title: Effects of the tumor necrosis factor-α antagonist adalimumab on arterial inflammation assessed by positron emission tomography in patients with psoriasis: results of a randomized controlled trial.
abstract: BACKGROUND
  Psoriasis is a chronic inflammatory disease associated with increased risks of myocardial infarction and stroke. Systemic treatments for moderate to severe psoriasis can reduce skin and joint inflammation; however, their effects on vascular inflammation are unknown.
  
  
  RESULTS
  This randomized, controlled trial included 30 patients with moderate to severe psoriasis and a history, or multiple risk factors, of coronary atherosclerosis. Patients were randomized (2:1) to receive either adalimumab subcutaneously for 4 months or to control nonsystemic treatment (topical therapies or phototherapy). Vascular inflammation was measured in the carotid artery and ascending aorta at baseline and week 15, by (18)F-fluorodeoxyglucose uptake on positron emission tomography. The change in target:
  
  
  BACKGROUND
  =0.004) but not for the control group (-0.10 [95% CI, -0.32 to 0.12]; P=0.35). The difference between study arms for this primary end point did not reach statistical significance (-0.13 [95% CI, -0.01 to 0.14]; P=0.32). The change in target:
  
  
  BACKGROUND
  =0.021) and in carotid arteries (-0.32±0.15, P=0.037) when analyzed separately (secondary end points). Changes in other positron emission tomography indices also improved significantly with adalimumab compared with controls in the ascending aorta and carotids. High-sensitivity C-reactive protein decreased by 51% at week 16 with adalimumab compared with 5% in controls (P=0·002).
  
  
  CONCLUSIONS
  The study did not meet its primary end point because the change in target:background ratio in patients randomized to adalimumab was not different from controls. Although adalimumab may reduce vascular inflammation in patients with moderate to severe psoriasis, this effect is not large enough to be demonstrated in a study with a small sample size.
  
  
  BACKGROUND
  URL: http://www.clinicaltrials.gov. Unique identifier: NCT00940862.
authors.affiliation: Department of Dermatology, Innovaderm Research Inc, Montreal, Quebec, Canada. rbissonnette@innovaderm.ca
authors.forename: Robert
authors.initials: R
authors.lastname: Bissonnette
authors.forename: Jean-Claude
authors.initials: JC
authors.lastname: Tardif
authors.forename: François
authors.initials: F
authors.lastname: Harel
authors.forename: Joséphine
authors.initials: J
authors.lastname: Pressacco
authors.forename: Chantal
authors.initials: C
authors.lastname: Bolduc
authors.forename: Marie-Claude
authors.initials: MC
authors.lastname: Guertin
mesh_terms: D000068879:Adalimumab; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage; D061067:Antibodies, Monoclonal, Humanized / Q000008:administration & dosage*; D050197:Atherosclerosis / Q000150:complications / Q000000981:diagnostic imaging*; D002340:Carotid Artery Diseases / Q000000981:diagnostic imaging* / Q000209:etiology; D005260:Female; D019788:Fluorodeoxyglucose F18; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D049268:Positron-Emission Tomography / Q000379:methods*; D011446:Prospective Studies; D011565:Psoriasis / Q000150:complications / Q000000981:diagnostic imaging / Q000188:drug therapy*; D019275:Radiopharmaceuticals; D016037:Single-Blind Method; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D000893:Anti-Inflammatory Agents; D061067:Antibodies, Monoclonal, Humanized; D019275:Radiopharmaceuticals; D014409:Tumor Necrosis Factor-alpha; D019788:Fluorodeoxyglucose F18; D000068879:Adalimumab