Z Gastroenterol 2009; 47 - A81
DOI: 10.1055/s-0029-1224060

Expression of protease-activated receptor-2 (PAR-2) in Barrett's esophagus.

A Rosztóczy 1, I Németh 2, F Izbéki 1, K Vadászi 1, R Róka 1, K Gecse 1, L Tiszlavicz 2, T Wittmann 1
  • 11st Department of Medicine, University of Szeged
  • 2Department of Pathology, University of Szeged

Background: Protease-activated receptor-2 mediates a variety of gastrointestinal functional processes, including the ability to induce tissue regeneration and cell proliferation. The metaplastic process resulting in Barrett's esophagus is considered as a regenerative answer to mixed duodenogastric reflux. In our present preliminary study we hypothetized that PAR-2 may have a role in the metaplastic-dysplastic changes in the columnar lined esophagus.

Materials and methods: Mucosal biopsy samples were taken during upper gastrointestinal endoscopy from 57 patients with endoscopically suspected esophageal metaplasia. Sixteen patients had cardia/oxynthic (CO), 18 had intestinal metaplasia (IM) without dysplasia, 12 had IM with low grade dysplasia (LGD), and 11 had IM with high grade dysplasia (HGD) or adenocarcinoma. PAR-2 expression was determined by immunohistohemistry and scored blindly, by two independent pathologists from 0 to 4.

Results: PAR-2 expression in CO metaplasia was significantly lower than in IM (1,19±0.24 vs. 1.78±0.10, p<0.01). Patients with IM dysplasia had further increase in their PAR-2 expression (LGD: 2.83±0.21, HGD/adenocarcinoma: 3.36±0.20, p<0.01 to IM without dysplasia). Correlation analysis showed a significant association between PAR-2 expression and the histological stage of the disease (p<0.001).

Conclusion: The marked presence of PAR-2 in esophageal metaplasias and its correlation with the histological stage may refer to the importance of PAR-2 in the metaplasia-dysplasia sequence of esophageal carcinogenesis.

The study was organized by the South Hungarian Regional Surveillance Group for the Study of Barrett's Esophagus (B Bod, L Czakó, J Csanádi, K Csefkó, Zs F. Kiss, P. Fritz, C Góg, J Hudák, K Intzédy, K Jármay, Zs Kálló, M Karácsony, Gy Lázár, Zs Lénárt, K Lovik, T Molnár, F Nagy, L Oczella, A Paszt, S Radics, L Szalay, K Szentpáli, A Szepes, Z Szepes, Gy Szlovák, A Tiszai, A Titz, M Varga, A Váry, J Zombori). Grant support: ETT T02–515/2006.