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)

Serum pepsinogen I and pepsinogen II levels in 369 healthy controls, 38 duodenal ulcer, 30 gastric ulcer and 46 stomach cancer including 21 early and 25 advanced gastric cancer patients were measured by enzyme-linked immunosorbent assays using pepsin moiety-reacting monoclonal antibodies to pepsinogens I and II. Serum pepsinogen I and pepsinogen II levels were higher in the duodenal and gastric ulcer groups than in the control. Although there was no significant difference in serum pepsinogen II between stomach cancer and control, serum pepsinogen I was significantly lower in the former than in the latter and also in advanced gastric cancer than in early gastric cancer. A specific negative correlation of serum pepsinogen I with patient age was observed in stomach cancer but not in peptic ulcer or control groups. Receiver operating characteristic analysis was performed and indicated that serum pepsinogen I, compared with serum pepsinogen II or the pepsinogen I/pepsinogen II ratio, is the most effective marker for stomach cancer.
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PMID:Enzyme-linked immunosorbent assays for serum pepsinogens I and II using monoclonal antibodies--with data on peptic ulcer and gastric cancer. 316 82

The current therapeutic approach to peptic ulcer disease includes agents that reduce gastric acidity and hence peptic activity, inactivate or adsorb pepsin, create a physical barrier against the effects of acid and pepsin, or enhance mucosal defence. Profound gastric acid reduction may predispose to infection, and it has been suggested that carcinogenesis is possible, although a cause-effect relationship has never been established. The side-effects of therapy are well-described, and may limit the therapeutic approach. Healing rates correlate closely with acid suppression in duodenal ulcer, but not entirely in gastric ulcer. Maintenance therapy lowers the relapse rate, but does not alter the ulcer diathesis. The optimal strategy for long-term management remains unclear, but in the future one should consider outcome measures which include a decrease in pain, improvement in the quality of life, reduction work loss, and a reduction of complications, in addition to ulcer healing. The ideal therapy should be efficacious, safe, and convenient--with no side-effects--and cost-effective. New agents should suppress acid and peptic activity, while enhancing the gastric mucosal defence mechanisms (such as mucosal blood flow, mucus, and bicarbonate secretion) and stimulating gastric cellular regeneration and restitution.
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PMID:The limitations of current therapy in peptic ulcer disease. 330 47

De-Nol (colloidal bismuth subcitrate, CBS) precipitates in an acid environment and adheres to the exudate layer covering an ulcer crater; moreover, CBS blocks pepsin activity, retards hydrogen-ion back-diffusion and stimulates prostaglandin synthesis. The average healing rate in duodenal ulcer (DU) after 4 weeks' treatment with CBS is 78% versus 63% with cimetidine. In a direct comparison, CBS gives 84% healing as opposed to 78% with ranitidine. The average healing rate after 4 weeks' treatment with CBS in gastric ulcer (GU) is 68% compared to 54% with cimetidine. The percentage of relapse-free patients, 1 year after DU or GU healing, with CBS is substantially higher than is the case with H2-receptor blockers.
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PMID:Colloidal bismuth subcitrate in peptic ulcer--a review. 330 17

We measured serum pepsinogen I (sPG-I) in 269 patients undergoing upper GI endoscopy and then classified by endoscopic diagnosis, gastric mucosal histology, and smoking habit. Both ulcer-free and duodenal ulcer smokers had significantly higher sPG-I levels than their non-smoking controls. In contrast, sPG-I values were not different in smokers and non-smokers with gastric ulcer. In ulcer-free smokers the overall increase in sPG-I simply reflected the high prevalence of patients with superficial gastritis and elevated sPG-I levels. Conversely, in duodenal ulcer smokers the increase in sPG-I, which was related to the number of cigarettes smoked daily, was not an epiphenomenon of concomitant gastritis. The smoking-induced increase in sPG-I in duodenal ulcer is proposed to reflect an augmented pepsin secretory capacity, which can be of aetiologic significance in the association between cigarette smoking and duodenal ulcer.
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PMID:Serum pepsinogen I elevation in cigarette smokers. 339 33

Ulcer formation after pylorus ligation was assessed in control, testosterone treated and castrated male rats after cimetidine treatment. The stomach was studied for incidence of ulcers and its contents analysed for pH, volume, total acidity, free acidity, pepsin and mucin activity. Testosterone and cimetidine when used alone protected from ulceration while when used in combination the degree of protection was decreased. Castration per se ead no effect on ulcer index but potentiated cimetidine induced gastric ulcer protection.
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PMID:Relevance of male hormonal status with antiulcer effect of cimetidine in pylorus ligated rats. 345 Jun 32

Somatostatin (SS) has been reported to exert potent inhibitory effects on gastric acid, pepsin and gastrin secretion. Although still controversial, the results of several studies have shown a possible influence of a local decrease in gastric somatostatin in the physiopathologic characteristics of peptic ulcer disease. In the present study, immunoreactive SS content (SLI) of antral (SLI-a), corpal (SLI-c) and fundic (SLI-f) mucosal extracts was measured by radioimmunoassay (RIA) in control patients (C) and in those patients with duodenal ulcer (DU) or gastric ulcer (GU) to further study a possible role of SS in peptic ulcer disease. Fifty-five patients (C = 20, DU = 21 and GU = 14) were included in the study. Gastric mucosal samples were obtained either by endoscopic biopsy (4.6 +/- 0.2 milligrams of weight) or operation (52.3 +/- 3.8 milligrams of weight). RIA was performed after a modified Arimura's method and results were expressed as nanograms per milligram of tissue plus or minus standard error of the mean. Chromatographic analysis of gastric mucosal extracts was performed on a Sephadex G-25 fine column. A great interindividual variation in SLI levels was observed (a range of 0.02 to 5.30 nanograms per milligram of weight). The mean SLI concentrations were: C (SLI-a, 2.55 +/- 0.45, SLI-c, 0.99 +/- 0.46 and SLI-f, 1.03 +/- 0.21); DU (SLI-a, 0.48 +/- 0.16, SLI-c, 0.43 +/- 0.13, and SLI-f, 0.58 +/- 0.12), and GU (SLI-a, 1.10 +/- 0.25, SLI-c, 0.40 +/- 0.10, and SLI-f, 0.81 +/- 0.24). Significantly greater amounts of SLI contents were found in the antrum of control patients as compared with those found in the corpus or fundus (p less than 0.05 and p less than 0.01, respectively). SLI-a levels were lower in peptic ulcer patients (DU, p less than 0.001 and GU, p less than 0.05) than in control patients. There was also a significant difference between SLI-a levels in DU versus GU patients (p less than 0.05). No significant differences were found in SLI-c and SLI-f contents in all three groups studied. In conclusion, these results suggest that decreased SS levels in antral gastric mucosa could be the alteration underlying the various physiopathologic mechanisms involved in the development of peptic ulcer disease.
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PMID:Gastric mucosal somatostatin-like immunoreactivity in peptic ulcer. 356 43

Colloidal bismuth subcitrate (CBS) precipitates in an acid environment, adheres to mucus, blocks pepsin activity, retards hydrogen-ion back diffusion and stimulates prostaglandin synthesis. The average healing rate after 4 weeks' treatment with CBS is 78% in duodenal ulcer versus 67% with cimetidine. A direct comparison with ranitidine gives healing rates of 78% (CBS) as opposed to 78% with ranitidine. The corresponding figures in gastric ulcer are 68% (CBS) and 54% (cimetidine). The percentage of relapse-free patients is substantially higher after CBS ulcer healing than after H2-blockers. Bismuth subsalicylate eliminates Campylobacter pylori in 71% after 4-weeks' therapy. Parallel to this elimination a decrease and normalization of the acute inflammatory process can be seen in antral mucosa.
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PMID:[Therapy of peptic ulcer and chronic gastritis with bismuth salts]. 368 49

The role of histamine in the gut is reviewed in relation to gastric secretion of acid, pepsin and intrinsic factors. Species-dependence of some of these actions are also discussed. Interactions with other agonists and antagonists in intact and isolated systems provide the basis for models of the role of histamine in control of gastric secretion. This review deals further with histamine H1 and H2 effects on gastrointestinal circulation and musculature including sphincters. The most dramatic application of the development of histamine H2 antagonists has been in the treatment of duodenal ulcer. The use of H2 antagonists in the treatment of duodenal and gastric ulcer, gastrinoma, gastritis, and esophagitis is critically evaluated.
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PMID:Histamine and the gut. 391 79

The dose response curves for acid and pepsin output to increasing intravenous doses of pentagastrin (0.01, 0.02, 2, 8, and 16 micrograms/kg per hour) were determined in six male patients with duodenal ulcer and six with type 1 corporeal gastric ulcer before and 3 to 6 months after selective proximal vagotomy and excision of the gastric ulcer. The maximal secretory capacity (maximal response) of acid and pepsin was greater in the duodenal ulcer patients than in the corporeal gastric ulcer patients, but the sensitivity of the oxyntic and peptic cells to pentagastrin (the dose required for half the maximal response) was equal for the two ulcer groups. Selective proximal vagotomy reduced the acid response to insulin by 96 to 100 percent. The acid secretory capacity and the sensitivity of the oxyntic cells to pentagastrin was reduced by selective proximal vagotomy to the same extent in the duodenal ulcer patients and the corporeal gastric ulcer patients. Selective proximal vagotomy reduced the pepsin secretory capacity in the duodenal ulcer patients but did not reduce the already low capacity in the corporeal gastric ulcer patients. Selective proximal vagotomy decreased the sensitivity of the peptic cells in both ulcer groups. Similar results were obtained when the dose response curves were analyzed according to Michaelis-Menten kinetics. Our results justify clinical trials of selective proximal vagotomy with complete ulcer excision for treatment of type 1 corporeal gastric ulcer.
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PMID:Acid and pepsin responses to graded doses of pentagastrin in duodenal and corporeal gastric ulcer patients before and after selective proximal vagotomy. 393 70

Heterogeneity is the most important consideration in the pathophysiology of peptic ulcer disease. Acute ulcers and erosions present clinically with gastrointestinal bleeding or perforation. If they heal there is no predictable recurrence. Factors concerned with mucosal defense are relatively more important than aggressive factors such as acid and pepsin. Local ischemia is the earliest recognizable gross lesion. The gastric mucosa is at least as vulnerable as the duodenal mucosa and probably more so. Most drug-induced ulcers occur in the stomach. Chronic or recurrent true peptic ulcers (penetrating the muscularis mucosae) usually present with abdominal pain. Many duodenal ulcer patients report that the pain occurs when the stomach is empty or is relieved by food, and follows a pattern of relatively long periods of freedom from symptoms between recurrences. Approximately 50% of patients experience a recurrence within a year if anti-ulcer medication is stopped. In most western countries recurrent duodenal ulcer is more common than gastric ulcer. Peptic ulcer disease is also more common in men. Recent evidence indicates genetic and familial factors in duodenal ulcer and increased acid-pepsin secretion in response to a variety of stimuli. However, it is also becoming clear that of all the abnormal functions noted, few are present in all subjects and many are clustered in subgroups. In chronic gastric ulcer of the corpus, defective defense mechanisms, such as duodenogastric reflux and atrophic gastritis, seem to be more important than aggressive factors. Nevertheless, antisecretory medications accelerate the healing of such ulcers. It remains to be seen whether prostaglandins, mucus secretion, or gastric mucosal blood flow are impaired in chronic ulcer disease.
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PMID:The pathophysiology of peptic ulcer disease. 405 22


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