Development of Fibrosis in Acute and Longstanding Ulcerative Colitis

Intestinal fibrosis is a process driven by chronic inflammation leading to increased presence of myofibroblasts and collagen deposition. Although strictures are rarely seen in ulcerative colitis [UC], longstanding disease is believed to cause fibrosis resulting in altered bowel function.

The presence of fibrosis was studied in colectomy specimens from patients with recent-onset UC refractory to medical treatment [n = 13] and longstanding UC [n = 16], and colon cancer patients without UC [n = 7] as controls. Severity of inflammation was scored according to the Geboes score on haematoxylin and eosin stainings. Immunohistochemistry was performed to detect α-smooth muscle actin, fibronectin and collagen I and III.

Colectomy specimens from patients with acute UC showed significantly more inflammation than those with longstanding disease [19 vs 9 points, p = 0.01]. Both acute and longstanding UC showed a thicker muscularis mucosa than controls [0.10 vs 0.10 vs 0.05 mm, respectively, p = 0.019]. An increase in collagen I and III deposition in the mucosa was observed in UC compared with controls (40% [30-75] vs 25% [10-25], p = 0.033), but this did not differ significantly among acute and longstanding UC patients.

Collagen deposition is enhanced in UC compared with controls. However, UC collagen deposition does not increase significantly over time and does not seem to aggravate the entire fibrotic process.