Development of Fibrosis in Acute and Longstanding Ulcerative Colitis

Autor: Gijs R. van den Brink, Sybren L. Meijer, Jessica R. de Bruyn, Willem A. Bemelman, Geert R. D'Haens, Manon E. Wildenberg
Přispěvatelé: Graduate School, Gastroenterology and Hepatology, Pathology, AII - Amsterdam institute for Infection and Immunity, AGEM - Amsterdam Gastroenterology Endocrinology Metabolism, Surgery
Rok vydání: 2015
Předmět:
Zdroj: Journal of Crohn s & colitis, 9(11), 966-972. Elsevier
ISSN: 1876-4479
1873-9946
Popis: 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 α-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 0.05mm, 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.
Databáze: OpenAIRE