TY - JOUR
T1 - Development of Fibrosis in Acute and Longstanding Ulcerative Colitis
AU - de Bruyn, Jessica R.
AU - Meijer, Sybren L.
AU - Wildenberg, Manon E.
AU - Bemelman, Willem A.
AU - van den Brink, Gijs R.
AU - D'Haens, Geert R.
PY - 2015
Y1 - 2015
N2 - Background: 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. Methods: 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 alpha-smooth muscle actin, fibronectin and collagen I and III. Results: 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. Conclusions: 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
AB - Background: 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. Methods: 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 alpha-smooth muscle actin, fibronectin and collagen I and III. Results: 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. Conclusions: 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
U2 - https://doi.org/10.1093/ecco-jcc/jjv133
DO - https://doi.org/10.1093/ecco-jcc/jjv133
M3 - Article
C2 - 26245217
SN - 1873-9946
VL - 9
SP - 966
EP - 972
JO - Journal of Crohn s & colitis
JF - Journal of Crohn s & colitis
IS - 11
ER -