In:
European Surgical Research, S. Karger AG, Vol. 52, No. 1-2 ( 2014), p. 73-82
Abstract:
〈 b 〉 〈 i 〉 Background: 〈 /i 〉 〈 /b 〉 Secondary biliary carcinomas are associated with persistent reflux cholangitis after bilioenterostomy. Cyclooxygenase-2 (COX-2) has been a target for cancer prevention. The aim of this study was to evaluate the chemopreventive efficacy of long-term treatment with a selective COX-2 inhibitor medication during the natural course after bilioenterostomy without chemical induction. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 Syrian golden hamsters which underwent choledochojejunostomy were randomly divided into two groups: the control group (n = 31), which was fed a normal diet, and the etodolac group (n = 33), which was fed 0.01% etodolac (a selective COX-2 inhibitor) mixed in the meal. The hamsters were killed at the postoperative weeks 20-39, 40-59, 60-79, or 80-100. Biliary neoplasms, cholangitis, proliferating cell nuclear antigen labeling index (PCNA-LI) of the biliary epithelium, and prostaglandin E 〈 sub 〉 2 〈 /sub 〉 (PGE 〈 sub 〉 2 〈 /sub 〉 ) production were evaluated. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 The occurrence rates of biliary neoplasm were 43.8 and 15.2% in the control and etodolac groups, respectively (p 〈 0.05). The incidence of biliary neoplasm increased as time progressed in the control group, whereas it remained at a low level throughout the experimental period in the etodolac group. PGE 〈 sub 〉 2 〈 /sub 〉 products tended to be lower in the etodolac group, and PCNA-LI was significantly lower in the etodolac group (p 〈 0.01). These results suggest that the medication etodolac suppresses cell proliferation of the biliary epithelium, thereby preventing biliary carcinogenesis. 〈 b 〉 〈 i 〉 Conclusions: 〈 /i 〉 〈 /b 〉 Etodolac is expected to prevent secondary biliary carcinogenesis caused by persistent reflux cholangitis after bilioenterostomy.
Type of Medium:
Online Resource
ISSN:
0014-312X
,
1421-9921
Language:
English
Publisher:
S. Karger AG
Publication Date:
2014
detail.hit.zdb_id:
1468505-X
