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  • 1
    Electronic Resource
    Electronic Resource
    Helicobacter pylori and Zollinger-Ellison syndrome (1991)
    Springer
    Digestive diseases and sciences 36 (1991), S. 15-18 
    Details
    ISSN: 1573-2568
    Keywords: Campylobacter pylori ; Helicobacter pylori ; Zollinger-Ellison syndrome ; peptic ulcer ; gastric acid secretion ; gastrin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Helicobacter pylori (previouslyCampylobacter pylori) is almost invariably associated with chronic duodenal ulcer disease. The relationship betweenH. pylori infection and duodenal ulcer in Zollinger-Ellison syndrome is unknown. We investigated the frequency ofH. pylori infection in Zollinger-Ellison syndrome and also what effectH. pylori infection had on gastric function in patients with Zollinger-Ellison syndrome.H. pylori infection was diagnosed based on a specific serologic (ELISA) assay based on high-molecular-weight cell-associated proteins ofH. pylori. We studied 20 patients with Zollinger-Ellison syndrome; 15 men and 5 women ranging in age from 24 to 71 years, median age 51. Six Zollinger-Ellison syndrome patients hadH. pylori infection compared to 100 consecutive patients with chronic recurrent duodenal ulcer disease (P〈0.05). Pretreatment basal acid output in Zollinger-Ellison syndrome patients ranged from 7.9 to 95.0 mmol/hr, median 35.2. Pentagastrin-stimulated maximal acid output ranged from 8.5 to 132 mmol/hr, median 52.7. Acid secretion was lower in theH. pylori-infected patients than the uninfected patients (BAO 24.5±6.5 vs 45.4±6.6, and MAO 44.3±11.8 vs 67.9±10.7, forH. pylori infected vs uninfected patients, respectively). The difference in BAO was statistically significant (P〈0.05). The present results indicate thatH. pylori is not a major contributing factor in duodenal ulcer associated with Zollinger-Ellison syndrome. The association of a reduced BAO withH. pylori suggests that these findings may be related.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01300080
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  • 2
    Electronic Resource
    Electronic Resource
    Search for Putative Virulence Factors of Helicobacter pylori (The Low-Molecular-Weight (33-35 K) Antigen) (1998)
    Springer
    Digestive diseases and sciences 43 (1998), S. 1482-1487 
    Details
    ISSN: 1573-2568
    Keywords: HELICOBACTER PYLORI ; LOW-MOLECULAR-WEIGHT ANTIGEN ; 33-35 K ANTIGEN ; CagA ; VacA ; PATHOGENESIS
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Early studies suggested that two Helicobacterpylori proteins, CagA and VacA, were virulence factors.Support for that hypothesis has been undermined bygeographic differences in prevalence of these antigens. To identify other possible putative virulencefactors by establishing a relationship between antigensand different H. pylori diseases, two commercialavailable immunoblot assay kits, HelicoBlot 2.0(Genelabs Diagnostics, Singapore) and RIDA BlotHelicobacter (R-Biopharm GmbH, Darmstadt, Germany), wereused to investigate the prevalence of various specificantigen seropositivity in 80 H. pylori-infected Japanese (20 each with gastritis, duodenal ulcer,gastric ulcer, or gastric cancer). The production ofinterleukin-8 (IL-8) in biopsy specimens was alsomeasured by enzyme-linked immunosorbent assay (ELISA).Both assays had 100% sensitivity; specificity was90% for HB2.0 and 80% for RIDA-BH. With the exception ofthe 33-35 K antigen, there was no relationship betweenantigens, endoscopic diagnoses, histological findings, or mucosal IL-8 levels. The 33-35 Kantigen was present in 97.5% (39 of 40) patients withgastric or duodenal ulcer compared to 70% (14 of 20)those with chronic gastritis (P 〈 0.006). The mean IL-8 levels in the corpus wassignificantly higher in those with antibody to the 33-35K antigen compared to those without (105.4 ± 22pg/mg vs 10.2 ± 8.8 pg/mg) (P = 0.015). There wasno relationship between other antigens including CagA andproduction of IL-8. In conclusion, thelowmolecular-weight 33-35 K antigen may play animportant role in the pathogenesis of H. pylori-relateddisease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1018850412148
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  • 3
    Electronic Resource
    Electronic Resource
    Omeprazole versus placebo in duodenal ulcer healing (1990)
    Springer
    Digestive diseases and sciences 35 (1990), S. 66-72 
    Details
    ISSN: 1573-2568
    Keywords: Duodenal ulcer ; peptic ulcer ; controlled trial ; omeprazole ; ulcer therapy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The study objective was to study the ulcer healing effects and safety of the proton pump inhibitor, omeprazole, given in a dose of 20 mg once daily before breakfast. The study design was a randomized, double-blind, multicenter comparison of omeprazole and placebo using endoscopy to assess ulcer healing after two or four weeks of therapy. One hundred fifty-three patients with endoscopically documented active duodenal ulcer were studied. One hundred two patients received omeprazole and 51 received placebo. Patients in both groups were similar with regard to age, sex, duration of disease, initial ulcer size, smoking history, and alcohol use. A “per protocol” analysis of healing rates showed a significant advantage for omeprazole (P〈0.01) at both week 2 (41% vs 13%) and week 4 (75% vs 27%). Concomitant factors (including smoking and ulcer size) did not alter the significance of the differences in healing rates between omeprazole and placebo. Complete relief of day and night pain was more often achieved (P〈0.01) in the omeprazole group. “All-patients treated” analyses for healing and pain relief gave results similar to the respective “per protocol” analyses. Omeprazole was well tolerated; fewer patients had clinical and laboratory adverse experiences in the omeprazole group than in the placebo group. Fasting serum gastrin levels increased with omeprazole therapy (mean 34.9 to 73.5 pg/ml) but exceeded the normal range (〉150 pg/ml) in only 12.3% of patients. Two weeks after therapy was stopped, serum gastrin levels showed a decrease toward baseline but had not yet completely returned to pretreatment levels (mean 49.7 pg/ml). Observations from Europe and Australia of 〉90% healing of duodenal ulcers after four weeks of omeprazole therapy were not confirmed in this study. No single factor explains this difference. Considerable variation in the degree of suppression of acid secretion has been demonstrated with the 20-mg daily dose of omeprazole; it is possible that, in US populations, a greater degree of antisecretory effect may be required to achieve the healing rates observed in Europe and Australia. In conclusion, omeprazole was more effective than placebo in the treatment of active duodenal ulcer, as determined by ulcer healing and relief of pain, and was well tolerated in the short-term treatment of patients with duodenal ulcer.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01537225
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