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| 1 | Breath and string test: A diagnostic package for the identification of treatment failure and antibiotic resistance of Helicobacter pylori without the necessity of upper gastrointestinal endoscopy显示文摘AIM: Helicobacter pylori ( H pylofi) resistance after failed eradication has a major impact on the outcome of a further treatment regimen. The aim of this study was to assess the validity of a non-invasive strategy using the 13C-urea breath test (UBT) and the gastric string test in identifying post-treatment resistance of Hpylori.METHODS: The UBT was routinely performed 4 to 6 wk after H pylorieradication therapy. Forty-two patients (24 females, 18 males, mean age 48 years) with a positive UBT were included in the study. A gastric string test using a capsule containing a 90 cm-long nylon fiber was performed.Before the capsule was swallowed, the free end of the string was taped to the cheek. After one hour in the stomach, the string was withdrawn. The distal 20 cm of the string was inoculated onto an agar plate and processed under microaerophilic conditions. Following the string test, upper gastrointestinal endoscopy was performed to obtain gastric biopsies for conventional culture.RESULTS: H pyloriwas successfully cultured from the gastric string in 34 patients (81%), but not in 5 patients due to contamination with oropharyngeal flora. Hpyloriwas cultured from the gastric biopsies obtained at endoscopy in 39 patients (93%).CONCLUSION: The UBT followed by the gastric string test in the case of treatment failure is a valid diagnostic strategy with the aim of determining the post-therapeutic antibiotic resistance of Hpyloriwith little inconvenience to the patient.Upper GI-endoscopy can be avoided in several cases by applying consequently this diagnostic package. | Andreas Leodolter Kathlen Wolle Ulrike von Arnim Stefan Kahl Gerhard Treiber Matthias P.Ebert Ulrich Peitz Peter Malfertheiner | 2005 | World Journal of Gastroenterology2005，11，4： | 10 |
| 2 | Prevalence of H pylori associated 'high risk gastritis' for development of gastric cancer in patients with normal endoscopic findings显示文摘AIM: To investigate the prevalence of H pylori associated corpus-predominant gastritis (CPG) or pangastritis, severe atrophy, and intestinal metaplasia (IM) in patients without any signifi cant abnormal fi ndings during upper- GI endoscopy. METHODS: Gastric biopsies from 3548 patients were obtained during upper GI-endoscopy in a 4-year period. Two biopsies from antrum and corpus were histologically assessed according to the updated Sydney-System. Eight hundred and forty-fi ve patients (mean age 54.8 ± 2.8 years) with H pylori infection and no peptic ulcer or abnormal gross fi ndings in the stomach were identifi ed and analyzed according to gastritis phenotypes using different scoring systems. RESULTS: The prevalence of severe H pylori associated changes like pangastritis, CPG, IM, and severe atrophy increased with age, reaching a level of 20% in patients of the age group over 45 years. No differences in frequencies between genders were observed. The prevalence of IM had the highest increase, being 4-fold higher at the age of 65 years versus in individuals less than 45 years. CONCLUSION: The prevalence of gastritis featuring at risk for cancer development increases with age. These findings reinforce the necessity for the histological assessment, even in subjects with normal endoscopic appearance. The age-dependent increase in prevalence of severe histopathological changes in gastric mucosa, however, does not allow estimating the individual risk forgastric cancer development-only a proper follow-up can provide this information. | Andreas Leodolter Matthias P Ebert Ulrich Peitz Kathlen Wolle Stefan Kahl Michael Vieth Peter Malfertheiner | 2006 | World Journal of Gastroenterology2006，12，34： | 4 |
| 3 | Helicobacter pylori infection and fundic gastric atrophy are not associated with esophageal squamous cell carcinoma: a case–control study显示文摘 | Marino Venerito Sabine Kohrs Thomas Wex Daniela Adolf Doerthe Kuester Daniel Schubert Ulrich Peitz Klaus M?nkemüller Peter Malfertheiner | 2011 | European Journal of Gastroenterology & Hepatology2011，，10： | 1 |
| 4 | Upregulation of cathepsin W-expressing T cells is specific for autoimmune atrophic gastritis compared to other types of chronic gastritis显示文摘AIM: To investigate a pathophysiological role of cathepsin W (CatW), a putative thiol-dependent cysteine protease,which is specifically expressed in cytotoxic lymphocytes,in different types of chronic inflammation of the gastric mucosa.METHODS: Gastric and duodenal biopsies of patients with Helicobacter pylori ( H pylori)-associated active gastritis ( Hp,n = 19), chemically induced reactive gastritis (CG, n = 17),autoimmune atrophic gastritis (AIG, n = 20), lymphocytic corpus gastritis (LG, n = 29), celiac disease (CD, n = 10),and corresponding controls (n = 24) were analyzed by immunohistochemistry for the expression of CatW and CD45. Furthermore, immunohistochemical double staining with anti-CD3 and anti-cathepsin was performed for the samples of AIG.RESULTS: Median values of CatW-expressing cells among CD45-positive immune cells were between 2% and 6% for normal gastric mucosa, CG, and LG, whereas the corresponding value was significantly increased for AIG (24.7%, P<0.001) and significantly decreased for HP (0.7%, P<0.05). Double staining with anti-CD3 and antiCatW antibodies revealed that >90% of CatW-expressing cells in gastric mucosa of AIG were T cells. Duodenal mucosa had significantly more CatW/CD45-positive cells than normal gastric mucosa (median: 17.8% vs 2%, P<0.01).The corresponding proportion of CatW/CD45-positive cells was decreased in CD compared to duodenal mucosa (median: 2.1% vs 17.8%, P<0.05).CONCLUSION: The opposite findings regarding the presence of CatW-positive cells in AIG (increase) and CD (decrease) reflects the different cellular composition of immune cells involved in the pathogenesis of these diseases. | Doerthe Kuester Michael Vieth Ulrich Peitz Stefan Kahl Manfred Stolte Albert Roessner Ekkehard Weber Peter Malfertheiner Thomas Wex | 2005 | World Journal of Gastroenterology2005，11，38： | 0 |
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