**2. The metabolic syndrome**

The metabolic syndrome (MetS) is a cluster of risk factors including obesity, atherogenic dyslipidaemia, hypertension, glucose intolerance and a proinflammatory and prothrombotic state predisposing the patients to cardiovascular diseases (CVD), type 2 diabetes (DM), renal failure and stroke (Gisondi et al, 2007).

Furthermore, it has recently been suggested that the metabolic syndrome might be a risk factor for cancer, in particular colon cancer (Gottlieb A et al, 2007).

The MetS prevalence in Western Europe population ranges from 15% to 35% and it strictly correlates with age, increasing sharply after the age of 60 (Gisondi et al, 2007).

The National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATP III) have proposed the criteria for the metabolic syndrome diagnosis; other organizations, such as The World Health Organization (WHO) and the European Group on Insulin resistance, agree with it in the essential components, differing from it in the details and criteria (Chung CP et al, 2005).

According to NCEP ATPIII the diagnosis of MetS requires at least three of these following criteria:

Metabolic Features in Psoriasis 109

Fig. 1. The molecular mechanisms involved in psoriasis-associated dysregulation of

Among different MetS components, the association between obesity and psoriasis is the best

Several studies have shown that the severity of PsO may be linked to obesity and a population-based study of mild or severe PsO has demonstrated that the risk of obesity was significantly increased in PsO patients compared with healthy controls. Unlike in other inflammatory diseases, such as rheumatoid arthritis, the risk of obesity is strongly

Although it is controversial if psoriasis is the result or the cause of obesity itself , recent data support the obesity is a consequence of psoriasis (Henseler T et al, 1995; Neimann AL et al,

Obesity is considered the main pathogenic factor in the metabolic syndrome and it is characterized by a low and persistent sistemic inflammatory status, whose mainstay is the

Adipose tissue is principally divided into two compartments, subcutaneously and centrally: the central one is characterized by omental adipose tissue and other intra-abdominal fat sources such as mesenteric fat. Central adipose tissue, also called visceral fat, is considered more metabolically active than peripheral subcutaneous fat (Kershaw EE et al, 2004; Galic S

metabolic function.

documented.

et al, 2010).

**3. Obesity and psoriasis** 

2006; Herron MD et al. 2005).

adipose tissue (Greenberg et al., 2006).

associated with disease severity (Sterry W et al, 2004).


It is now thought that non-alcoholic fatty liver disease (NAFLD) is a component of metabolic syndrome, that may progress to steatoepatitis (NASH) with complications of fibrosis and cirrhosis (Capeau J, 2008).

Recent study have demonstrated that the prevalence of metabolic syndrome is significantly higher in psoriatic patients compared to controls after the age of 40 years and psoriatic patients have an increased risk for the individual components of MetS (Gisondi et al, 2007).

Moreover, the association between psoriasis and metabolic syndrome is also true for mild severity psoriasis and it is independent from the tendency of psoriatic patients to be obese ( Mallbris L et al, 2006; Neimann AL et al, 2006; Sommer DM et al, 2006).

Although the link between psoriasis and metabolic syndrome is not completely elucidated, the pathophysiology of both these entities shows many shared cytokines contributing to the underlying chronic inflammatory status.

It is known that both innate and adaptive immunity are involved in psoriatic pathogenesis and, in particular, NK cells appear crucial in the inflammatory process initiation, with an increased release of proinflammatory cytokines, such as TNF-alpha and IFN-gamma and the subsequent interaction with TH1 and Th17 cells (Teunissen MBM et al , 2007).

Dysregulation of T-cell antigen presenting cell interactions and overexpression of proinflammatory cytokines lead to the hyperproliferation of keratinocytes and the activation of neutrophils and endothelial cells until the development of the characteristic psoriatic skin lesions (Kimball AB et al, 2008).

The molecular mechanisms involved in psoriasis-associated dysregulation of metabolic functions are believed to be due to an underlying low and persistent inflammatory status with increased levels of proinflammatory factors, such as tumor necrosis factor-alpha and IL-6 (Fig.1).

TNF-alpha is a proinflammatory cytokine produced by many cell lines, such as keratinocites, T cells, NK cells, dendritic cells, neutrophils, mast cells and adipocytes (Ronti T et al, 2006).

It is expressed as a 26-kD cell surface trans-membrane protein that undergoes cleavage to produce a 17-kD soluble, biologically active form of TNF-α (Ronti T et al, 2006).

IL-6, a pleiotropic circulating cytokine, shows multiple effects ranging from inflammation to host defence and tissue injury. It is secreted by many cell types, including immune cells, fibroblasts, endothelial cells, skeletal muscle and adipocytes (Ronti T et al, 2006).

Abdominal obesity, defined as waist circumference ≥ 102 cm in men and ≥ 88 cm in

It is now thought that non-alcoholic fatty liver disease (NAFLD) is a component of metabolic syndrome, that may progress to steatoepatitis (NASH) with complications of

Recent study have demonstrated that the prevalence of metabolic syndrome is significantly higher in psoriatic patients compared to controls after the age of 40 years and psoriatic patients have an increased risk for the individual components of MetS

Moreover, the association between psoriasis and metabolic syndrome is also true for mild severity psoriasis and it is independent from the tendency of psoriatic patients to be obese

Although the link between psoriasis and metabolic syndrome is not completely elucidated, the pathophysiology of both these entities shows many shared cytokines contributing to the

It is known that both innate and adaptive immunity are involved in psoriatic pathogenesis and, in particular, NK cells appear crucial in the inflammatory process initiation, with an increased release of proinflammatory cytokines, such as TNF-alpha and IFN-gamma and the subsequent interaction with TH1 and Th17 cells (Teunissen

Dysregulation of T-cell antigen presenting cell interactions and overexpression of proinflammatory cytokines lead to the hyperproliferation of keratinocytes and the activation of neutrophils and endothelial cells until the development of the characteristic psoriatic skin

The molecular mechanisms involved in psoriasis-associated dysregulation of metabolic functions are believed to be due to an underlying low and persistent inflammatory status with increased levels of proinflammatory factors, such as tumor necrosis factor-alpha and

TNF-alpha is a proinflammatory cytokine produced by many cell lines, such as keratinocites, T cells, NK cells, dendritic cells, neutrophils, mast cells and adipocytes

It is expressed as a 26-kD cell surface trans-membrane protein that undergoes cleavage to

IL-6, a pleiotropic circulating cytokine, shows multiple effects ranging from inflammation to host defence and tissue injury. It is secreted by many cell types, including immune cells,

produce a 17-kD soluble, biologically active form of TNF-α (Ronti T et al, 2006).

fibroblasts, endothelial cells, skeletal muscle and adipocytes (Ronti T et al, 2006).

HDL cholesterol plasma levels less than 40 mg/dl in men and 50 mg/dl in women

 Blood pressure more than 130 mmHg (systolic) and 85 mmHg (diastolic) Fasting plasma glucose levels more than 100 mg/dL [Grundy et al., 2005]

( Mallbris L et al, 2006; Neimann AL et al, 2006; Sommer DM et al, 2006).

women

(Gisondi et al, 2007).

MBM et al , 2007).

IL-6 (Fig.1).

(Ronti T et al, 2006).

lesions (Kimball AB et al, 2008).

Tryglicerides plasma levels ≥ 150 mg/dl

fibrosis and cirrhosis (Capeau J, 2008).

underlying chronic inflammatory status.

Fig. 1. The molecular mechanisms involved in psoriasis-associated dysregulation of metabolic function.
