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 10 peptic ulcer patients, 5 duodenal ulcer and 5 gastric ulcer patients, the relation of nocturnal intragastric pH to EEG sleep stages was examined. The nocturnal intragastric pH was monitored by pH-measuring telemeter and sleep stages were recorded simultaneously by electroencephalography throughout the night. The EEG sleep stages were classified after the criteria of Dement and Kleitman. The average of intragastric pH level at each sleep stage was higher in gastric ulcer than the duodenal ulcer. The intragastric pH level became low as the patients' sleep advanced to deep stage. This tendency was more likely in duodenal ulcer patients than the gastric ulcer patients, which indicated that the cephalic phase might play an important role in the pathogenesis of hyperacidity in duodenal ulcer.
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PMID:The nocturnal intragastric pH in EEG sleep stages in peptic ulcer patients. 1 3

The enzyme, aspirin esterase, which converts acetylsalicyclic acid to the less toxic salicyclic acid, was found to be present in gastric mucosal specimens obtained from surgically resected tissue. The enzyme was found to be stable to storage and active at two pH optima. Alcohol in the reaction mixture produced a net effect of slowing the rate of aspirin hydrolysis; this was attributable to a marked inhibitory effect on aspirin esterase activity which was not completely counteracted by the increased rate of spontaneous breakdown of aspirin by alcohol. Age, sex, or gastric disease state of the patient from whom the tissue was obtained, did not significantly alter the level of enzyme activity measured, nor were different levels obtained from body or antral mucosa. In patients with gastric ulcer, those with a previous history of regular aspirin consumption did not show significantly different levels from those without such a history. It is concluded that aspirin esterase activity of gastric mucosa is not alone a significant factor in any role acetylsalicyclic acid may play in the etiology and natural history of chronic peptic ulcer.
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PMID:Aspirin esterase of gastric mucosal origin. 1 7

Eight patients with a clinical, radiology and endoscopic diagnosis of benign peptic ulcer were studied in a prospective fashion using Cimetidine (H2-Receptor antagonist). With this outgoing form of therapy the need for antiacid diminished greatly and pain totally disappeared. We discuss the possible etiological pathways of gastric ulcer and finally propose the simultaneous use of H2-Receptor antagonist and colesteramine with the goal of eliminating the two predominant factors that cause the lesion.
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PMID:[Histamine 2 receptor antagonists in the treatment of gastric ulcer]. 1 9

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

In an attempt to elucidate the etiology of acute gastric bleeding and/or erosion and chronic peptic ulcer, a measurement of gastric juice and mucosal pepsin was carried out in surgically-treated patients. Patients with massive gastric mucosal bleeding in the fundic gland area showed high levels of fundic mucosal pepsin without acid-pepsin appearance in the gastric contents. In these patients, a significantly high value of the peptic activity ratio of gastric mucosa to gastric juice (MJPR, 36.4 +/- 6.7) was observed. It can be suggested that transient blockage of pepsin output from peptic cells with occur in the course of the acute mucosal bleeding, while acid-peptic digestion could be carried out within the fundic gland mucosa. On the other hand, a close correlation between relatively high acid-and-pepsin concentration of the gastric contents and a low level of MJPR (5.6 +/- 1.2) was observed in patients with chronic gastric ulcer. Patients who had a gastric ulcer within the pyloric gland mucosa had a highest acid-peptic activity among three groups with ulcers in fundic gland area, border zone and pyloric gland area. There is a rule that acid-peptic activity becomes low when the site of gastric ulcer moves from pylorus to fundus. A marked increase in acid-and-pepsin secretion into the gastric cavity was observed in patients suffering from chronic duodenal ulcer showing the lowest level of MJPR (3.40 +/- 0.50).
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PMID:Relationship between site of peptic ulceration and gastric acid-peptic activity: new evaluation of gastric analysis in patients with acute gastric bleeding and chronic peptic ulcer. 2 12

The authors have investigated some organic phosphoric esters such as dimethoate, malatione, and trichlorphone in order to see whether they influence the genesis of the reserpine ulcer induced in rats or whether they act on the existing ulcer. Another objective of the investigation was to determine whether the aggravating effect of these compounds on the experimental gastric ulcer can be mitigated or prevented with isopropamide and gastrixon, two compounds known to be used in the therapy of ulcers. It was found that 1. dimethoate and trichlorphone considerably aggravate the genesis of the experimental peptic ulcer in rats, and that also malathione exercises this exacerbating effect still to some extent, 2. that the already existing experimental ulcer is aggravated by all three organic phosphoric esters and that 3. the severe experimental damage to the stomach can be reduced or prevented with Isopropamide and even more effectively with Gastrixon. As to the interpretation of the phenomena observed the authors take the view that--provided the effects mentioned apply also to man--with this a new risk was detected in the field of the chemical plant protection which may well gain importance for the health of a population.
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PMID:[The effect of organic phosphoric esters on the experimental peptic ulcer (author's transl)]. 3 54

Antacids can reduce gastroduodenal acidity for long periods if taken in substantial quantities after food. Their healing effect on gastric ulcer is minimal, if present at all, and easily overwhelmed by the benefit obtained from admission to hospital. Intensive antacid therapy appears effective in healing duodenal ulcer and preventing haemorrhage from stress ulcer, and is comparable in these respects with cimetidine but with a higher incidence of side-effects. Clinical impression strongly suggests that antacids relieve pain in peptic ulcer but objective confirmation is lacking.
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PMID:Antacids and peptic ulcer--a reappraisal. 3 92

The effect of cimetidine on the risk of further bleeding shortly after acute gastrointestinal haemorrhage from peptic ulcer was investigated in a double-blind randomised trial. 34 patients were given cimetidine and 32 placebo, the two groups being matched for age, sex, and severity of haemorrhage. Further bleeding within a week of admission was detected clinically in 8 patients on cimetidine and 15 on placebo. Cimetidine had no effect on bleeding from duodenal ulcer, but only 2 of 14 patients with gastric ulcer treated with cimetidine bled again, compared with 10 of 19 patients on placebo. Cimetidine, therefore, may help to prevent haemorrhage from gastric ulcer but not duodenal ulcer.
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PMID:Cimetidine in bleeding peptic ulcer. 9 Jul 61

The relationship between the secretion of pepsin 1 (the most electronegative of the pepsins), and the smoking habits of 219 patients has been investigated. Significantly more cigarette smokers with peptic ulceration (72.5%) secreted pepsin 1 in greater than trace amounts after pentagastrin or histamine than did non-smokers with ulceration (51.2%). Differences of a similar order were found for men with duodenal ulcer, women with duodenal ulcer, and all patients with gastric ulcer, but the difference was statistically significant only for men with duodenal ulcer. Significantly more patients with peptic ulcer smoking six to 15 cigarettes/day secreted moderate or high concentrations of pepsin 1 than did heavier smokers or non-smokers. There was no significant association between cigarette smoking and pepsin 1 secretion among 74 patients without ulceration. Maximal acid output was not significantly related to smoking in any group studied. The findings add to the increasing body of evidence linking pepsins and pepsin 1 with the pathogenesis of peptic ulceration.
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PMID:Cigarette smoking, chronic peptic ulceration, and pepsin 1 secretion. 11 97

Pepsin 1, the ulcer-associated pepsin, occurred significantly more frequently in the gastric juice of those patients with duodenal ulcer who did not secrete A, B, or H antigens into gastric juice than in those secreting these antigens. This observation may explain the increased proportion of such non-secretors among patients with duodenal ulceration. In patients with gastric ulcer and non-ulcer dyspepsia, and in a miscellaneous group of patients, there was no association of pepsin 1 secretion with secretor status, suggesting that the association noted in duodenal ulceration is an indirect rather than a direct one. No increase of pepsin 1 occurred in group O patients with peptic ulcer, so that the increased proportion of such patients in peptic ulcer does not arise from differences in pepsin 1 secretion.
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PMID:Hereditary aspects of duodenal ulceration: pepsin 1 secretion in relation to ABO blood groups and ABH secretor status. 11 57


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