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Psoriasis is a chronic inflammatory skin condition characterised by clearly defined, red and scaly plaques (thickened skin). It is classified into several subtypes.
Psoriasis affects 2–4% of males and females. It can start at any age including childhood with peaks of onset at 15–25 years and 50–60 years. It tends to persist lifelong, fluctuating in extent and severity. It is particularly common in Caucasians, but may affect people of any race. About one third of patients with psoriasis have family members with psoriasis.
Psoriasis is multifactorial. It is classified as an immune-mediated inflammatory disease (IMID).
Genetic factors are important. An individual’s genetic profile influences their type of psoriasis and its response to treatment.
Genome-wide association studies report that HLA-Cw6 is associated with early onset psoriasis and guttate psoriasis. This major histocompatibility complex is not associated with arthritis, nail dystrophy or late onset psoriasis.
Theories about the causes of psoriasis need to explain why the skin is red, inflamed and thickened. It is clear that immune factors and inflammatory cytokines (messenger proteins) such is IL1β and TNFα are responsible for the clinical features of psoriasis. Current theories are exploring the TH17 pathway and release of the cytokine IL17A.
Psoriasis usually presents with symmetrically distributed, red, scaly plaques with well-defined edges. The scale is typically silvery white, except in skin folds where the plaques often appear shiny and they may have a moist peeling surface. The most common sites are scalp, elbows and knees, but any part of the skin can be involved. The plaques are usually very persistent without treatment.
Itch is mostly mild but may be severe in some patients, leading to scratching and lichenification (thickened leathery skin with increased skin markings). Painful skin cracks or fissures may occur.
When psoriatic plaques clear up, they may leave brown or pale marks that can be expected to fade over several months.