Psoriasis is a chronic immune-mediated inflammatory skin disease affecting more than 2% of the world population (1, 2). The pathogenesis of psoriasis is complex and it has genetic, autoimmune and hormonal background (3). A number of recent studies have revealed an association between psoriasis and systemic disorders leading to the development of concomitant immune-mediated inflammatory diseases (3-5). It has been noted that systemic chronic inflammation associated with increased interaction of inflammatory mediators of various origin, including cytokines, growth factors, platelet-derived factors, adipokines, abnormal lipid profile and the activation of vascular endothelium, may be a common pathophysiological basis for psoriasis and other immune-mediated inflammatory diseases (6, 7). It appears, that the metabolic syndrome and its components, in particular, can constitute a link between cardiovascular diseases and type 2 diabetes mellitus in psoriatic patients (4, 5, 8). Understanding the importance of white adipose tissue as an endocrinologically and immunologically active organ has shed new light on the pathophysiological processes of psoriasis, especially on the possible role of bioactive mediators produced by the adipose tissue cells, namely adipokines (6, 9). Recent data indicate that adipokines are involved in the homeostasis maintenance through regulating bodily functions, such as: glucose and lipid metabolism, blood pressure, tissue sensitivity to insulin as well as immune-mediated and inflammatory processes (6, 9-11). Epidemiological surveys reveal the association of psoriasis with obesity, glucose intolerance/diabetes mellitus, hypertension and cardiovascular diseases.

Chemerin is a recently discovered 18 kDa primarily inactive protein that regulates adipocyte differentiation and stimulates chemotaxis and activation of dendritic cells and macrophages (11, 12). This adipokine has low biological activity and requires further extracellular C-terminal processing (11, 13, 14). More recent studies have shown that chemerin is elevated in tissues and fluids in inflammatory conditions and serum chemerin levels correlate with levels of the proinflammatory cytokines such as: tumor necrosis factor α (TNF-α), interleukin 6 (IL-6) and also with CRP (13, 14). In the dermis of early psoriasis leasions Albanesi et al. reported high expression of chemerin together with increased number of plasmacytoid dendritic cells (pDCs) however in the chronic plaques low chemerin expression and pDCs were found (15, 16). Nakajima et al. described elevated chemerin levels in the serum of psoriatic patients (16). Recently chemerin was reported as an adipokine regulating adipogenesis and adipocyte metabolism (11, 14, 17). In another study serum level of chemerin was highly correlated with several markers of inflammation and components of the metabolic syndrome (12). Chemerin has also been detected on dermal endothelial vessels of systemic lupus erythematosus (SLE) (15, 18). The dual role of this adipokine may be a link between chronic inflammation and obesity related disorders.

PEDF is a multifunctional glycoprotein that belongs to the superfamily of serine protease inhibitors with potent antiangiogenic and neurotrophic properties (19-21). It was first purified from the conditioned medium of human retinal pigment epithelial cells but a recent study showed that PEDF is widely distributed in variety of human tissues, including adipocytes, vascular, inflammatory cells and skin (20, 22). Recently published studies found that serum levels of PEDF are strongly associated with components of metabolic syndrome (19, 20, 22). Chen et al. recently reported that increased serum level of PEDF independently predicted the development of the metabolic syndrome in a 10 year prospective study (23). Serum PEDF correlated with several factors closely related to insulin resistance, BMI, triglycerides, systolic blood pressure. Two other studies describe a significant correlation between serum level of PEDF and obesity in humans indicating adipose tissue as the main source of PEDF (19, 21, 24). Rychli et al. suggested that PEDF can have a protective role in atherosclerosis because of its anti-oxidant, anti-inflammatory and anti-thrombotic properties in the vessel wall (25). Nakajima et al. examined PEDF levels in the serum of patients with psoriasis compered to healthy controls (22). Circulating PEDF levels were significantly higher in psoriatic patients than in control subjects. Their findings might suggest that PEDF could mediate anti-inflammatory actions in psoriasis.

Taking into consideration, that the results of previous studies are often inconclusive, the own study has been undertaken to evaluate the selected adipokines in the psoriatic patients and to investigate the potential role of adipokines in systemic abnormalities as part of the metabolic syndrome. In particular, the present study focuses on:

1. The assessment of the serum levels of selected adipokines – chemerin and PEDF in patients suffering from psoriasis as compared with healthy controls.

2. The assessment of the possible relationship between the disease severity and the serum levels of selected adipokines in patients with psoriasis.

3. The assessment of the possible correlations between the serum levels of selected adipokines and selected laboratory indicators of inflammation, lipid profile and the components of the metabolic syndrome.

The study was carried out on 66 adult male patients diagnosed with the plaque-type psoriasis and treated at the Department of Dermatology, Venereology and Paediatric Dermatology of the Medical University of Lublin. The control group consisted of 40 healthy volunteers whose sex and age matched the study group. The complete medical histories of patients with psoriasis were reviewed, their general health condition was assessed. The used protocol was approved by the Committee on Ethics of the Medical University of Lublin and all the psoriatic patients gave informed consent to participate in the study.

Psoriasis severity was evaluated by the PASI score. The PASI score below 10 defined psoriasis as mild, a score >10 was considered as moderate to severe. The weight and height of all patients and volunteers from the control group were measured.

BMI was calculated as the weight in kilograms divided by square of height in metres and participants were classified as being of normal weight (≥ 18.5 and < 25), overweight (≥ 25 and < 30), or obese (≥ 30).

Venous blood samples were collected from both psoriatic patients and healthy individuals. The laboratory tests included: lipid profile parameters (total cholesterol, high density lipoprotein cholesterol (HDL), low density lipoprotein cholesterol (LDL), triglycerides), CRP concentration and SR. The serum concentrations of chemerin and PEDF were measured by enzyme-linked immunosorbent assay (ELISA) using commercially available kits according to the manufacturer’s instructions (Biovendor Human Chemerin ELISA; Biovendor GmbH Heidelberg, Germany, PEDF ELISA Kit; Wuhan EIAAB Science CO Wuhan, China).

Statistical analyses were performed using Statistica ver. 10.0 PL. Results are presented as mean, standard deviation (SD) or median with interquartile as appropriate. The statistical comparison among groups was calculated by the Mann-Whitney test. The correlation analysis was performed by calculating the Spearman coefficient correlation. A p value < 0.05 was considered as statistically significant.

In our study no statistically significant differences were found between patients and controls (p > 0.05) regarding age, sex. The mean PASI was 21.09 (tab. 1).