Atherosclerosis progression in psoriatic arthritis patients despite the treatment with tumor necrosis factor-alpha blockers: a two-year prospective observational study.
OBJECTIVE
To evaluate the progression of subclinical atherosclerosis in Psoriatic Arthritis (PsA) patients treated with anti-tumor necrosis factor (TNF)-α agents.


METHODS
Thirty-two PsA patients classified according to the CASPAR criteria and attending the Rheumatology Unit of the University of Padua Medical Center were enrolled in a two-year prospective, observational study. In accordance with the ASAS/EULAR recommendations on the management of these patients, those studied were prescribed biological agents [etanercept (n=21), adalimumab (n=6), infliximab (n=5)]. Plasma lipids, inflammatory biomarkers, including C-reactive protein (CRP), interleukin-6 (IL-6), vessel endothelium growth factor (VEGF), osteoprotegerin (OPG), and TNF-α, as well as Disease Activity Score 28 calculated with CRP (DAS 28-CRP) were evaluated at baseline and after two years of treatment. Bilateral carotid B-mode ultrasound measurements [the mean-intima media thickness (mean-IMT), the mean maximum-IMT (M-Max)] of each carotid artery segment (common, bulb, and internal carotid artery) and the post-occlusion flow-mediated dilation (FMD) of the brachial artery were also assessed at baseline and after two years.


RESULTS
Despite an improvement in the DAS 28-CRP score (P<0.0005) and lower low-density lipoprotein cholesterol (P<0.013) and triglyceride (P<0.036) values, there was a significant progression in both the mean-IMT (P<0.0005) and M-Max (P<0.0005). Moreover, no recovery in FMD (P=ns) was observed after two years of anti TNF-α treatment. Serum TNF-α levels were increased (P=0.003) and OPG values were decreased (P=0.011) at the end of follow- up with respect to baseline values.


CONCLUSIONS
Despite improvement in clinical status, arterial remodelling was observed in the PsA patients who were treated with anti TNF-α agents for two years.
Rheumatology Unit, Department of Medicine DIMED, University of Padova, Via Giustiniani 2, 35128 Padova, Italy. Electronic address: roberta.ramonda@unipd.it.
Roberta
R
Ramonda
Clinica Medica 4, University of Padova, Padova, Italy.
Massimo
M
Puato
Rheumatology Unit, Department of Medicine DIMED, University of Padova, Via Giustiniani 2, 35128 Padova, Italy.
Leonardo
L
Punzi
Medicina I, Ospedale Ca' Foncello, Treviso, Italy.
Marcello
M
Rattazzi
Clinica Medica 4, University of Padova, Padova, Italy.
Marta
M
Zanon
Clinica Medica 4, University of Padova, Padova, Italy.
Giulia
G
Balbi
Rheumatology Unit, Department of Medicine DIMED, University of Padova, Via Giustiniani 2, 35128 Padova, Italy.
Augusta
A
Ortolan
Rheumatology Unit, Department of Medicine DIMED, University of Padova, Via Giustiniani 2, 35128 Padova, Italy.
Paola
P
Frallonardo
Clinica Medica 4, University of Padova, Padova, Italy.
Elisabetta
E
Faggin
Laboratory Medicine, University of Padova, Padova, Italy.
Mario
M
Plebani
Laboratory Medicine, University of Padova, Padova, Italy.
Martina
M
Zaninotto
Rheumatology Unit, Department of Medicine DIMED, University of Padova, Via Giustiniani 2, 35128 Padova, Italy.
Mariagrazia
M
Lorenzin
Medicina I, Ospedale Ca' Foncello, Treviso, Italy.
Paolo
P
Pauletto
Rheumatology Unit, Department of Medicine DIMED, University of Padova, Via Giustiniani 2, 35128 Padova, Italy.
Andrea
A
Doria
D000328:Adult; D018501:Antirheumatic Agents / Q000627:therapeutic use*; D015535:Arthritis, Psoriatic / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D050197:Atherosclerosis / Q000000981:diagnostic imaging / Q000209:etiology / Q000503:physiopathology*; D018450:Disease Progression; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*; D014463:Ultrasonography
D018501:Antirheumatic Agents; D014409:Tumor Necrosis Factor-alpha
Atherosclerosis; Carotid ultrasound; Flow-mediated dilation; Intima media thickness; Psoriatic arthritis; Tumor necrosis factor-α