**5. NAFLD**

The liver plays a central role in lipid metabolism, importing serum free fatty acids and manufacturing, storing and exporting lipids and lipoproteins (Adams LA et al, 2005).

Metabolic Features in Psoriasis 115

Many evidences suggest a strong link between PsO and abnormalities in fatty acid metabolism: psoriatic patients show dyslipidemia with increased plasma cholesterol, triglycerides (TG), low-density lipoprotein (LDL) cholesterol, very low-density lipoprotein (VLDL) cholesterol, and decreased HDL cholesterol and antioxidant capacity. In particular, a recent study has underlined that the dyslipidemic profile could precede the psoriasis

Studies on lipid profile in psoriatic patients have been conducted since 1994 focusing on the presence of a significant content in total cholesterol and of the cholesterol/protein ratio in low-density lipoproteins (LDL) and in high-density lipoproteins (HDL) of psoriatic children. The compositional changes were associated with alterations of fluidity in LDL and HDL of

In PsO patients, the detection of raised levels of LDL and low levels of HDL cholesterol is associated with coronary artery disease and with accelerated mortality for cardiovascular

In PsO patients a higher occurrence of hypertension compared with controls has been reported. The underlying mechanism of hypertension in psoriasis has been discussed and

The pathogenesis of hypertension in psoriasis seems to be linked to increased production of angiotensinogen by adipose tissue, subsequently converted to angiotensin II through

Angiotensin II not only promotes salt retention by kidney but also it regulates vascular tone, acting a vasoconstrictor and stimulates T-cell proliferation promoting inflammation and the

The association between psoriasis and hypertension may also be attributed to the increased oxidative stress in psoriasis patients. Greater levels of reactive oxygen species can damage

Other studies emphasized the role of endothelin-1 in hypertension development among PsO patients. Endothelin-1 is a protein produced by several different cell types including keratinocytes; it induces blood vessels vasoconstriction increasing blood pressure. In PsO patients endothelin-1 expression appears to be altered in lesional skin and serum and

A proinflammatory and/or prothrombotic state has been associated with MetS and PsO, probably linked to elevated serum levels of PAI-1, fibrinogen and CRP. Elevated CRP levels are induced by IL-6 and they have been shown to be predictive of future CVD in initially

multiple hypothesis have been emerged on this topic (Gottlieb A et al, 2008).

ACE serum levels are increased in psoriasis patients (Gottlieb A et al, 2008).

angiotensin converting enzyme (ACE) (Armstrong AW et al, 2011).

development of atherosclerosis (Armstrong AW et al, 2011).

endothelium-dependent vasodilation (Armstrong AW et al, 2011).

correlated to psoriasis disease severity (Armstrong AW et al, 2011).

**6. Atherogenic dyslipidemia** 

manifestations (Gottlieb A et al, 2008).

psoriatic patients (Offidani AM et al, 1994).

disease (Jones SM et al, 2000).

**7. Hypertension** 

**8. Protrombotic state** 

NAFLD is the acronym for nonalcoholic fatty liver disease and it includes a wide spectrum of liver pathology, from hepatocellular steatosis to nonalcoholic steatohepatitis (NASH) (Browning JD et al, 2004).

The prevalence of NAFLD is 10–25% in the western world and it is a an emergent condition now recognized as the most frequent cause of abnormal liver tests, especially in obese individuals (Papatheodoridis GV et al, 2007).

NAFLD is considered the hepatic manifestation of the metabolic syndrome closely associated to visceral obesity and insulin resistance (Marchesini G et al, 2003; Tsochatzis EA et al, 2009).

Adipocytokines, free fatty acids, mitochondrial dysfunction, bacterial endotoxin and vascular disturbance have all been implicated in the development of hepatic inflammation and fibrosis in patients with NAFLD (Adams LA et al, 2005).

The pathogenesis of NAFLD is currently seen as a two steps process, initially characterized by the accumulation of liver fat followed by the development of necroinflammation and fibrosis (Day CP et al,1998).

Insulin resistance results in both increased adipose tissue lipolysis and increased hepatic lipogenesis leading to lipid accumulation in the hepatocytes, mainly in the form of triglycerides and FFAs (Emmanuel A et al, 2009).

The increased liver deposition of TG and FFAs contributes to lipotoxicity and predisposes hepatocytes to the second step: the mythocondrial disfunction and the oxidative stress (Emmanuel A et al, 2009).

A recent study has emphasized that NAFLD is highly prevalent among psoriasis patients and it seems that patients with NAFLD and psoriasis are at higher risk for severe liver fibrosis than their age, sex and BMI-matched counterparts with NAFLD without psoriasis (Marra M et al, 2007).

Psoriasis, metabolic syndrome and NAFLD might share a common underlying mechanism characterized by a low level inflammatory status characterized by a pro-inflammatory cytokines generalized activation (Marra M et al, 2007).

As in obesity and insulin resistance, TNF-alpha seems to have a pivotal role: both serum and hepatic levels of TNF-alpha are elevated in patients with NAFLD and it is directly correlated considering the markers of liver damage (Marra M et al, 2007).

AST, ALT and mostly AST/ALT ratio are considered important parameters of liver damage and they appear correlated to the severity of the hepatic damage to histological disease severity.[ Pulzi FBU et al, 2011]

It has already demonstrated that psoriatic patients with NAFLD show a higher mean AST/ALT ratio, a parameter proved to be an independent predictor factor of liver fibrosis in NAFLD patients (Angulo P et al, 2007).

AST serum levels increase more than those of ALT with the progression of the hepatic disease; therefore, an higher than 1 AST/ALT ratio may be one element of more advanced disease (Vanni E et al, 2010).

NAFLD is the acronym for nonalcoholic fatty liver disease and it includes a wide spectrum of liver pathology, from hepatocellular steatosis to nonalcoholic steatohepatitis (NASH)

The prevalence of NAFLD is 10–25% in the western world and it is a an emergent condition now recognized as the most frequent cause of abnormal liver tests, especially in obese

NAFLD is considered the hepatic manifestation of the metabolic syndrome closely associated to visceral obesity and insulin resistance (Marchesini G et al, 2003; Tsochatzis EA

Adipocytokines, free fatty acids, mitochondrial dysfunction, bacterial endotoxin and vascular disturbance have all been implicated in the development of hepatic inflammation

The pathogenesis of NAFLD is currently seen as a two steps process, initially characterized by the accumulation of liver fat followed by the development of necroinflammation and

Insulin resistance results in both increased adipose tissue lipolysis and increased hepatic lipogenesis leading to lipid accumulation in the hepatocytes, mainly in the form of

The increased liver deposition of TG and FFAs contributes to lipotoxicity and predisposes hepatocytes to the second step: the mythocondrial disfunction and the oxidative stress

A recent study has emphasized that NAFLD is highly prevalent among psoriasis patients and it seems that patients with NAFLD and psoriasis are at higher risk for severe liver fibrosis than their age, sex and BMI-matched counterparts with NAFLD without psoriasis

Psoriasis, metabolic syndrome and NAFLD might share a common underlying mechanism characterized by a low level inflammatory status characterized by a pro-inflammatory

As in obesity and insulin resistance, TNF-alpha seems to have a pivotal role: both serum and hepatic levels of TNF-alpha are elevated in patients with NAFLD and it is directly

AST, ALT and mostly AST/ALT ratio are considered important parameters of liver damage and they appear correlated to the severity of the hepatic damage to histological disease

It has already demonstrated that psoriatic patients with NAFLD show a higher mean AST/ALT ratio, a parameter proved to be an independent predictor factor of liver fibrosis in

AST serum levels increase more than those of ALT with the progression of the hepatic disease; therefore, an higher than 1 AST/ALT ratio may be one element of more advanced

correlated considering the markers of liver damage (Marra M et al, 2007).

(Browning JD et al, 2004).

fibrosis (Day CP et al,1998).

(Emmanuel A et al, 2009).

(Marra M et al, 2007).

severity.[ Pulzi FBU et al, 2011]

disease (Vanni E et al, 2010).

NAFLD patients (Angulo P et al, 2007).

et al, 2009).

individuals (Papatheodoridis GV et al, 2007).

and fibrosis in patients with NAFLD (Adams LA et al, 2005).

triglycerides and FFAs (Emmanuel A et al, 2009).

cytokines generalized activation (Marra M et al, 2007).
