**1. Introduction**

Epidemiological data have provided evidence of an association between psoriasis and adverse cardiovascular outcomes [1]. This association may be determined by assessing their shared pathogenesis involving endothelial dysfunction [2,3]. Vascular cell adhesion molecule 1 (VCAM-1) is an inducible glycoprotein, and E-selectin is a soluble cell adhesion molecule. Both molecules are primarily expressed in the endothelium [4–7]. The serum levels of soluble VCAM-1 appear to be correlated with the degree of atherosclerosis and may be used for diagnosing the early stages of the condition [8]. Endothelial activation, resulting in E-selectin expansion, induces leukocyte rolling along the vascular wall and mediates inflammation in various diseases, including atherosclerosis [9]. A common feature of the

inflammatory process in psoriasis and atherosclerosis is leukocyte migration, to which VCAM-1 and E-selectin significantly contribute. These adhesion molecules, being the indicators of endothelial activation, might be potential biomarkers of inflammatory activity and of the severity of atherosclerosis and cardiovascular disease coexisting with psoriasis [10].

In clinical practice, atherosclerosis and its severity are assessed by determining the 10-year risk of fatal cardiovascular disease, which is estimated using the European Risk Chart: Systematic Coronary Risk Evaluation (SCORE) [11,12]. Methotrexate (MTX) is used to treat psoriasis, and one of its main mechanisms of action is believed to be based on its effect of decreasing E-selectin expression [13,14]. Endothelial function, which is significantly altered in psoriasis patients, may also improve during treatment with tumor necrosis factor alpha (TNF-alpha) inhibitors [15].

This study aimed at determining VCAM-1 and E-selectin levels and evaluating their relationship with psoriasis severity compared to those in healthy controls. We also estimated atherosclerosis severity by evaluating cardiovascular risk in patients with plaque psoriasis who were assigned to receive a systemic treatment. The objective was also to assess the impact of 12-week MTX and adalimumab (ADA) treatments on the VCAM-1 and E-selectin concentrations in psoriasis patients. We believe our research will supplement information concerning cardiovascular and atherosclerosis risks in patients with plaque psoriasis, as well as the effects of MTX and ADA on endothelial activation markers in psoriasis. Understanding the impact of systemic psoriasis treatment on E-selectin and VCAM-1 serum levels will enable the selection of the appropriate therapy for both cardiovascular disease and skin lesions as coexisting conditions.
