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Tumor Necrosis Factor‐ α Antagonism Improves Endothelial Dysfunction in Patients With Crohn's Disease
Author(s) -
Schinzari F,
Armuzzi A,
De Pascalis B,
Mores N,
Tesauro M,
Melina D,
Cardillo C
Publication year - 2008
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1038/sj.clpt.6100229
Subject(s) - medicine , ulcerative colitis , inflammatory bowel disease , tumor necrosis factor alpha , crohn's disease , infliximab , endothelial dysfunction , sodium nitroprusside , inflammation , immunology , cytokine , endothelium , disease , gastroenterology , nitric oxide
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)‐ α 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‐ α 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‐ α neutralization. These findings underscore the role of selective cytokine targeting in improving endothelial function in patients with Crohn's disease. Clinical Pharmacology & Therapeutics (2008) 83 , 70–76; doi: 10.1038/sj.clpt.6100229 ; published online 16 May 2007