Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013395 (dyspepsia)
 4,879 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The 13C-urea breath test was used for diagnosing noninvasively the possible presence of Helicobacter (formerly called Campylobacter) pylori in 20 patients with dyspepsia (ten men and ten women, mean age 40.2 [24-74] years). H. pylori was cultured from 14 patients, while in six the culture was negative. The proportion of 13C in expired air was measured by isotope mass-spectrometer and expressed as Delta (basal value about 20%). A dose of 2.5 mg urea per kg body-weight (BW) was ingested after a standard meal. The test was repeated with 1.75 and 1.0 mg/kg BW in five subjects. Delta had increased significantly after 30 min in all H. pylori-positive patients (P less than 0.001). The maximal value after 90 min ranged from 38 to 114%; in the H. pylori-negative patients it was 24%. After 1.75 and 1.0 mg/kg urea the maximal value after 90 min was 39-52% and 30-52%, respectively. Using a dose of 2.5 or 1.75 mg/kg BW tagged urea one can reliably distinguish between presence and absence of H. pylori. It is sufficient to test a basal and a 90-min expired-air sample.
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PMID:[13C-urea breath test as a non-invasive method for the detection of Helicobacter (Campylobacter) pylori]. 231 11

129 patients, Panamanians and North Americans, with chronic dyspepsia, were prospectively studied regarding infection by H. pylori and the type of gastroduodenal pathology diagnosed by endoscopy and histology. The rapid urea split test was compared with the culture. The percentage of patients infected by H. pylori increased with age. Patients under 30, 37%; 31 to 40, 61%; 41 to 76, 75%. H. pylori was found in 70% of the Panamanians and 54% of the americans. H. pylori infected 81%, 75%, 54% and 29% of the patients with duodenal ulcer, chronic gastritis, duodenitis, and patients with normal endoscopy and histology, respectively. The rapid urea split test had a positive predictive value of 98%. The results were discussed and the literature reviewed.
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PMID:[Helicobacter pylori and gastroduodenal pathology in the Republic of Panama]. 239 79

Campylobacter pylori is a newly described, spiral-shaped, gram-negative bacillus that is oxidase positive, catalase positive, and urease positive and grows slowly in culture. Although observed in human tissue at the beginning of the century, it was not cultured until 1982. Because there are significant morphological and genetic differences between this organism and other species of Campylobacter, it will probably be reclassified in a new genus. Current information indicates that the organism primarily resides in the stomach tissue of humans and nonhuman primates and may occasionally spread to the esophagus or other parts of the alimentary tract under appropriate conditions. Significant evidence has accumulated in the last several years to show that it causes gastritis, and there is mounting evidence that it may participate in the development of duodenal ulcers. It may also be associated with gastric ulcers and nonulcer dyspepsia. It can be detected in patients by culture of biopsy specimens or histological staining of biopsy tissue. Indirect evidence for the presence of the organism can be obtained by detection of urease in a tissue biopsy specimen, by urea breath tests, or by detection of specific antibody. It may not be necessary to implement these procedures for routine use, however, until the role of the organism can be defined better. Ultimately, the discovery of this organism may lead to radical changes in the diagnosis and treatment of gastric disease.
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PMID:Campylobacter pylori and gastroduodenal disease. 240 65

Campylobacter pylori has been associated with gastro-duodenal inflammatory disease. Ninety-five adults with dyspepsia were examined for the presence of C. pylori in the gastric antrum and near gastric or duodenal ulcers (when present) by means of culture, Gram and acridine orange stains, and urease activity of biopsies. C. pylori was identified from 51 out of 67 patients with chronic gastritis, from 9 out of 9 patients with duodenal ulcer, and from 8 out of 10 patients with gastric ulcer. Acridine orange stain revealed the highest number of positive cases, followed by culture, Gram stain and urease test. The latter showed a 100% specificity when carried out with a selective urea broth containing colistin, trimethoprim, vancomycin and amphotericin B. It has to be considered a further diagnostic tool which enables clinicians and microbiologists to diagnose the etiology of a dyspeptic syndrome even at the patient's bedside.
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PMID:[Comparison of methods for the identification of Campylobacter pylori in gastric biopsies of patients with dyspepsia]. 245 24

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

14C-urea breath test was used to detect Campylobacter pylori colonisation in 129 consecutive non-ulcer dyspepsia patients. Fasting patients were given 3 microCi (110 kBq) of 14C-labelled urea after a test meal. Breath samples were collected at 10 minute intervals for 90 minutes and the C-14 activity was counted on a liquid scintillation analyser. Urea derived 14CO2 appears in the exhaled breath of Campylobacter pylori culture positive individuals within 20-30 minutes. Likelihood analysis revealed a most favourable cut off level of [0.07% dose 14C-urea/mmol CO2] multiplied by body weight at t = 40 minutes, to separate culture positive from culture negative subjects. Using this upper limit of normal, a positive likelihood ratio of 50 and a negative likelihood ratio of 0.05 was calculated. Sensitivity of the test was 95% and specificity 98%. The 14C-urea breath test is a simple, sensitive and non-invasive test, that detects viable C pylori microorganism and semiquantitatively assesses the bacterial load of C pylori colonisation. Administration of a single dose of colloidal bismuth subcitrate resulted in a rapid decrease in 14CO2 excretion, so this test can be used to confirm eradication of the bacterium in therapeutic trials without endoscopy, or need for culture.
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PMID:14C-urea breath test in C pylori gastritis. 259 50

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

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.
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PMID:A sensitive and specific serologic test for detection of Campylobacter pylori infection. 277 37

The effect of experimental metabolic acidosis and its correction for nitrogen and energy metabolism was studied in new-born calves. It was discovered that a change in the acid-base balance towards acidosis causes a sharp increase in "ammoniogenesis", urea formation and inhibition of the tricarboxylic acid cycle, which is also observed in calves suffering from dyspepsia with symptoms of acute diarrhea. Alongside with the use of therapeutic measures for treating dyspepsia of new-born calves, it is necessary to control the acid-base balance of blood in the calves and in case of revealing the acidosis state to use means of its correction.
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PMID:[Changes in the levels of various substrates of nitrogen metabolism and tricarboxylic acid cycle during experimental acidosis in calves]. 303 45

Since Warren and Marshall rediscovered in 1983 the presence of a spiral microorganism on the gastric mucosa, and named it Campylobacter Pylori (CP), its significance and characteristics have been largely studied. CP has fulfilled Koch's postulates, which need to proven before a microorganism can be said to cause a disease. The natural source of infection is unknown, but in human volunteer studies, ingestion of a suspension of CP was followed by the development of severe dyspepsia associated with colonization of gastric antrum and histologically proven gastritis B. CP is found overying the gastric epithelium, in the gastric crypts and in the mucus gel layer that protects it from gastric acid. There it causes infiltration of the mucosa by polymorphonuclear leucocytes and mononuclear cells, and mucin depletion. It is found in 60-70% of children with chronic active antral gastritis and can cause various lesions of upper intestinal tract, like esophagitis, duodenitis and gastric or duodenal ulcers. Several tests have been proposed to detect serum antibody against CP, but they are not yet commercially available. Breath test with C 13 or C 14-urea are promising, but up to now the diagnosis can be made only by upper G.I. endoscopy and antral biopsy. A pseudopolypoid antral gastritis seems to be the peculiar lesion caused by CP, but in children it is present only in 40% of cases. CP is easily seen in antral biopsies by Giemsa or Hematoxylin-Eosin staining, or can be cultured in Skirrow's agar under microaerophilic conditions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Campylobacter pylori and gastroduodenal pathology in children]. 328 48


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