April 2000
AGAA1303
Updated Sydney System. In 10 patients with marked antral 1M and 10 without 1M, Ki-67 lavelling index (LI) in the antral mucosa was assessed. The immunostaining was performed using MIB-I antibody (Immunotech, Marseille, France) and by the avidin-biotin method with microwave retrieval. LI was calculated by counting MIB-I-positive cells in the entire gastric pits longitudinally sectioned and was expressed as a percentage ratio of the total cells in a gastric pit. Results: Table shows the number of patients in each category of change after the therapy. There was no significant difference in the grade of atrophy or 1M between before and after the therapy. After eradication, Ki-67 LI in the antral mucosa without 1M decreased significantly (from 34 to 25%, p<0.05), but that in the 1M did not change (from 36 to 39%). Conclusions: During 1-4 years after H. pylori eradication, regression or improvement of atrophy was found in 40% of patients. No significant regression of 1M, however, was found. 1M keeps proliferating after eradication of H. pylori.
and corpus. Macroscopic and microscpic inflammation was documented and was ranked according to the Sydney classification. Immunohistochemistry is currently under investigation. Results: Both e-defensins were present in the duodenum of almost every individual. Various sites in stomach and esophagus contained low transcript levels of HD-5 and 6, but there was no clear correlation to HP status. HBD-I was ubiquitously expressed in every part of the upper GI tract, supporting its constitutive character. HBD-2 was primarily found in the squamous epithelium of the esophagus. However, in almost half of the cases, parts of the stomach expressed considerable HBD-2 message. Conclusion: Human epithelial defensins are ubiquitously expressed in the upper gut. Highest expression levels of HD-5 and 6 were found in the duodenum whereas HBD-2 was located in the esophagus. There was no clearcut border of epithelial defensin expression longitudinally but a broad transitional zone in the stomach which varied interindividually. No correlation existed between helicobacter infection and defensin expression.
Number ofpatients ineach category ofchange after the therapy Reg Antral atrophy Body atrophy Antral 1M Body 1M
4 6 1 7
Imp
Dev
5950
Prog
Ne
ND
4 2 6
12 6 9 7
14 9 13
3
Reg, regression; Imp, improvement; Dev, development: Prog, progress;NC, nochange: ND, no development.
5948 SHORT SEGMENT BARRETT'S ESOPHAGUS: PREVALENCE OF HELICOBACTER PYLORI INFECTION IN COMPARISON TO PATIENTS WITH EROSIVE GERD, LONG SEGMENT BARRETT'S ESOPHAGUS AS WELL AS A ASYMPTOMATIC CONTROL GROUP. A PROSPECTIVE EVALUATION. Dieter Schilling, Margit Hahne, Tina Weinerth, Andreas Spiethoff, Ralf Jakobs, Juergen Ferdinand Riemann, Dept of Gastroenterology and Hepatology, Ludwigshafen, Germany; Dept of Gastroenterology, Ludwigshafen, Germany; Dept of Pathology, Ludwigshafen, Germany. Introduction: Diagnosis of short segment Barrett's esophagus (SSBE) depends on the histological finding of specialized intestinal metaplasia in biopsies from the typical endoscopical lesions at the squamocolunmar junction (z-line). The clinical and prognostic importance of SSBE in comparison to long segment Barrett's esophagus (LSBE) is still unclear. Recent reports have suggested that gastric infection with Helicobacter pylori (Hp)actually may protect the esophagus by preventing the development of gastroesophageal reflux esophagitis. Methods: We compared the clinical data concerning gastroesophageal reflux disease [(GERD);symptoms, 24 hour pH monitoring] and the prevalence of Hp infection (rapid urease test, Histology) in patients with SSBE (n=94),LSBE (n=51),erosive GERD (n=85) and in an age matched control group without evidence of GERD or associated diseases ( statistical analyses by chi square test). In SSBE patients at least three biopsie were obtained from the suspected areas at th z-line and were presented a pathologist not knowing the endoscopical diagnosis. Results: The prevalence of SSBE was 6 % in all patients of our endoscopic unit. Corresponing endoscopical and histological diagnosis was found in 66 %. Clinical features and results of pH monitoring did not differ between patients with SSBE and LSBE but between LSBE and GERD and between SSBE and GERD. The prevalence of Hp infection in patients with SSBE was 29.8 %, whereas it was 48.9 % in the control group (p=O.OOOI), in patients with erosive GERD 34.2 % (p=O.003) and 18 % of patients with LSBE (p=0.009). Conclusion: The prevalence of Hp infection differed significantly between the various reflux associated diseases and the control group, but did not differ significantly within these diseases. However a tendency towards a lower prevalence in LSBE and, according to our data also in SSBE can be seen. I
5949 DISTRIBUTION OF DEFENSIN EXPRESSION IN THE UPPER GASTROINTESTINAL TRACT. Klaus Schmidt, Klaus Fellermann, Jan Wehkamp, Klaus Robert Herrlinger, Frank Martin Reimann, Steffi Baxmann, Eduard Friedrich Stange, Univ of Luebeck, Luebeck, Germany. Background: Defensins are widely expressed antimicrobial peptides counteracting invasion by various pathogens. Interest has focussed on human beta defensin 2 (HBD-2), an inducible defensin, which is predominantly expressed in skin and lung. Elevated levels have been found in certain infections and ulcerative colitis. Recent studies speculated on an association of helicobacter pylori (Hp) infection and defensin expression. Cag pathogenicity island positive strains were incapable of inducing HBD-2 in a gastric carcinoma cell line . Aim of the present study was to investigate RNA expression in the upper GI tract and relate it to Hp status. Methods: During upper GI endoscopy 2 biopsies were taken from duodenum, antrum, corpus, fundus and esophagus of 13 patients (6 Hp positive). Total RNA was extracted and RT-PCR performed with a multiplex protocol for a-defensins (human defensin 5 and 6) and separately for /3-defensins (human /3defensin-I and 2), GAPDH serving as an internal housekeeping gene. HP-status was assessed by urease testing and histology from antrum
LEPTIN IS A CONTRIBUTING FACTOR TO THE INTEGRITY OF GASTRIC MUCOSA. Ralph Schneider, Matthias G. Breidert, Stefan R. Bornstein, George P. Chrousos, Gerhard Ehninger, Med Dept I, Tech Univ Hosp, Dresden, Germany; NIH, Bethesda. Background: Recently, the rat stomach was reported as a source of leptin, a hormone mainly secreted by adipocytes. Also Helicobacter pylori-induced gastritis in humans was associated with locally elevated leptin levels. In addition, it was suggested that gastric leptin adjusts the function of the intestinal tract in parallel to the function of hypothalamic satiety centers. Aims: Here we examined the synthesis and potential physiologic role of leptin in the human stomach. Methods: RT-PCR was employed to detect leptin mRNA in the human stomach and the human gastric carcinoma cell line AGS, while immunogold staining and electron microscopy were used to detect leptin protein. The in vitro effects of leptin on cell proliferation were examined in the AGS cell line. Results: No leptin mRNA could be detected by RT-PCR, yet immunogold labeling and electron microscopy allowed visualization of leptin protein in the human gastric mucosa. Leptin at concentrations of 100 to 200nM led to a significantly, increased proliferation rate of AGS cells (+27%, p
5951 PANTOPRAZOLE 40MG (PANTO) RELIEVES PRIMARY REFLUX SYMPTOMS MORE RAPIDLY THAN OMEPRAZOLE MUPS 20MG (OME) IN PATIENTS WITH SEVERE GERD SYMPTOMATOLOGY. Theo Scholten, Gudrun Gatz, Peter Sander, Med Clin Hosp of Hagen, Hagen, Germany; Byk Gulden, Konstanz, Germany. Methods: In this double-blind, randomized, multi-centre, parallel group comparison of GERD patients treated for 4 weeks with either Panto or Orne, the following symptoms were assessed: heartburn, acid eructation, general gastric complaints as were the patients assessment of their treatment and their use of antacids. These assessments were made every second or third day by telephone interview and the severity of symptoms was scored and a factor analysis conducted. The influence of treatment and of heartburn severity at baseline on symptoms was investigated by use of analysis of variance (ANOVA). Results: 360 patients (198 male, 162 female) were recruited into the study with a mean age of 54.3:':: 14.7 years. 185 Patients were randomized to receive Panto and 175 patients to receive Orne. At baseline the degree of heartburn was nearly identical in both groups (2.34 :':: 0.48 versus 2.34 :':: 0.47). Factor analysis of symptoms recorded revealed 2 factors: the first was acid eructation and heartburn (reflux symptoms) and the second was gastric complaints and assessment of treatment. Overall Panto showed an advantage compared to Orne. In patients with severe heartburn (63 of the Panto and 57 of the Orne groups respectively) Panto therapy was associated with at least lower or even significantly lower reflux symptom scores at the first telephone interview (scores: 3.32 vs. 3.60, p=0.472), second interview (score: 2.73 vs. 3.33, p=0.012) and at the third interview (scores: 2.43 vs. 2.74, p= 0.081). Similarly, an analysis of factor 2 also yielded a trend to higher efficacy for Panto compared to Orne, though this did not reach statistical significance. Conclusions: in patients with severe heartburn pantoprazole 40mg brings faster relief of primary GERD symptoms than omeprazole 20mg.