Cyclooxygenase-2 (COX-2) polymorphisms and risk of inflammatory bowel disease in a Scottish and Danish case–control study

✍ Scribed by Vibeke Andersen; Elaine Nimmo; Henrik B. Krarup; Hazel Drummond; Jane Christensen; Gwo-tzer Ho; Mette Østergaard; Anja Ernst; Charlie Lees; Bent A. Jacobsen; Jack Satsangi; Ulla Vogel

• Publisher: John Wiley and Sons
• Year: 2011
• Tongue: English
• Weight: 243 KB
• Volume: 17
• Category: Article
• ISSN: 1078-0998
• DOI: 10.1002/ibd.21440

✦ Synopsis

Background:

Inflammatory bowel diseases (ibds) are a result of interactions between luminal pathogens and the intestinal immune response. cyclooxygenase-2 (cox-2) plays a key role in the regulation of the inflammatory response upon stimulation by luminal pathogens via toll-like receptors.

Methods:

Genotypes of the cox-2/ptgs2/pghs2 a-1195g (rs689466), g-765c (rs20417), and t8473c (rs5275) polymorphisms were assessed in a scottish and danish case-control study including 732 crohn's disease (cd) cases, 973 ulcerative colitis (uc) cases, and 1157 healthy controls using logistic regression.

Results:

Carriers of the cox-2 a-1195g variant allele had increased risk of uc (odds ratio [or], 95% confidence interval [ci] = 1.25 [1.02-1.54], p = 0.03) and of both uc and ibd among never smokers (or [95% ci] = 1.47 [1.11-1.96], p = 0.01 and or [95% ci] = 1.37 [1.06-1.77], p = 0.02, respectively). furthermore, this variant genotype was associated with increased risk of diagnosis of uc before age 40 years and with extensive uc (or [95% ci] = 1.34 [1.11-1.62], p = 0.002 and or [95% ci] = 1.32 [1.03-1.69], p = 0.03, respectively).

Conclusions:

Cox-2 a-1195g polymorphism was associated with the risk of uc, especially among never-smokers, suggesting that low activity of cox-2 may predispose to uc. our results suggest that inclusion of smoking status may be essential for the evaluation of the role of genetic predisposition to ibd.