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P073. Fibrosis does not increase with disease duration in ulcerative colitis

J. de Bruyn1,2, S. Meijer3, M. Wildenberg1, G. van den Brink1,2, G. D'Haens2, 1Academic Medical Center, Tytgat Institute for Liver and Intestinal Research, Amsterdam, Netherlands, 2Academic Medical Center, Gastroenterology & Hepatology, Amsterdam, Netherlands, 3Academic Medical Center, Pathology, Amsterdam, Netherlands


Intestinal fibrosis in Crohn's disease is a process stimulated by chronic inflammation leading to an increased presence of myofibroblasts in all layers of the intestinal wall. Ulcerative colitis (UC) is classically considered to be a purely mucosal disease although rarely transmural complications such as strictures and stenosis develop. Fibrogenesis in UC has not been studied systematically yet and may be a neglected phenomenon.

We therefore investigated whether there is a different fibrotic load in acute vs longstanding UC and whether the degree of fibrosis in UC correlates with the severity of inflammation.


Colectomy specimens from all UC patients operated at the AMC between 2007–2012 were reviewed. Specimens from patients with recent onset refractory therapy UC (diagnosis <2 years) and longstanding UC with dysplasia (>10 years) were selected. Patients operated for colon cancer without UC served as controls. On H&E stainings the Geboes histological inflammatory activity score (0–22 points) was determined by an experienced IBD pathologist. Sirius Red stainings and collagen I and III immunohistochemistry stainings were performed for collagen, and α-smooth muscle (αSMA) for detection of myofibroblasts and smooth muscle cells. Staining intensity signals were investigated by image analysis software (Image J, NIH).


We examined 13 colectomy specimens from patients with acute UC, 16 from patients with longstanding UC, and 7 colorectal cancer controls.

Patients with short disease duration had a higher Geboes score of 19 (13–20) points, versus 8.5 (2–16) points in specimens with longer disease duration (p = 0.001). Acute and longstanding UC had a thicker muscularis mucosa (MM) than controls (0.10 vs 0.10 vs 0.05 mm, p = 0.019). Both UC groups had less submucosal αSMA expression (number of αSMA positive vs total number of cells; 29% vs 33% vs 54%, p = 0.009). Between acute and late UC there was no difference in collagen deposition, however between UC together and controls there was more collagen I expression in the mucosa, MM and muscularis externa (50% vs 10%, p = 0.02; 28% vs 10%, p = 0.048; 71% vs 20%, p = 0.003).

In both early and long UC duration, we did not find a correlation between inflammation or collagen deposition or MM thickness. There was a negative correlation between inflammation and αSMA positivity in the submucosa (R = −0.51, p = 0.003) and MM (R = −0.37, p = 0.04).


In our series of colectomy specimens, there is more collagen deposition in UC than in controls. No association between disease duration and increased collagen deposition could be found. Expression of αSMA however is lower in UC and correlates with inflammation. Fibrosis in UC does not appear to increase significantly over time.