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Query: UMLS:C0013395 (dyspepsia)
 4,879 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Campylobacter pylori may cause type B gastritis. C. pylori produces urease, and the presence of this enzyme in gastric mucosal biopsies is a marker for colonization with the microorganism. The value of a breath test to detect C. pylori colonization in non-ulcer dyspepsia patients was investigated. We compared the 14C-urea breath test with the culture results obtained from antral mucosal biopsies. The 14C-urea breath test is comparable to culture results in detecting C. pylori colonization.
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PMID:14C-urea breath test as a method to detect Campylobacter pylori colonization. 266 97

The presence of Campylobacter pylori was investigated in gastric antral biopsy specimens. In 50 consecutive patients undergoing upper gastrointestinal tract endoscopy microbiological cultures, histological examination and rapid urease test were parallel performed, and a 92 per cent sensitivity and 100 per cent specificity of rapid and cheap urease test were determined. Afterwards--in a prospective study--311 patients were examined for C. p. by the rapid urease test only. C. p. was detected in 92 per cent of duodenal ulcer patients, in 52 per cent of patients with gastric ulcer, in 67 per cent of non-ulcer dyspepsia, in 62 per cent of mixed diabetic patient material, and in 21 per cent only of asymptomatic volunteers. It has been found by the authors, that the rate of C. p. infection increased parallel with the continuance of diabetes and did not follow the increasing with age as in the general population. This is the first observation in the world literature concerning the correlation between C. p. and diabetes mellitus. Very close, significant correlation has been found between C. p. infection and chronic active gastritis. C. p. may play an important role in the recurrences of duodenal ulcer and in the pathogenesis of non-ulcer and diabetic dyspepsia. Further studies are planned to the correct evaluation of pathogeneity of Campylobacter pylori.
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PMID:[The significance of Campylobacter pylori infection in gastroenterologic and diabetic practice]. 266 37

The occurrence of Campylobacter pylori (CP) was studied in 180 patients referred for endoscopy. The bacterium was detected by culture, histology (Warthin-Starry staining) and urease test of antral biopsy samples. Patient groups were formed according to endoscopic diagnoses, clinical symptoms and antral mucosal histology. 50 CP positive patients with chronic antral gastritis were treated by bismuth subsalicylate (2,4 g/day) for 3 weeks. Positivity by culture and/or silver-stained histology proved to be the most reliable way for detecting CP. CP was proved in about 30% in patients with normal gastroduodenum (13/42) or with stump gastritis (4/15), in 75% with endoscopic antral gastritis (51/68) and in 89% with duodenal ulcer (49/55). A close relationship between CP and histological chronic antral gastritis could be demonstrated. No causal link between CP positive chronic active antral gastritis and non-ulcer dyspepsia could be verified. The decrease in histological activity of chronic gastritis and in dyspeptic complaints after bismuth salt therapy was found to be independent of CP elimination. The results of control investigations following a therapy-free interval of 7-10 days speak in favour of CP recolonialisation within a relativelly short period. It can be concluded that, despite the undeniable relationship between CP and chronic antral gastritis and duodenal ulcer, further studies are necessary to clarify the clinical relevance of the CP infection.
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PMID:[Has Campylobacter pylori infection any clinical relevance? Methodologic, epidemiologic and clinical studies]. 268 46

From August 1987 through July 1988, we evaluated antral biopsy specimens for Campylobacter pylori (CP) in 212 patients undergoing upper endoscopy. For those patients who had multiple endoscopies, the first endoscopy in which a urease test, histology, and culture were done was used to determine CP status. A patient was regarded as CP-positive if the culture was positive or if both a urease test and the histology were positive. Blacks had an increased CP positivity (61.2%) compared to whites (31.5%). Among non-ulcer patients, CP positivity was 52% in black patients and 18% in white patients. Age and gender were unrelated to CP positivity among controls and those without ulcers. There was increased CP positivity in patients with duodenal ulcers (85%), compared with those without ulcers (37%), and a trend toward increased positivity in those with gastric ulcer (53%) and duodenitis (50%). There was no increased CP positivity in patients with gastroesophageal reflux disease (28%), gastritis (29%), non-ulcer dyspepsia (43%), or the control patients with no gastroduodenal mucosal abnormalities (40%). CP-negative DU patients were older (average 71 yr) than CP-positive DU patients (43 yr), and female DU patients had a lower CP positivity (71%) than males (94%).
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PMID:Prevalence of Campylobacter pylori in patients undergoing upper endoscopy. 272 34

Of 1,100 patients checked by at least two diagnostic tests (urease, histology, culture) 574 (52.1 p. 100) were found to have Campylobacter pylori (C. pylori) in their antral mucosa. Significantly different frequencies of C. pylori (p less than 0.005) were evidenced in the group of patients with active gastroduodenal ulcer (212/298, 71 p. 100), in non-ulcer dyspepsia (NUD) with a previous history of GD ulcer (108/177, 61 p. 100) and NUD without antecedent history of GD ulcer (254/625, 41 p. 100). Whatever the group, males and immigrants were significantly at risk. Chronic alcoholism (greater than 60 g/day) and non-steroid anti-inflammatory drug (NSAID) intake were not predictive for the presence of C. pylori but smokers were significantly at risk when the total (n = 1,100) population was taken into consideration. C. pylori was found in 29 p. 100 of asymptomatic controls (n = 31). There was no significant difference in the frequency and intensity of symptoms when comparing C. pylori+ and C. pylori- patients. The macroscopic aspect of the antral mucosa was not predictive since 51 p. 100 of patients with normal endoscopy were C. pylori+. A strong correlation was observed between the incidence of C. pylori and the severity of gastritis at histology (p less than 0.001) and C. pylori was found in 7 p. 100 of patients with normal histology.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical, endoscopic and histologic findings in 1,100 patients of whom 574 were colonized by Campylobacter pylori]. 274 27

In order to understand the relation between the prevalence of Campylobacter pylori and the severity of gastritis, we conducted a survey of 166 randomly selected dyspeptic patients. The presence of C. pylori on the antral mucosa was aseptically determined by both urease and bacterial culture tests. Specimens of antral mucosa were obtained for pathologic gradings of inflammation: active gastritis, mononuclear cell infiltration C0 (nil) to C3 (lymphoid follicle); presence or absence of intestinal metaplasia. Pathologically, chronic gastritis was invariably present in almost all patients with dyspepsia: three-fourths of them showed evidence of active gastritis, one-third showed intestinal metaplasia. Half of the dyspeptic individuals had C. pylori colonization. The results suggest that the prevalence of C. pylori was closely related to the different grades of active gastritis; neither the different grades of chronic gastritis nor intestinal metaplasia affected the prevalence of C. pylori on gastric mucosa. We conclude from this study that C. pylori is closely related to active chronic gastritis because of the common presence of chronic gastritis in patients with dyspepsia.
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PMID:The relation between Campylobacter pylori and inflammatory cell infiltration of antral mucosa in patients with dyspepsia. 275 23

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

The association of Campylobacter pylori (C.p.) colonization of the upper gastrointestinal tract with five predefined anamnestic variables, seven symptoms of dyspepsia, and various blindly evaluated histological criteria, was prospectively investigated in a consecutive series of 149 patients submitted to upper gastrointestinal tract endoscopy. Colonization was determined by biopsy urease tests and histological searches. Significant differences (P less than 0.05) between C.p.-positive and C.p.-negative patients were found for smoker status and the frequency of therapy with ulcer-healing drugs (positive association with C.p.) and antibiotics (negative association), but not for any other of the anamnestic data or symptoms. These data were further submitted to stepwise multiple logistic regression analyses. Concerning histological findings, C.p. colonization was significantly associated with the degree of antrum and body gastritis (P less than 0.01), and also with lymphocellular infiltration in antrum and body biopsies and neutrophil cellular grading in gastric antra. We conclude that C.p. colonization of the upper gastrointestinal tract is associated with gastritic change of the antrum and, albeit to a lesser extent, of the body mucosa. However, a specific pattern of symptoms to predict C.p. colonization could not be established.
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PMID:Campylobacter pylori: prospective analysis of clinical and histological factors associated with colonization of the upper gastrointestinal tract. 313 19

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


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