1. ¹Division of Terapia Medica, Department of Internal Medicine, Complesso Integrato Columbus, Università Cattolica del Sacro Cuore, Rome, Italy
2. ²Istituto di Farmacologia, Università Cattolica del Sacro Cuore, Rome, Italy
3. ³Department of Internal Medicine, Università di Tor Vergata, Rome, Italy

Correspondence: C Cardillo, (carmine.cardillo@rm.unicatt.it)

Received 31 January 2007; Accepted 9 April 2007; Published online 16 May 2007.

Abstract

This study assessed the presence of endothelial dysfunction in patients with inflammatory bowel diseases (IBDs) and evaluated the possible role of tumor necrosis factor (TNF)- in the pathophysiology of this abnormality. Similar elevations in circulating markers of inflammation (C-reactive protein and interleukin-6) were observed in Crohn's disease and ulcerative colitis compared to controls. Endothelium-dependent vasodilation to acetylcholine was impaired in Crohn's disease, but not in ulcerative colitis. Endothelium-independent vasodilation to sodium nitroprusside, by contrast, was not different among the three groups. The TNF- neutralizing antibody, infliximab, enhanced the responsiveness to acetylcholine, but not to nitroprusside, in Crohn's disease, without modifying vascular responses to both drugs in ulcerative colitis. In conclusion, despite comparable degrees of systemic inflammation in the two IBDs, endothelial dysfunction is a selective feature of Crohn's disease and is beneficially affected by intravascular TNF- neutralization. These findings underscore the role of selective cytokine targeting in improving endothelial function in patients with Crohn's disease.