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More than just a skin condition


Psoriasis – more than just a skin condition


Several epidemiological studies have confirmed the association between chronic plaque psoriasis and comorbidities, including immune-mediated, cardio-metabolic and psychological disorders, as discussed during this chapter


Paolo Gisondi Department of Medicine, Section of Dermatology and Venereology, University of Verona, Italy


Psoriasis is an immune-mediated chronic inflammatory disease affecting 2–3% of Caucasians, being less common in Asians and rarely seen in Africans.1


It


can occur at any age, although the majority of cases occur before the age of 40 years and it is quite uncommon in children (0.7% of prevalence).1


Psoriasis


affects genetically predisposed individuals and it is commonly considered as a complex disease. So far, between ten and 20 chromosome regions have been proposed to harbour psoriasis-susceptible genes. One locus consistently identified is the class I region of the major histocompatibility locus antigen cluster, which harbours the human leukocyte antigen Cw6.2


However, its low 2


penetrance — about 10% — indicates that other genetic and environmental factors are also involved. The disease is characterised by a series of linked cellular changes in the skin, including hyperplasia of epidermal keratinocytes, vascular hyperplasia and ectasia, and infiltration of T lymphocytes, neutrophils and other types of leucocyte in the affected skin.3 The current understanding of the molecular pathogenesis of psoriasis assigns central importance to an interaction between acquired and innate


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Figure 1: Classical well delineated red-scaly psoriatic plaque of the trunk and elbows


immunity. At the onset of the disease, plasmocitoid dendritic cells are activated in the epidermis and dermis and produce tumor necrosis factor (TNF)-α and interleukin (IL)-23, which promote the development of T helper (Th)1 and Th17 cells.4


These T cells secrete several


mediators, including interferon-γ, TNF-α, IL-6, IL-22 and IL-17, which are responsible for inflammatory changes and epidermal hyperplasia. Epidermal keratinocytes are the primary target of the immune responses, but strongly contribute to disease chronicity by releasing chemokines and cytokines, which attract and activate inflammatory cells. Plaque psoriasis is by far the most common clinical form of the condition


(90% of patients with psoriasis) and is characterised by well-delineated red and scaly plaques. The extent of involvement is variable, ranging from a few localised plaques at extensor sites to generalised involvement (Figure 1). Rarely, psoriasis may involve the whole body, configuring erythroderma. Flexural (also known as inverse or intertriginous) psoriasis refers to plaque psoriasis at submammary, groin, axillary, genital and natal cleft sites, and is typically less scaly. Seborrhoeic psoriasis is localised on seborrhoeic areas of the face, scalp and trunk. Guttate psoriasis is characterised by an acute eruption of small (<1 cm) papules of psoriasis, which appear generally after a streptococcal infection.


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