TNF-α Antagonist and Vascular Inflammation in Patients with Psoriasis Vulgaris: A Randomized Placebo-Controlled Study

Robert Bissonnette, François Harel, James G Krueger, Marie-Claude Guertin, Malorie Chabot-Blanchet, Juana Gonzalez, Catherine Maari, Isabelle Delorme, Charles W Lynde, Jean-Claude Tardif, Robert Bissonnette, François Harel, James G Krueger, Marie-Claude Guertin, Malorie Chabot-Blanchet, Juana Gonzalez, Catherine Maari, Isabelle Delorme, Charles W Lynde, Jean-Claude Tardif

Abstract

Vascular inflammation is increased in patients with psoriasis. This randomized, double-blind, multicenter study evaluated the effects of tumor necrosis factor-α antagonist adalimumab on vascular inflammation in patients with psoriasis. A total of 107 patients were randomized (1:1) to receive adalimumab for 52 weeks or placebo for 16 weeks followed by adalimumab for 52 weeks. Vascular inflammation was assessed with positron emission tomography-computed tomography. There were no differences in the change from baseline in vessel wall target-to-background ratio (TBR) from the ascending aorta (primary endpoint) (adalimumab: TBR = 0.002, 95% confidence interval [CI] = -0.048 to 0.053; placebo: TBR = -0.002, 95% CI = -0.053 to 0.049; P = 0.916) and the carotids (adalimumab: TBR = 0.031, 95% CI = -0.005 to 0.066; placebo: TBR = 0.018, 95% CI = -0.019 to 0.055; P = 0.629) at week 16 between adalimumab and placebo. After 52 weeks of treatment with adalimumab there was no significant change from start of treatment in TBR from the ascending aorta (TBR = -0.006, 95% CI = -0.049 to 0.038; P = 0.796), but there was an increase in TBR in carotids (TBR = 0.027, 95% CI = 0.000 to 0.054; P = 0.046). This study showed no difference over 16 weeks in vascular inflammation in patients treated with a tumor necrosis factor-α antagonist or placebo and a modest increase in vascular inflammation in carotids after 52 weeks of treatment with adalimumab.

Trial registration: ClinicalTrials.gov NCT01722214.

Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.

Source: PubMed

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