Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pyrrole aldehydephenyl semicarbazone was shown to be an effective anti-ulcer agent in five experimental models in rats, namely, the indomethacin-induced, acetic acid-induced, pyloric ligation-induced and 0.6 mol HCl, absolute alcohol-induced ulcers, at doses of 40-100 mg/kg. Its anti-ulcer activity and characteristics are similar to those of furazolidone. Its oral acute toxicity in mouse is much lower than furazolidone. This compound exhibited mild inhibitory effects on gastric pepsin secretion, caused increases in hexosamine level and decreases of DNA content in gastric juice. It showed no influence on gastric acid secretion and was considered to have "cytoprotective action" on the gastric mucosa. However, this compound was found to be ineffective against the stress-restraint gastric ulcer model.
 ...
PMID:[The effects of pyrrole aldehydephenyl semicarbazone on experimental gastric peptic ulcer models in rats]. 251 45

In peptic ulcer disease, antacids present a therapeutic effect by neutralizing gastric acid and reducing acid delivery to the duodenum. Furthermore, they reduce the activity of pepsin and have the capacity to bind bile acids. Despite the opinion of most clinicians, the effect of antacids relieving pain in patients with peptic ulcer has not been definitely demonstrated. Furthermore, antacids do not seem to improve the healing rate of gastric ulcer. Earlier studies showed that antacids could hasten the healing of duodenal ulcer when administered at a very high dose. However, recent papers demonstrate that this therapeutic effect is also achieved with a dose with very low neutralizing capacity. Severe side effects are rare, although they can occur in high-risk patients. However, minor problems, such as changes in bowel habits, are more frequent.
 ...
PMID:Antacids in the treatment of peptic ulcer disease. 265 91

Although current concepts of ulcer pathophysiology postulate an imbalance between the principal aggressive factors of acid and pepsin and an impairment of mucosal defence, effective acid reduction by a variety of antisecretory drugs is associated with a significant acceleration of duodenal and gastric ulcer healing in controlled clinical trials. The healing of duodenal ulcer is related to the degree and duration of acid reduction with currently available H2-receptor antagonists. The highly significant correlation between the reduction of nocturnal acidity and ulcer healing reflects the ability of these drugs to inhibit basal and nocturnal acid secretion to a greater extent than stimulated daytime secretion. The extent to which the addition of daytime acid inhibition to that of nocturnal acid inhibition is responsible for further accelerating ulcer healing has not yet been determined, although a model has been proposed recently to explore this effect. Omeprazole has a marked effect on the duration and the degree of inhibition of intragastric acidity which is dose-dependent. In clinical trials of duodenal ulcer treatment, this efficacy and duration of effect is associated with an increased rate of healing and a leftward shift of the healing time curve.
 ...
PMID:Relationship between inhibition of acid secretion and healing of peptic ulcers. 269 Mar 31

Campylobacter pylori, a spiral-shaped bacterium, commonly colonizes the gastric epithelium where it induces chronic gastritis; this organism has also been implicated in the etiology of chronic peptic ulcer disease. Once introduced to the gastric mucosa or an area of gastric metaplasia, it tends to migrate to the vicinity of the epithelial tight junction where it probably utilizes host urea and other substances to sustain itself. Campylobacter pylori also produces a proteolytic enzyme that degrades mucin. As the mucous layer slowly degrades, noxious luminal contents such as acid and pepsin have an opportunity to diffuse closer to the epithelium. We hypothesize that C. pylori, which is sensitive to low-pH environments, eventually migrates away from the compromised area to an area where the mucous layer is still protective. The injured epithelial focus left behind either regenerates its mucous layer and heals, or ulcerates depending upon the balance between other aggressive and protective factors. This interaction between C. pylori and the mucous layer is then repeated at the organism's new location. This hypothesis is consistent with existing data regarding C. pylori. It explains how C. pylori can be present in most duodenal ulcer patients and many gastric ulcer patients, as well as in otherwise healthy individuals. It also explains why ulceration is localized rather than diffuse when it does occur.
 ...
PMID:Campylobacter pylori, mucus, and peptic ulceration. A dynamic interaction. 279 27

The epidemiology, pathophysiology, diagnosis, clinical presentation, and treatment of peptic ulcer disease (PUD) are reviewed. PUD occurs commonly, with about 4 million Americans affected in a year. Cigarette smoking, aspirin use, and prolonged corticosteroid use are associated with PUD. The disease's etiology is multifactorial; the long-held assumption that ulcers develop solely because of increased gastric acid secretion is no longer valid. Although duodenal ulcer patients are frequently hypersecretors of acid, gastric ulcer patients more commonly have defective mechanisms for protecting the mucosal lining from acid, pepsin, and other agents. PUD is best diagnosed using an upper gastrointestinal roentgenographic series or using endoscopy. The clinical presentations, which involve epigastric abdominal pain that is relieved by food, milk, or antacids, may aid in diagnosis but are not usually definitive. Treatment is designed to relieve symptoms, heal the ulcer, prevent recurrences, and prevent complications. Of the four currently available drug treatments (cimetidine, ranitidine, antacids, and sucralfate), the treatment of first choice is cimetidine or ranitidine for four or six weeks, respectively, for duodenal and gastric ulcer patients. Antacids should be used as needed for pain, and the patient should be reassessed at the end of this period. For most patients, neither cimetidine nor ranitidine is demonstrably superior to one another. Several agents are under investigation in the U.S., including other H2-receptor antagonists (famotidine and nizatidine), proton-pump inhibitors (omeprazole), prostaglandins (misoprostol, arbasprostil, enprostil, and trimoprostil), antimuscarinic agents (pirenzepine), and tricyclic antidepressants (doxepin and trimipramine). peptic ulcer disease is an important disease. It is best treated with H2-receptor antagonists supplemented with antacids as needed for pain.
 ...
PMID:Current concepts in clinical therapeutics: peptic ulcer disease. 286 52

In this revision article it was tried to focus on the role played by pepsinogen/pepsin since its discovery until its practical use. Pepsinogen determination as the gastric acid secretion has different basal or stimulated secretion levels in the peptic ulcer, gastritis, etc. The methods for pepsinogen determination are evaluated, verifying that, in spite of radioimmunoassay utilization another methods less sophisticated have been used successfully. The pepsinogen seric levels (PSL) after stimulation with Histalog, discriminate the patients suffering from duodenal ulcer from normal individuals, and they are higher among men than women. A parallelism is made between pepsinogen-I and II finding out pepsinogen-I higher level in smoking individuals. The pepsinogen-I is increased in the duodenal ulcer and II in the gastric ulcer and both of them bent to be characterized as a genetic marker for peptic ulcer. Finally, the main clinical applicability for PSL group I determination is the detection of atrophic gastritis considering its potential for gastric malignancy.
 ...
PMID:[Pepsinogen I and duodenal ulcer]. 306 7

The pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage and administration of omeprazole are reviewed. Omeprazole, a substituted benzimidazole, has a unique site and mechanism of action because it inhibits the proton pump--i.e., hydrogen, potassium adenosine triphosphatase (H+,K+-ATPase)--and consequently blocks the final common step in the gastric acid secretory pathway. Omeprazole inhibits basal and histamine-, gastrin- and pentagastrin-stimulated gastric hydrochloric acid secretion. It produces a dose-dependent reduction in gastric acidity, gastric acid output, and gastric juice volume and has variable effects on pepsin secretion. Omeprazole has no documented effect on esophageal motility or lower esophageal sphincter pressure. Omeprazole is variably absorbed from the gastrointestinal tract, and food appears to decrease the rate, but not the extent, of drug absorption. The drug is approximately 95% bound to plasma proteins and is metabolized to inactive components that are enterohepatically or renally eliminated. Omeprazole is more effective (in most studies) than H2-receptor antagonists in treating duodenal ulcer, at least as effective in treating benign gastric ulcer, and more effective in treating reflux esophagitis. Omeprazole has been used successfully in patients with Zollinger-Ellison syndrome refractory to treatment with H2-receptor antagonists. Gastrointestinal complaints (nausea and diarrhea) are the most commonly reported adverse effects associated with omeprazole therapy. The most frequently reported laboratory abnormality occurring with omeprazole use is elevation of serum aspartate aminotransferase and alanine aminotransferase concentrations. Omeprazole will serve a valuable role in the management of gastrointestinal tract ulcers and hypersecretory conditions.
 ...
PMID:Therapeutic evaluation of omeprazole. 306 85

Basal and pentagastrin stimulated gastric secretion was measured in seven patients with duodenal, and six with gastric ulcers before and after four weeks' treatment with colloidal bismuth subcitrate (as De-Nol), one tablet four times a day. Each duodenal and all but one of the gastric ulcers healed. After De-Nol there were no significant changes in basal, or pentagastrin stimulated volume, acid output, or primary parietal component. There were marked decreases in basal (duodenal ulcer -25%; gastric ulcer -16%) and pentagastrin stimulated total pepsin outputs, (duodenal ulcer -42%, gastric ulcer -36%). There were insignificant decreases in basal output of mucus, but postpentagastrin stimulated mucus output was significantly inhibited (p less than 0.05) in patients with duodenal (-16%) and with gastric ulcer (-27%). The drop in gastric proteolysis after De-Nol is unlikely to be because of the healing of the ulcers and is more likely to be because of the drug. The ulcer healing efficacy of De-Nol may be related to this decline in the proteolytic action of gastric juice, but is unlikely to be because of a quantitative change in mucus, or in acid secretion.
 ...
PMID:Acid, pepsin, and mucus secretion in patients with gastric and duodenal ulcer before and after colloidal bismuth subcitrate (De-Nol). 308 45

Important problems currently under study or requiring investigation for better understanding of the pathophysiology and management are reviewed under three major categories: acute peptic erosions and ulcers, gastric ulcer, and duodenal ulcer. In patients with acute erosions and ulcers, we need to identify patients at risk for major bleeds, to prevent lesions induced by anti-inflammatory, non-steroidal drugs, as well as bleeding from stress ulcers, and to perfect and establish the efficacy of endoscopic methods for coagulation of bleeding ulcers. In patients with gastric ulcers, we need to establish the relative importance of gastric acidity and mucosal resistance to ulcerogenesis, to determine factors that influence healing rates, and to uncover the factors responsible for recurrence. In duodenal ulcer patients, we need to determine the relative importance of post-prandial versus interdigestive secretion, the role of pepsin, and the importance of local defense mechanisms such as bicarbonate and mucus secretion, cellular defense, and blood flow. The mechanisms of failure to heal during treatment need attention. The relation of symptoms and clinical course to healing of ulcer craters should continue to be considered, as well as the long-term course of ulcer disease. The consequences of long-term suppression of acid secretion are a potential hazard, and, finally, the prevention of recurrence remains the major clinical problem in duodenal ulcer.
 ...
PMID:Peptic ulcer--current status. 311 95

The role of pepsin in the pathogenesis of peptic ulcer has been the subject of intense study and debate for many years. Two difficulties inherent in distinguishing between the role of acid alone vs acid and pepsin are that a) acid-containing gastric juice always contains pepsin, and, b) that hydrogen ion concentration (pH) is a major determinant of the activity of pepsin. However, studies in animal models of peptic ulcer indicate clearly that pepsin, in combination with acid, produces much more severe and more extensive mucosal damage than acid alone. Recent interest in pepsin and its precursor, pepsinogen, has stemmed from the finding that each is remarkably heterogeneous, and that the heterogeneity has a genetic basis. Results of studies using radioimmunoassays specific for the 2 major forms of pepsinogen, pepsinogen I and pepsinogen II, have shown that serum levels of pepsinogen I and pepsinogen II, and the ratio of pepsinogen I to pepsinogen II, can be used as noninvasive probes of gastric mucosal structure and function, indicators of the genetics and heterogeneity of duodenal ulcer, and as markers of increased risk for duodenal ulcer and gastric ulcer.
 ...
PMID:Pepsinogens, pepsins, and peptic ulcer. 311 99


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>