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Psoriasis is a complex autoimmune inflammatory disease that occurs in genetically susceptible individuals and presents with the development of inflammatory plaques on the skin (picture 1A-B). Although early concepts of the pathogenesis of psoriasis focused primarily on keratinocyte hyperproliferation, dysregulation of the immune system is now recognized as a critical event in this disease. The evolving knowledge of the role of the immune system in psoriasis has had a significant impact on treatment development. Many new and emerging therapeutic agents target specific immunologic aspects of psoriatic disease. (See"Treatment of psoriasis".) The pathophysiology of psoriasis will be discussed here. The epidemiology, genetics, clinical features, diagnosis, and management of psoriasis are reviewed separately. Involvement of the immune system in psoriasis was first indicated in early studies that identified complex infiltrates of leukocytes involved in both innate and adaptive immunity in psoriatic skin [1,2]. Subsequent studies have supported the concept that interactions between dendritic cells, T cells, keratinocytes, neutrophils, and the cytokines released from immune cells likely contribute to the initiation and perpetuation of the cutaneous inflammation that is characteristic of psoriasis [3]. A basic sequence of the immunologic events that are theorized to occur in psoriasis is described below [3]: * Antigenic stimuli contribute to the activation of plasmacytoid dendritic cells and other innate immune cells in the skin. * Proinflammatory cytokines produced by innate immune cells, including interferon (IFN)-alpha, stimulate the activation of myeloid dendritic cells in the skin. * Myeloid dendritic cells produce cytokines, such as interleukin (IL)-23 and IL-12 that stimulate the attraction, activation, and differentiation of T cells. * Recruited T cells produce cytokines that stimulate keratinocytes to proliferate and produce proinflammatory antimicrobial peptides and cytokines. * Cytokines produced by immune cells and keratinocytes perpetuate the inflammatory process via participation in positive feedback loops http://www.uptodate.com/contents/pathophysiology-of-psoriasis Psoriasis Pathophysiology

• Localized and systemic inflammation
– Increased antigen presentation
– Defects in T regulatory cells
– Upregulation of Th1 and Th17 cells,
APCs, and cytokines
– Associated with increased CRP values and
other markers of inflammation
• Epidermal hyperproliferation
– Clinically appreciated as scaling, cracking
– Associated with elevated uric acid and
oxidative stress
• Angiogenesis
– Clinically appreciated as “Auspitz” sign
– Associated with increased circulating VEGF
Plaque Psoriasis
Bottom right photo by Dr Joel Gelfand, used with permission. Other photos by National Psoriasis Foundation.
Menter A, et al. J Am Acad Dermatol. 2008;58:826-850.
• Most common type
– 80%-90% of psoriasis patients
• Plaques:
– 10 mm to several cm
– Well-defined
– Erythematous
– Irregular, round to oval in shape
– Most often located on the scalp,
trunk, buttocks, and limbs,
(especially elbows and knees)
– Have a dry, thin, silvery white or
micaceous scale
– Tend to be symmetrically
distributed over the body
Psoriasis Risk Factors
• Genetics:
– ~40% of people with psoriasis have a positive family history for the disease
1– At least 9 chromosomal loci are linked to psoriasis
(PSORS1-PSORS9)
PSORS1 accounts for 35%-50% of heritability of psoriasis
Environmental and behavioral triggers:
Smoking
Obesity
Medications (eg, lithium, antimalarials, β-blockers)
Infection (streptococcal infection can trigger guttate psoriasis) Guttate Psoriasis
Photo by National Psoriasis Foundation.
Menter A, et al. J Am Acad Dermatol. 2008;58:826-850.
• Characterized by dew drop–like, 1- to
10-mm salmon-pink papules, usually with
a fine scale
• Common in those younger than 30 years
• Primarily found on...
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