Hyperresponsiveness of the mucosal barrier in Crohn's disease is not tumor necrosis factor-dependent.

摘要: Background: Crohn's disease (CD) is associated with gut barrier dysfunction. Besides the baseline defect, a subgroup of patients also expresses an intestinal hyperresponsiveness to nonsteroidal anti-inflammatory drugs. We studied whether reducing inflammation and restoring dysfunction anti-tumor necrosis factor (TNF) antibody treatment antagonizes permeability increase by oral drug intake in CD. Methods: Thirty-one healthy control subjects 25 active CD were studied. The 31 controls performed testing for 51Cr-EDTA before (baseline) after indomethacin (50 + 75 mg). Twenty-five carried out indomethacin-mediated test infliximab infusion. repeated either (12/25) or tests (13/25), 1 month this treatment. Intestinal was measurement urinary excretion intake. Results: Increased whole permeation (3.16%; interquartile range [IQR], 2.92-5.72) restored normal values (2.47%; IQR, 1.97-2.78) anti-TNF Indomethacin increased significantly more (before anti-TNF: 6.50%; 4.84-10.38; 5.50%; 3.97-10.09) compared (4.66%; 3.51-5.64). Eleven (44%) had abnormal response anti-TNF, 9 them remained hyperresponsive infusion, despite clinical remission. Conclusions: Although suppresses restores function CD, it does not antagonize indomethacin. These data support notion underlying mucosal subset independent inflammation.