**7. Biological drugs**

244 Psoriasis

Recently, some studies have also shown that in psoriasis patients, the increased risk for myocardial infarction varies by age (higher in younger individuals) and disease severity (higher in severe forms) (Gelfand et al., 2006; Kremers et al., 2007; Mallbris et al., 2004). As such, a young patient with severe psoriasis is burdened by a CVD risk comparable with what is seen in the presence of traditional risk factors such as diabetes and hypertension. Moreover, a variety of data indicates that psoriasis and CVD (mostly atherosclerosis) share common pathogenic features: both Th1 mediated, with an up-regulation of Th1 cytokines (TNF-, IFN-) and a systemic expression of adhesion molecules, neoangiogenesis factors, and superantigens, these latter potentially able to activate the T cells (Biedermann et al.,

2004; Ettehadi et al., 2004; Gudjonsson et al., 2004). The table 1 summarizes the

psoriasis and atherogenesis.

**6. Disease evaluation** 

al., 2007b).

et al., 2009).

consequences of the TNF- over-expression in promoting inflammatory conditions such as

Overlapping of genetic susceptibility loci between psoriasis and atherosclerosis is also worth

Lastly, the two conditions also show similar histological aspects, mainly involving T cells, macrophages, mast cells and connective tissue matrix. (Nickoloff et al., 2007a; Nickoloff et

Alongside the similar pathogenesis, other indirect factors might be responsible for psoriasis-CVD association; in fact some authors have found that a number of conventional systemic psoriasis treatments (e.g. methotrexate, acitretin, cyclosporine) might increase the effects of

To assess the severity of psoriasis and PsA (baseline/in response to treatment), a number of tools are now available, of which the Psoriasis Activity and Severity Index (PASI) is the most frequently used (Fredriksson & Pettersson, 1978). The PASI combines assessments of the extent of body surface involvement in four anatomical regions (head, trunk, arms and legs) and the severity of desquamation, erythema and plaque induration (thickness) in each region, yielding an overall score of 0 (no psoriasis) to 72 (severe psoriasis) (Fredriksson & Pettersson, 1978). PASI 75 is defined as a 75% reduction in PASI compared with baseline, instead a PASI score of >10 is defined as moderate to severe disease, necessitating systemic therapy (PUVA, UVB 311, MTX, cyclosporin A or biological drugs) (Pathirana et al., 2009)

An additional tool to assess the psoriasis severity is the physician's global assessment (PGA). The PGA takes into account the involvement of the body surface area, induration, scaling and erythema and grades the patient's psoriasis overall, relative to baseline, as 1

In trials investigating patients with PsA, the American College of Rheumatology Criteria (ACR) are most commonly used. The ACR clinical response criteria are defined as percentage reduction [20% (ACR 20), 50% (ACR50) and 70% (ACR 70)] in tender and swollen joint counts and in 3 of the, remaining, 5 ACR core items (patient and physician global assessments, pain, disability and an acute phase reactant) (Montecucco, 2006; Radtke

(clear), 2 (excellent), 3 (good), 4 (fair), 5 (poor) or 6 (worse) (Pathirana et al., 2009).

mentioning, even though its role has yet to be fully understood (Becker et al., 1998).

specific CVD risk factors (Katz et al., 1994; Strober & Menon, 2005; Taler et al., 1999).

Biological therapies for the treatment of psoriasis are defined by their mode of action and are classified into 3 groups, the inhibitors of TNF- (adalimumab, certolizumab, etanercept, golimumab, and infliximab), the T-cell modulating agents (such as alefacept) and the inhibitors of IL-12 and IL-23 (ustekinumab and briakinumab).
