Affects 1-3% of people.
Psoriasis is an immunologic disease with contributions from genetic susceptibility and genetic factors. It is not known if the inciting antigens are self or environmental.
Sensitised populations of T cells enter the skin, including dermal CD4+ TH1 cells and CD8+ T cells that accumulate in the epidermis.
T cells homing to the skin secrete cytokines and growth factors that induce keratinocyte hyper-proliferation, resulting in the characteristic lesions.
Psoriatic lesions can be induced in susceptible individuals by local trauma, a process known as the Koebner phenomenon. The trauma may induce a local inflammatory response that promotes lesion development.
Morphology
- Marked epidermal thickening (acoanthosis).
- Regular donward elongation of the rete ridges. This downward growth has been likened to test-tubes in a rack.
- Increased epidermal cell turnover and lack of maturation results in loss of the stratum granulosum with extensive overlying parakeratotic scale.
- There is thinning of the epidermal cell layer overlying the tips of dermal papillae (suprapapillary plates).
- Blood vessels within the papillae are dilated and tortuous. These vessels bleed rapidly when the scale is removed, giving rise to multiple punctate bleeding points (Auspitz sign).
- Neutrophils form small aggregates within both the spongiotic superficial epidermis (pustules of Kogoj) and the parakeratotic stratum corneum (Munro microabscesses).
- Similar changes can be seen in superficial fungal infections, and it is important to exclude this possibility with special stains in new diagnoses of psoriasis.
The most typical lesion is a well-demarcated, pink plaque covered by loosely adherent silver-white scale.
Nail changes occur in 30% and consist of yellow-bown discoloration, with pitting, thicking and onycholysis (crumbling and separation of the nail bed from the underlying bed).
There are a variety of clinical subtypes.
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