Pancreatic acinar cells normal finding at the gastroesophageal junction Data from a prospective Central European multicenter study

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• 作者：Nora I. Schneider (1)
  Wolfgang Plieschnegger (2)
  Michael Geppert (3)
  Bernd Wigginghaus (4)
  Gabriele M. Hss (5)
  Andreas Eherer (6)
  Eva-Maria Wolf (1)
  Peter Rehak (7)
  Michael Vieth (8)
  Cord Langner (1)
  
• 关键词：Pancreatic acinar metaplasia ; Prevalence ; Gastric cardia ; Reflux disease ; Gastritis
• 刊名：Virchows Archiv
• 出版年：2013
• 出版时间：November 2013
• 年：2013
• 卷：463
• 期：5
• 页码：643-650
• 全文大小：
• 作者单位：Nora I. Schneider (1)
  Wolfgang Plieschnegger (2)
  Michael Geppert (3)
  Bernd Wigginghaus (4)
  Gabriele M. Hss (5)
  Andreas Eherer (6)
  Eva-Maria Wolf (1)
  Peter Rehak (7)
  Michael Vieth (8)
  Cord Langner (1)
  
  1. Institute of Pathology, Medical University of Graz, Auenbruggerplatz 25, 8036, Graz, Austria
  2. Department of Internal Medicine, Krankenhaus der Barmherzigen Brer, Academic Teaching Hospital, St. Veit/Glan, Austria
  3. Bayreuth, Germany
  4. Osnabrk, Germany
  5. Department of Surgery, Division of General Surgery, Medical University of Graz, Graz, Austria
  6. Department of Internal Medicine, Division of Gastroenterology and Hepatology, Medical University of Graz, Graz, Austria
  7. Department of Surgery, Research Unit for Biomedical Engineering and Computing, Medical University of Graz, Graz, Austria
  8. Institute of Pathology, Klinikum Bayreuth, Bayreuth, Germany
  
• ISSN：1432-2307

文摘

Pancreatic acinar cells are a well-recognized finding at the gastroesophageal junction, but their histogenesis and biological significance are unclear. From the prospective Central European multicenter histoGERD trial, we recruited 1,071 individuals undergoing gastroscopy for various non-selected reasons. Biopsy material was systematically sampled from the gastroesophageal junction and from the stomach. The study aimed to assess the prevalence of pancreatic acinar cells and to relate their presence to various histologic and clinical features. Overall, pancreatic acinar cells were observed in 184 (17.2%) participants. Individuals diagnosed with pancreatic acinar cells were slightly younger than those without (median 50 vs. 53years; p=0.009). There was no association with patientssymptoms and/or complaints or with an endoscopic diagnosis of esophagitis or Barrett esophagus. Regarding histology, pancreatic acinar cells were not associated with features of the squamous epithelium indicating reflux disease, such as basal cell hyperplasia, papillary elongation, dilation of intercellular spaces, and inflammatory cell number, but were associated with the presence of cardiac mucosa (p<0.001), oxyntocardiac mucosa (p<0.001), and intestinal metaplasia (p=0.038), respectively. No association with Helicobacter pylori infection or diagnosis of gastritis was noted. In conclusion, pancreatic acinar cells are a common finding at the gastroesophageal junction, and no association with either reflux disease (histologically or endoscopically) or diagnosis of gastritis was observed. These data suggest a congenital rather than an acquired (metaplastic) origin of pancreatic acinar cells at the gastroesophageal junction. This questions the term ancreatic acinar metaplasiawhich is currently widely used for their diagnosis.