levels may be explained by artificial prostaglandin formation during the aspiration procedure.
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PMID:Effect of carbenoxolone on gastric prostaglandin E2 levels in patients with peptic ulcer disease following vagal and pentagastrin stimulation. 641 22


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