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)

One hundred and ninety-six symptomatic Saudi patients with dyspepsia underwent gastroscopy, and multiple biopsies were taken from the antrum of the stomach for identification of Helicobacter pylori. Three methods were studied for diagnosis of Helicobacter pylori, including urease test, culture and histopathology. The commonest gastroscopic findings were gastritis in 82 patients (41.84%) and duodenal ulcer in 40 patients (20.41%). Among the 196 patients, Helicobacter pylori was identified by histopathology in 145 patients (73.98%), the urease test was positive in 126 patients (64.29%), and a positive culture was obtained in 102 patients (52.04%). These results show that there is a high incidence of Helicobacter infection among Saudi patients with peptic ulcer disease or non-ulcer dyspepsia. Helicobacter pylori identification was more successful by histopathology than by the urease test or culture.
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PMID:Helicobacter pylori: incidence and comparison of three diagnostic methods in 196 Saudi patients with dyspepsia. 817 15

In a prospective study we examined 20 Helicobacter pylori (HP)-positive duodenal ulcer patients (5 female, 15 male; age 26-70 [mean 43] years), 20 HP-positive patients with non-ulcer dyspepsia (10 female, 10 male; age 26-79 [mean 48] years) and 10 HP-negative patients with non-ulcer dyspepsia (5 female, 5 male; age 21-76 [mean 45] years) during upper GI-endoscopy. HP was detected by histology (H&E, Giemsa), rapid urease test (CLO) and serology (Cobas Core Anti-H. pylori EIA). IgA anti-HP in gastric juice was determined by ELISA. HP-positivity included positivity in all methods, and HP-negativity failure to detect HP-infection by all methods used. Of the 20 duodenal ulcer patients, 10 patients (2 female, 8 male; age 26-70 [mean 42] years) had an endoscopically documented duodenal ulcer at an earlier endoscopy with no current ulcer, 10 patients had florid duodenal ulcer disease at the time of examination. Duodenal ulcer patients compared with non-ulcer dyspepsia patients were tended to have higher serum IgG anti-HP (551 +/- 240 vs. 338 +/- 159 U/ml) and significantly higher gastric juice IgA anti-HP (50.0 +/- 7.3 vs. 26.5 +/- 4.3 relative units). Concentrations of both serum IgG anti-HP and gastric juice IgA anti-HP tended to be higher in patients with positive ulcer history but no present ulcer compared with patients with florid ulcer disease (934 +/- 456 vs. 170 +/- 63 U/ml and 60.0 +/- 8.6 vs. 40.8 +/- 10.4 relative units).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Duodenal ulcer disease: a defect in the secretory immune response to Helicobacter pylori?]. 819 Dec 63

The systemic IgG response to Helicobacter pylori was examined in 70 patients with gastric cancer. H pylori IgG antibodies were assayed by enzyme linked immunosorbent assay (ELISA), and serological recognition of H pylori antigens was characterised by western blotting. A percentage of 78.5 were seropositive by ELISA. Two of five patients under age 50 were seronegative. Positivity was unrelated to age, sex, tumour type, or site. Ninety one per cent of ELISA positive cancer patients recognised the H pylori cytotoxin associated 120 kilodalton (kD) protein, significantly more than a control group of 47 ELISA positive patients with non-ulcer dyspepsia (72%). Four of 15 ELISA negative cancer patients also showed recognition of this protein in western blots. Mucosal IgA responses to H pylori were examined by immunoblotting supernatants of in vitro cultured resected antral mucosa in an overlapping group of 19 gastric cancer patients. Eighteen had a positive response, including 10 of 11 negative for H pylori by biopsy urease testing. The systemic and local immunoblotting results show that the high seroprevalence of H pylori antibodies detected by ELISA is nevertheless an underestimate of past infection. Dyspepsia screening policies based solely on H pylori ELISA would miss some young patients with gastric cancer. Further study of the relation of the H pylori cytotoxin to gastric precancerous lesions is warranted.
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PMID:Systemic and mucosal humoral responses to Helicobacter pylori in gastric cancer. 824 98

Although a high prevalence of antibodies to Helicobacter pylori has been documented within families, culture and DNA typing of strains from infected children and their parents has not been evaluated. This study aimed to analyse H pylori infection within family groups. Endoscopy, gastric biopsy, and H pylori culture were performed on all eight parents of four children who presented with dyspepsia and who had a positive H pylori culture. All biopsy specimens were cultured on Columbia based blood agar under microaerophilic conditions for four days. The DNA from each strain was extracted and electrophoretic patterns were compared after digestion with restriction endonucleases Hae III or Hind III. Ribotyping using a biotinylated cDNA probe prepared from 16S and 23S rRNA of H pylori NCTC 11638 was also used. Seven of the parents were positive for H pylori on urease testing, histology, and on culture. DNA typing showed the same or a similar strain to be present in at least two family members in three of the four family groups. In family 1, the mother, father, and child all had an identical strain; in family 2, father and son had a similar related strain; father and mother had the same strain in family 3; and all strains were unique in family 4. These data provide evidence for either intrafamilial cross infection or a common source of infection within family groups.
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PMID:Helicobacter pylori: comparison of DNA fingerprints provides evidence for intrafamilial infection. 824

The purpose of the work was a comparison of the incidence of Helicobacter pylori (HP) infections in persons with dyspeptic symptoms of non-ulcer dyspepsia (NUD) character in relation to the presence or absence of duodenogastric reflux (DGR). The study included 80 patients aged from 17 to 80 years, 21 males and 59 females. In all studied patients endoscopy of upper digestive tract segment was performed with biopsy specimen taking for microbiological investigations. From each patient two biopsy specimens were taken from the prepyloric part and the fundus. The specimens were subjected to a microbiological analysis using the rapid urease test, culturing, and direct preparation. The presence of duodenogastric reflux was evaluated during endoscopy. In persons with diagnosed NUD and duodenogastric reflux, lower incidence of HP infections was found than in patients with the same diagnosis but without the reflux.
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PMID:[Incidence of Helicobacter pylori infections in patients with duodenogastric reflux]. 824 13

Antibodies to H.pylori were investigated in the serum of 50 patients with dyspepsia and 25 healthy controls with ELISA method. The antibody positivity was found in all of the 40 cases (100%) for whom H.pylori was demonstrated in at least two tests of rapid urease, Gram stain, culture and silver staining and in eight of the ten cases (80%) whom H.pylori tests were all negative. Twenty-two of the 25 healthy controls (88%) had also antibodies to H.pylori. The sensitivity of the test was found high (100%), but the specificity was found too low (20%).
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PMID:[Evaluation of the ELISA method for the diagnosis of Helicobacter pylori]. 826 42

A prospective study of infection due to Helicobacter pylori in 104 Southern Appalachian veterans with upper gastrointestinal symptoms revealed a prevalence of 67%. There was no age difference observed between those with and without H pylori. The organism was shown to be present in 12 of 13 patients with duodenal ulcer (92%), 6 of 10 with gastric ulcer (60%), and 52 of 81 with nonulcer dyspepsia (64%). Using culture as standard, the urease test showed a sensitivity of 76% and specificity of 100%, while the biopsy stain had a sensitivity of 97%. The presence of acute inflammation in the antrum and body of the stomach closely correlated with the presence of the organism. Somewhat at variance with previous studies, our study indicated that H pylori in the body mucosa was strongly associated with chronic superficial gastritis with and without acute inflammation. Such a finding may reflect the natural history of infection due to H pylori and the advanced age of our patients.
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PMID:Chronic gastritis associated with infection due to Helicobacter pylori in southern Appalachian veterans with dyspepsia. 827 11

Colonisation with Helicobacter pylori may influence susceptibility to gastroduodenal injury and ulceration in patients taking non-steroidal anti-inflammatory drugs (NSAIDs). The aim of this study was to determine if Helicobacter pylori colonisation altered eicosanoid synthesis by gastric mucosa in these patients. Sixty five patients with long-standing NSAID intake and 23 control subjects underwent endoscopy. In vitro gastric antral biopsies were stimulated by vortex mixing and eicosanoid measurements determined by radioimmunoassay. Helicobacter pylori colonisation was determined by a CLO test (a gel based rapid urease test) and histological assessment. Median prostaglandin E2 synthesis by gastric mucosa was 61.0 (interquartile range: 19.2-73.1) pg/mg in control subjects colonised with Helicobacter pylori compared with 46.5 (23.3-65.5) pg/mg in Helicobacter pylori negative subjects. This was not significantly different. Treatment with NSAIDs was associated with a significant difference (p < 0.001) in prostaglandin E2 (PGE2) synthesis between those colonised with Helicobacter pylori (37.5(22.0-77.3) pg/mg) compared with patients not infected (12.6(7.0-19.3) pg/mg). Values in patients taking NSAIDs who were colonised were not different from control subjects. Synthesis of PGE2 was strongly associated with type B (chronic active), but not type C (chemical) gastritis. Dyspeptic symptoms were more common in subject colonised with Helicobacter pylori (p < 0.002) and were associated with higher PGE2 synthesis. In patients taking NSAIDs Helicobacter pylori colonisation removes rather then enhances depression of PGE2 synthesis associated with NSAIDs and may promote dyspepsia associated with ulcers and prevent superficial mucosal injury.
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PMID:Effect of Helicobacter pylori colonisation on gastric mucosal eicosanoid synthesis in patients taking non-steroidal anti-inflammatory drugs. 831 5

Thirty-three consecutive patients with idiopathic gastric acid hypersecretion (defined as a basal acid output > 10.0 meq/hr with a normal fasting serum gastrin level and negative secretin stimulation test) who were being treated for duodenal ulcer disease and other acid-peptic disorders were evaluated for the presence of Helicobacter pylori by means of a rapid urease test. Fourteen patients had duodenal ulcer and 19 had other acid-peptic disorders (gastroesophageal reflux in 14, including six with Barrett's esophagus; four with nonulcer dyspepsia; and one with erosive gastritis). Helicobacter pylori was present in 12 of the 14 ulcer patients (86%) compared to only two of the 19 nonulcer patients (11%) (P < 0.0001). The distribution of basal acid output for patients with duodenal ulcer was similar to that for nonulcer patients, and no significant difference in the mean basal acid output was found among Helicobacter pylori-positive compared to Helicobacter pylori-negative patients. Seven of the duodenal ulcer patients with a basal acid output greater than 15.0 meq/hr were Helicobacter pylori-positive, suggesting that the organism can withstand even extreme levels of gastric acidity. In conclusion, this study demonstrates that the prevalence of Helicobacter pylori infection in patients with duodenal ulcer disease associated with idiopathic gastric acid hypersecretion is not different from a majority of ulcer patients with normal acid secretory profiles and offers additional evidence that extreme levels of gastric acid are not bactericidal for the organism.
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PMID:Helicobacter pylori in duodenal ulcer patients with idiopathic gastric acid hypersecretion. 842 Jul 45

In a prospective study, gastroscopy and biopsies from the gastric antrum and body were undertaken in 100 consecutive patients (67 women, 33 men; mean age 58.6 [11-90] years) with unknown Helicobacter pylori status. None had been on any bacteria-suppressing drugs. Main indications for gastroscopy were upper abdominal pain, dyspepsia, emesis and anaemia of unknown cause. The macroscopic criteria for the diagnosis of H. pylori gastritis were the presence of at least one of the following signs: (1) chronic antral erosions; (2) goose-pimple-like appearance of the antral mucosa; (3) spotty erythema in the antrum; (4) complex changes of the antral mucosa with both bizarre reddening and pale areas; and (5) increased areolar markings and diffuse or fine-spotty erythema in the mucosa of the body of the stomach. Four biopsies each from the antrum and body were examined with the urease quick-test, microscopically as smears, specific culture and histology as reference methods. 60 patients had H. pylori gastritis, recognized macroscopically in 59 (sensitivity 98.3%). A false-positive diagnosis was made in 10 of 40 H. pylori-negative patients (specificity 75%). The positive predictive value of macroscopic diagnosis was 85.5%, the negative predictive value 96.8%.
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PMID:[Is Helicobacter pylori gastritis a macroscopic diagnosis?]. 843 66


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