Vascular Endothelial Growth Factor and Cyclooxygenase-2 are Overexpressed in Ileal Pouch-Anal Anastomosis

Abstract

Cyclooxygenase-2 and vascular endothelial growth factor are overexpressed in the ileal pouch mucosa. This is associated with increased proliferative activity and neoangiogenesis. Cyclooxygenase-2 and vascular endothelial growth factor overexpression might play a role in the pathogenesis of pouchitis.

Risk of cancer in patients with chronic pouchitis after restorative proctocolectomy for ulcerative colitis

“…Moreover, no correlation was found between COX‐2 and either p53 or Ki‐67 in UC‐associated colorectal cancer [29], suggesting that COX‐2 expression may not be related to cell proliferation or to the grade of malignancy. Previously, COX‐2 was reported to be overexpressed in the pouch mucosa of IPAA‐operated patients without pouchitis [30]. In our study, COX‐2 was expressed in patients both with and without pouchitis, and the expression did not correlate with p53 or Ki‐67.…”

“…Ki‐67 is overexpressed in the pouch mucosa [30]. In UC, increased expression of Ki‐67 was observed in both normal and dysplastic colonic mucosa, but in dysplasia Ki‐67 is also located above two thirds of the crypt depth [14].…”

Pouchitis: lessons for inflammatory bowel disease

“…Pro-inflammatory cytokines, such as TNF-a, are released mostly in the inflamed mucosa by macrophages and monocytes, leading to tissue injury, and are considered to be involved in the mechanism of pouchitis [54]. Like in ulcerative colitis, the production of inflammatory mediators is increased, including pro-inflammatory cytokines [67,[73][74][75][76], cell-adhesion molecules [77], platelet-activating factor [78], lipoxygenase products of arachidonic acids [79,80], vascular endothelial growth factor [80], pro-inflammatory neuropeptides, and other mediators [74,[81][82][83]. In general, ulcerative colitis pouches express higher levels of inflammatory cytokines than FAP pouches [84].…”

Prophylactic negative pressure wound therapy in colorectal surgery. Effects on surgical site events: current status and call to action

“…IBD pathogenesis relies on a complex interaction between environmental and autoimmune mechanisms, which still remain largely unknown [67][68][69][70]. As a result, IBD patents have impaired responses to host factors, affecting reaction to environmental agents, and increasing the risk of malignancies through inflammatory pathways, different from those observed in sporadic carcinogenesis [70][71][72].…”

“…As a result, IBD patents have impaired responses to host factors, affecting reaction to environmental agents, and increasing the risk of malignancies through inflammatory pathways, different from those observed in sporadic carcinogenesis [70][71][72]. Approximately 80 % of CD patients undergo surgery during life, often at young age, and more than half may need repeated surgery in the following 20 years [73][74][75].…”