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)

The etiology of peptic ulcer disease is completely unknown. However, gastric acid secretion plays an important role in the pathogenesis of the disease. Acetylcholine, gastrin and histamine are recognized as the main stimulators of the acid secretion. Extensive studies on blood gastrin have not incriminated this hormone in the pathogenesis of the disease. The present study was done to evaluate the role of circulating histamine in peptic ulcer disease using a sensitive and specific radioimmunoassay method. Since gastrin at least in some species seems to exert its stimulatory effect by releasing histamine, serum gastrin was also determined. There was no significant difference in plasma histamine between patients with duodenal or gastric ulcer, nonulcer dyspepsia or ulcer patients after proximal gastric vagotomy. However, patients taking a histamine-2 blocker (cimetidine or ranitidine) had significantly higher plasma histamine than those not taking these drugs. This effect was not due to interference in the histamine assay. There was no correlation between plasma histamine and plasma gastrin. Plasma gastrin was significantly increased in patients having been operated on with a proximal gastric vagotomy. In conclusion, plasma histamine is similar in patients with different upper gastrointestinal disorders. However, histamine-2 blockers may increase plasma histamine.
 ...
PMID:Histamine and gastrin in plasma of patients with upper gastrointestinal diseases. 276 43

Campylobacter pylori causes type B gastritis and C. pylori infection has been associated with duodenal ulcer, gastric ulcer, non-ulcer dyspepsia, and gastric cancer. Although we have been able to culture C. pylori for only about 5 years, what we now know about this organism can explain many mysteries surrounding peptic ulcer disease. Whenever one investigates a population of ulcer patients for the presence of any accepted potentially important pathogenetic factors, one finds that the population of patients with duodenal ulcer disease differs (statistically) from those without duodenal ulcer disease, but that to a large degree they also overlap. None of the traditional factors can be considered essential and characteristic of chronic duodenal ulcer. The exception is the presence of a C. pylori infection, the presence of which is almost invariable. Several properties of C. pylori have been identified that might be virulence factors, including (a) provoking a marked acute and chronic inflammatory response, (b) rapid motility through gastric mucus, (c) urease activity, (d) a fibrillar adhesin(s), (e) several putative exotoxins, and (f) microinvasion. We can now add to the old dictum "no acid-no ulcer," "no C. pylori-no ulcer" at least as far as chronic duodenal ulcer disease in adults is concerned.
 ...
PMID:Campylobacter pylori. The organism and its clinical relevance. 280 38

40 patients with their first gastric ulcer diagnosed gastroscopically 4-8 years ago and who have not since undergone surgery for their ulcer disease or been on medical treatment for active ulcer were reexamined with endoscopy. In 22 patients one or more gastric ulcers were found. At the follow-up endoscopy, 14 of these patients were without dyspeptic complaints, 4 had minimal symptoms and did not need antacids, and 4 were taking antacids for the relief of dyspepsia. A high frequency of asymptomatic gastric ulcer in patients with previous symptomatic disease has not been reported before, and the natural course of gastric ulcer disease should be re-evaluated by long-term prospective studies.
 ...
PMID:Asymptomatic gastric ulcer: a follow-up study in patients with previous gastric ulcer disease. 286 46

Campylobacter pylori infection has been associated with duodenal ulcer, gastric ulcer, and non-ulcer dyspepsia. Although in vitro studies have shown that C. pylori is susceptible to most commonly used antibiotics, predictions from in vitro sensitivity studies have not led to a safe and generally effective therapy; C. pylori has proved to be very difficult to eradicate in vivo. We used the urea breath test to assess the susceptibility of C. pylori in vivo to various drugs. C. pylori was susceptible to bismuth subsalicylate, bismuth subnitrate, and furazolidone. C. pylori was not susceptible (i.e., urease activity remained despite administration of the drug) to the following drugs: 1) antiulcer agents (cimetidine, ranitidine, famotidine, omeprazole, misoprostol, sucralfate, liquid antacids); 2) NSAIDs (aspirin, indomethacin, ibuprofen, naproxen, tolmetin); 3) antibiotics (oral penicillin V, trimethoprim-sulfamethoxazole, dicloxacillin); 4) salts (lithium, ferrous sulfate, gold); 5) miscellaneous (acetaminophen, phenytoin, hydrochlorothiazide, propranolol, metoprolol, metoclopramide, ursodeoxycholic acid). Oral antimicrobials can be administered directly onto the site of infection, so that a very low oral dose will provide many multiples of the in vitro minimal inhibitory concentration. Furazolidone suspension (7 mg) was administered seven times daily (daily dose 49 mg) to three individuals infected by C. pylori during suppression of gastric acid secretion with famotidine (40 mg bid). After 4 days, all subjects had significant reductions in urease activity (two to normal and one to a borderline value). This response suggested that very low-dose therapy may be useful either alone or combined with bismuth. Conclusive establishment of an etiologic (or major contributory) relationship of C. pylori to ulcer disease will require a safe and reliable method to eradicate the organism from the stomach and duodenum.
 ...
PMID:In vivo susceptibility of Campylobacter pylori. 291 80

Campylobacter pylori has been associated with gastritis, duodenal ulcer, gastric ulcer, and nonulcer dyspepsia. Evidence that C. pylori may be the causative agent or at least a major contributory factor in peptic ulcer disease has generated intense interest in the development of reliable methods for detecting C. pylori infections. We have developed a specific and sensitive enzyme-linked immunosorbent assay (ELISA) that detects serum immunoglobulin G antibodies directed against high molecular weight cell-associated proteins (HM-CAP) of C. pylori. In a blinded fashion we tested sera from 300 individuals and found that all of 147 HM-CAP ELISA-negative individuals were also negative for C. pylori, as documented by a negative urea breath test; also, 151 of 153 C. pylori-positive (by urea breath test) individuals were HM-CAP ELISA-positive. Campylobacter pylori was cultured from the two ELISA-negative but infected patients and these isolates did possess HM-CAP antigens, showing that these two individuals had failed to seroconvert. Thus, the specificity and positive predictive value of the HM-CAP ELISA were each 100%; the sensitivity of the assay was 98.7%, and the negative predictive value was 98.6%. The HM-CAP ELISA and the urea breath test both proved valuable for detecting C. pylori infection, the urea breath test being a more direct method whereas the ELISA is less expensive and easier to perform. Furthermore, the results of a serologic test such as the HM-CAP ELISA would not be influenced by recent ingestion of bismuth compounds or antimicrobial therapy, which might suppress C. pylori and cause a transient false-negative result in the urea breath test.
 ...
PMID:A sensitive and specific serologic test for detection of Campylobacter pylori infection. 277 37

It is now possible readily to investigate dyspeptic symptoms using either a double-contrast barium meal or upper gastrointestinal endoscopy. The accuracy of endoscopy makes it preferable for routine use. As oesophagogastro-duodenoscopy (OGD) is invasive, some risks (albeit very small) are involved. Moreover, this technique has some weaknesses. For these reasons, selection of patients is important. Organic disease is most likely to occur in older patients: anyone presenting with dyspepsia for the first time over the age of 40 years should be investigated automatically. In individuals under 40 years of age, organic disease is less common and some selection criteria should be applied to reduce the number of negative investigations. After age, smoking is probably the single most important adverse factor. For gastric ulcer, endoscopy with biopsy, repeated after a course of therapy, is routine, but for duodenal ulcer repeat examination need not normally be undertaken owing to the effectiveness of modern healing drugs. Methods for improving the diagnostic accuracy of patient histories and clinical examinations need to be developed in order to utilize diagnostic investigations more efficiently for the patients' benefit.
 ...
PMID:When should endoscopy (or radiology) be used in dyspepsia and peptic ulcer disease? 297 3

An active 80-year-old woman without a history of peptic ulcer disease, recent nonsteroidal anti-inflammatory drug use, or smoking developed severe, symptomatic epigastric pain initially diagnosed as nonulcer dyspepsia secondary to esophagitis. Initial treatment consisted of 12 weeks of full-dose H2-receptor antagonist therapy. During this therapy the patient developed multiple gastric ulcers confirmed by endoscopy, and continued to have significant dyspeptic symptoms. An additional 16 weeks of combination therapy with ranitidine and sucralfate failed to ameliorate upper gastrointestinal symptoms, and there was significant increase in gastric ulcer size. Repeated ulcer biopsies showed no malignancy. Prior to scheduling elective gastric ulcer surgery, a trial of oral prostaglandin E1 analogue therapy was initiated with an investigational agent. Within the first three weeks of therapy, there was significant symptomatic improvement. Endoscopy of the upper gastrointestinal tract at 12 weeks revealed complete ulcer healing. This case report suggests that prostaglandin E1 analogue therapy should be considered as an alternative to elective gastric ulcer surgery for patients with refractory gastric ulcer.
 ...
PMID:Prostaglandin E1 analogue therapy in the treatment of refractory gastric ulcer in an elderly patient. 314 Jul 54

355 patients suffering from dyspepsia with an endoscopic pathological picture were examined. Campylobacter pylori was sought histologically and by culture. Histological and cultural results were compared. There were no bacteria on the gastric mucosa of 46 patients who had no histopathological evidence of lesions. Cultural studies were performed in 40 cases on endoscopic instruments used during the examination, before and after standard sterilization. Campylobacter pylori was found on the gastric mucosa of 224 patients (63.09%); 91.93% with duodenal ulcer; 71.87% with gastric ulcer; 54.23% with erosive duodenitis; 56.71% with erosive gastritis and 54.81% with chronic gastropathy. The agreement between the two techniques was 75.39%, with a male prevalence (p = 0.05). Campylobacter pylori was present on the gastric mucosa of 10.86% of patients without histopathological evidence of lesions. Standard sterilization with alkyl-dimethyl-benzyl ammonium eliminated the campylobacter in 100% of cases.
 ...
PMID:[Campylobacter pylori colonization and gastroduodenal pathology]. 320 Apr 72

Our review of evidence that Campylobacter pylori is an important factor in gastritis, peptic ulcer disease, and "nonulcer dyspepsia" suggests that C pylori is the most common cause of chronic active gastritis. The association between C pylori gastritis and duodenal ulcer, which approaches 100%, leads to the suggestion that this infection plays an important role in the pathogenesis of duodenal ulcer. Evidence supporting a central role in the pathogenesis of gastric ulcer and nonulcer dyspepsia is less compelling.
 ...
PMID:Campylobacter gastritis and associated disorders. 329 34

To determine the clinical importance of Campylobacter pyloridis infection, its association with gastric inflammation, and the response to drug therapy, patients with a duodenal or gastric ulcer (n = 63), patients with nonulcer dyspepsia (n = 240), and asymptomatic volunteers (n = 34) were studied. In a prospective longitudinal study, the type, intensity, and distribution of inflammation in antral biopsy specimens were correlated with the presence of C. pyloridis. Campylobacter pyloridis was cultured from antral biopsy specimens in 98% of the ulcer patients, 70% of the nonulcer dyspepsia patients, and 20% of the asymptomatic volunteers. The dependency of chronic active gastritis on the presence of C. pyloridis was shown by an association of gastritis with positive culture and healing of gastritis with negative culture after various therapeutic regimens. Spontaneous disappearance of C. pyloridis never occurred. Colloidal bismuth subcitrate, amoxicillin, and the combination of colloidal bismuth subcitrate and amoxicillin were effective therapies in eradicating C. pyloridis. Recolonization with the same bacterial subtype and recurrence of gastritis frequently occurred within 1 mo after initial eradication. In this study we demonstrate ultimate normalization of gastric mucosa after successful eradication of C. pyloridis. Especially complete normalization of gastric mucosa after amoxicillin monotherapy provides additional strong evidence for a true cause-effect relationship between C. pyloridis colonization and gastritis.
 ...
PMID:Campylobacter pyloridis-associated chronic active antral gastritis. A prospective study of its prevalence and the effects of antibacterial and antiulcer treatment. 333 95


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