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

The diagnostic performance of two different urease tests and of histologic search after modified Giemsa staining to detect Campylobacter pylori (CP) colonization of the upper gastrointestinal tract was prospectively investigated in 215 esophagogastroduodenoscopies, by using a sensitive culture technique as reference. Single antral urease tests had a high specificity of 95-96%, but a limited sensitivity of 78-83%, which increased to 91-94%, when one antral and one additional body biopsy were submitted to the biochemical tests. Giemsa stains were very sensitive, but less specific. The rate of colonization was similar in antrum and body biopsies, and increased with age. There was a close association of Campylobacter pylori colonization with duodenal and to a lower degree with gastric ulcer disease, but especially with gastritic mucosal changes. CP was never detected in patients without gastritis. Therefore, submitting one antral and one body biopsy specimen to validated urease tests represents a sensitive (91-94%) and specific (93%) method to detect Campylobacter pylori colonization, which appears to be a diffuse phenomenon affecting antral and body mucosae with similar frequency.
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PMID:[Campylobacter pylori: clinical correlations and prospective comparative studies of various diagnostic techniques]. 275 52

To investigate the prevalence of Campylobacter pylori (CP) and its association with histological inflammatory grading and intestinal metaplasia, biopsies were carried out in 388 patients with gastro-duodenal diseases from 2 sites in the stomach (body and antrum). In each case, 3 biopsy specimens were taken from each site for culture, acridine orange stain and urease test. CP was detected in 55% of 22 endoscopically normal patients, in 47% of 17 gastric cancer patients, in 73% of 205 gastritis patients in 91% of 99 gastric ulcer patients and in 100% of 45 duodenal ulcer patients. In gastric ulcer and duodenal ulcer patients, CP detection rate was significantly higher than in endoscopically normal patients (p less than 0.01). There was no difference in CP detection rate irrespective of ulcer stage (active, healing or scar). According to the histological gradings of inflammation (Warren's criteria), CP was detected in only 3% in grade 0-I, 20% in grade II and 83% in grade III. It was found that a close association between CP and histological gastritis with polymorphonuclear leukocytes infiltration exists (p less than 0.001). In a few cases, CP was found even in the areas of intestinal metaplasia. But the number of CP in the areas of intestinal metaplasia were fewer than in the areas of surrounding inflamed gastric mucosa. In most cases, CP was not seen in the areas of intestinal metaplasia, but was found in the areas of surrounding inflamed gastric mucosa in the same biopsy specimen.
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PMID:[Campylobacter pylori in gastro-duodenal diseases, with special reference to endoscopic diagnosis, histological inflammatory grading, and intestinal metaplasia]. 279 52

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.
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PMID:Campylobacter pylori. The organism and its clinical relevance. 280 38

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.
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PMID:In vivo susceptibility of Campylobacter pylori. 291 80

We examined the pathophysiological roles of the urea-urease-ammonia system in gastric ulcer disease using rats. Exposure of the stomach to ammonia (0.01-1.0%) decreased the transmucosal potential difference (PD) and histological injury in a concentration-dependent manner. Exposure of the stomach for 20 min to urea (0.025-0.2%) together with urease (100 IU) produced a decrease in PD and microscopic injury similarly, and the lesion was closely associated with the amount of ammonia produced. Urea and urease alone had no effect on the gastric mucosa. These results suggested the pathophysiological importance of urea, urease and ammonia in gastric ulcer disease.
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PMID:Effect of ammonia on the gastric mucosa in rats: pathophysiological importance of urease in gastric ulcer disease. 322 33

Biopsy specimens of human gastric mucosa of patients with gastric complaints and subjected to endoscopic examination were cultured microaerobically, and Campylobacter pyloridis was detected in 46 out of 80 cases (57.5%). The organism was found in 13 out of 22 patients with gastritis, 11 out of 16 with gastric ulcer scar, 7 out of 16 with gastric ulcer, 3 out of 9 with gastric polyp, 4 out of 5 with gastric carcinoma, 2 out of 2 with esophagus carcinoma, and 6 out of 9 with other gastric diseases. The isolates were identified as C. pyloridis, demonstrating its characteristic features such as positive for oxidase and catalase, negative for reduction of nitrite and nitrate, positive for urease, no growth at 25 C, growth at 37 C, not tolerant to 1% glycine, and resistant to nalidixic acid. Positive alkaline phosphatase activity was considered as an additional feature characteristic for the strains of C. pyloridis. The major cellular fatty acids were tetradecanoic acid and 19-carbon-cyclopropane acid. This pattern is unique among Campylobacter species. The survival of the organism for a longer period than 60 min at pH 2.5 indicates its significant resistance to acidic environment.
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PMID:Isolation of Campylobacter pyloridis from human gastric mucosa and characterization of the isolates. 343 27

Campylobacter pyloridis infection of the stomach has been associated with gastric ulcer, duodenal ulcer, nonulcer dyspepsia, and gastritis. The etiological role of C. pyloridis in most of those conditions remains unclear. We reviewed what is known about C. pyloridis infections in man. Considerable clinical data on C. pyloridis infections was available in older literature concerning gastritis and gastric urease. C. pyloridis causes a form of type B gastritis. In some individuals the acute infection is associated with abdominal pain and transient hypochlorhydria. C. pyloridis infection is difficult to eradicate with current therapies. The mechanisms by which C. pyloridis infection may lead to development of peptic ulcers, nonulcer dyspepsia, or atrophic gastritis are discussed. Recent technological advances, such as the 13C-urea breath test, provide rapid noninvasive methods of identifying active C. pyloridis infection. These methods will permit the rapid execution of definitive investigations of the epidemiology, transmission patterns, and possible reservoirs of C. pyloridis infection and will delineate the spectrum of C. pyloridis-associated disorders.
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PMID:Campylobacter pyloridis gastritis: the past, the present, and speculations about the future. 355 84

From Oct. 1986 to Jan. 1987, a total of 74 patients presenting for endoscopy were studied. These included 30 cases of active chronic gastritis and 44 cases of peptic ulcer. Biopsy specimens were taken during the endoscopy and sent to the laboratory for Campylobacter pyloridis culture within 2 hours. The culture was done by inoculated with chocolate agar, Brucella agar and 0.2% urea broth for urease activity. Results showed that, 53% (16/32) of active chronic gastritis, 77% (10/13) of gastric ulcer and 84% (26/31) of duodenal ulcer were positive for Campylobacter pyloridis. The specificity and sensitivity of urease positive rate are 64% and 90% respectively. It is higher as compared with bacteria culture. In addition, we found that 10 days would be needed for the routine culture and identification of this organism. But it took only 30 minutes to 6 hours for urease activity test. Therefore, we suggested that urease activity test could be a rapid diagnostic method for detecting Campylobacter pyloridis.
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PMID:[Campylobacter pyloridis in active chronic gastritis and peptic ulcer]. 365 84

Triple therapy has been recommended as the most effective treatment for Helicobacter pylori eradication. Despite achieving a comparatively high eradication result, however, around 10% of patients still fail to be cured. Omeprazole can enhance efficacy of single and double antibiotic protocols and is particularly effective when combined with clarithromycin and a nitroimidazole. This study examined the effect of combining triple therapy with omeprazole. A prospective, randomised, unblinded, single centre trial was carried out on consecutive patients with symptoms of dyspepsia and H pylori infection confirmed by rapid urease test, microbiological culture, and histological assessment. Patients were given a five times/day, 12 day course of colloidal bismuth subcitrate chewable tablets (108 mg), tetracycline HCl (250 mg), and metronidazole (200 mg) with either 20 mg omeprazole twice daily (triple therapy+omeprazole) or 40 mg famotidine (triple therapy+famotidine) at night. Compliance and side effects were determined using a standard questionnaire form. One hundred and twenty five of 165 triple therapy+omeprazole patients and 124 of 171 triple therapy+famotidine patients returned for rebiopsy four weeks after completion of treatment. Significantly more triple therapy+omeprazole patients achieved eradication 122 of 125 (97.6%) as assessed by negative urease test, culture, and histological assessment, when compared with 110 of 124 (89%) triple therapy+famotidine patients (p = 0.006; chi 2). There were 30 triple therapy+omeprazole (24%) and 26 triple therapy+famotidine (21%) patients with de novo metronidazole resistant H pylori included in the study. Side effects were mild and infrequent and were comparable in both groups, although pain in duodenal ulcer, gastric ulcer, and oesophagitis patients seemed to subside earlier in those taking omeprazole. Compliance (>95% of drugs taken) was achieved by 98% of patients of both groups. A 12 days regimen of triple therapy with omeprazole is more effective in achieving H pylori eradication than is triple therapy plus famotidine. Use of 20 mg omeprazole twice daily rather than 40 mg famotidine with a 12 day, low dose triple therapy enhances eradication to over 97% whether the H pylori is metronidazole sensitive or resistant.
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PMID:Omeprazole enhances efficacy of triple therapy in eradicating Helicobacter pylori. 748 31

The presence of Helicobacter pylori was investigated in 50 patients, mean age 54 years and age range 28-56 years. Gastroduodenoscopy and biopsy of the antral and/or pyloric part of gastric mucous membrane were performed in all study patients. Bioptic tissue was examined by culture and histologic staining, and tested by a rapid urease test. According to overall results, the urease test was most sensitive, i.e. positive in 23 (45%) patients, whereas histological staining was positive in 14 (29) patients. Endoscopic diagnosis revealed the following: duodenal ulcer--histologic stain 3/5 (55%), urease test 9/21 (43%); gastric erosion--histologic stain 4/13 (31%), urease test 7/13 (55%); gastroduodenitis--histologic stain and urease test 2/4 (50%). According to endoscopy, positive pyloriset test (Orion Diagnostica) was found as follows: duodenal ulcer 5/7 (71%), gastric ulcer 8/10 (80%), gastric erosion 10/12 (83%) and gastroduodenitis 5/7 (71%). The authors recommend the diagnosis of Helicobacter pylori as a routine approach in gastroenterological routine.
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PMID:Helicobacter pylori in a group of endoscopically examined patients in the county of Medimurje. 758 42


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