Time to Look Underneath the Surface: Ulcerative Colitis-Associated Fibrosis

Intestinal fibrosis is a common complication of inflammatory bowel diseases [IBD].1,2 Despite awareness of the clinical importance of this complication in Crohn’s disease [CD] very little attention has been devoted to colonic fibrogenesis and stricture formation in ulcerative colitis [UC].3–6 Fibrosis in patients with UC can lead to an increase in wall stiffness and has significant clinical implications, such as colonic motility abnormalities, anorectal dysfunction, rectal urgency, and incontinence.7 Importantly, these clinical presentations can occur in the absence of macroscopic or microscopic inflammation, with an entirely normal mucosa, and it is critical to take a thorough look underneath the mucosal surface. Fibrosis, defined as excessive accumulation of extracellular matrix [ECM] and expansion of the mesenchymal cell pool, has been characterised in UC. The muscularis mucosa [MM] is markedly thickened4 and excessive ECM deposition, mainly in the submucosa, is a significant component of stricturing as well as non-stricturing UC.5,6 In this issue of the Journal of Crohn’s and Colitis,8 De Bruyn and colleagues investigated whether disease duration in UC affects the degree of colonic fibrosis. The study was performed using colectomy specimens from UC subjects refractory to medical treatment with a disease duration < 2 years [n = 13], compared with specimens of longstanding UC with > 10 years’ disease duration and colectomy for diagnosis of dysplasia [n = 16]. At time of colectomy, the longstanding UC subjects had less severe inflammation than the therapy-refractory UC group. The study was controlled with seven subjects without UC.