Abstract
Studies on the inflammatory burden in recent-onset psoriatic arthritis (PsA) patients without conventional cardiovascular risk factors (CVRFs) are not available. This preliminary study focuses on cardiovascular risk in cutaneous psoriasis (CPs) and recent-onset PsA patients. Blood biochemistry (glucose, cholesterol, uric acid, lipid profile and apolipoprotein B) was analyzed using standard kits. Proatherogenic inflammation markers, C-reactive protein (CRP) and interleukin-6 (IL-6), and endothelial activators monocyte chemoattractant protein-1 (MCP-1) and soluble intercellular adhesion molecule-1 (sICAM-1), were determined by enzyme-linked immunosorbent assay. Ultrasound images allowed measuring carotid intima–media thickness (cIMT). Our study first shows an increase in cIMT, and in serum levels of sICAM-1 and CRP in recent-onset PsA patients not presenting conventional CVRFs over the non-medicated time-period, from disease diagnosis to the beginning of pharmacological treatment, compared with healthy subjects. The outcome highlights the importance of monitoring serum level of sICAM1, CRP, and cIMT, and the value of primary prevention in psoriatic patients even with no history of cardiovascular events.
Highlights
Psoriasis (Ps) and psoriatic arthritis (PsA) belong to the family of immune mediated inflammatory diseases (IMID) predominantly affecting skin and joints [1]
Three groups were matched for age and body mass index (BMI): C (9 control healthy patients), cutaneous psoriasis (CPs) (9 lowintermediate CPs patients to account for psoriasis inflammation), and PsA (14 patients with recent PsA onset following lowintermediate CPs)
Our results indicate an enhanced inflammatory burden reflected by carotid wall thickening and higher blood level of soluble intercellular adhesion molecule-1 (sICAM-1) and C-reactive protein (CRP) in PsA patients without conventional risk factors
Summary
Psoriasis (Ps) and psoriatic arthritis (PsA) belong to the family of immune mediated inflammatory diseases (IMID) predominantly affecting skin and joints [1]. Epidemiological studies show a peak incidence of Ps between the second and third decades of life [2] and a global prevalence around 2–3% regardless of sex [3]. Epidemiological studies show that PsA is a high-risk factor for cardiovascular disease (CVD) [7,8,9,10] likely related to chronic inflammation leading to endothelial dysfunction [11] and plaque formation [12]. Accelerated atherosclerosis has been linked to cutaneous psoriasis (CPs) according to its severity, even in the absence of joint symptoms [13]
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