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INTRODUCTION

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  • Psoriasis is a chronic T-lymphocyte–mediated systemic inflammatory disease characterized by recurrent exacerbations and remissions of thickened, erythematous, and scaling plaques and multiple comorbidities.

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PATHOPHYSIOLOGY

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  • Genetic predisposition coupled with an unknown precipitating factor triggers an abnormal immune response mediated via T-lymphocytes, resulting in keratinocyte proliferation and the initial psoriatic skin lesions.

  • Psoriasis susceptibility genes and variants reside on various chromosomes. The psoriasis susceptibility locus 1 (PSORS1) on chromosome 6p is a key gene locus, accounting for up to 50% of disease heritability. The major histocompatibility complex antigen HLA-Cw6 and tumor necrosis factor (TNF)-α are major psoriasis susceptibility genes, along with interleukin (IL)-23 and many other loci. Genes corresponding to these loci are involved in pathogenesis pathways in the immune system. There appears to be a general role for T lymphocytes and a specific role for TH17 lymphocytes in psoriasis pathogenesis and as indicators of psoriasis risk.

  • Interactions between dermal dendritic cells and activated Th-1 and Th-17 cells in concert with numerous growth factors and cytokines (eg, TNF-α, interferon gamma, interleukin-1) cause epidermal hyperplasia and dermal inflammation.

  • Precipitating factors implicated in the development of psoriasis include skin injury, infection, drugs, smoking, alcohol consumption, obesity, and psychogenic stress.

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CLINICAL PRESENTATION

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  • Plaque psoriasis (psoriasis vulgaris) is seen in about 90% of psoriasis patients. Lesions are erythematous, red-violet in color, at least 0.5 cm in diameter, well demarcated, and typically covered with silver flaking scales. They may appear as single lesions at predisposed areas (eg, knees and elbows) or generalized over a wide body surface area (BSA).

  • Pruritus may be severe and require treatment to minimize excoriations from frequent scratching. Lesions may be physically debilitating or socially isolating.

  • Preexisting psoriasis can be exacerbated by drugs (eg, lithium, nonsteroidal antiinflammatory drugs [NSAIDs], antimalarials such as chloroquine, β-adrenergic blockers, fluoxetine, and withdrawal of corticosteroids), times of stress, and seasonal changes.

  • Potential comorbidities resulting from the systemic immune response include psoriatic arthritis, heart disease, diabetes, metabolic syndrome, and other immune-mediated disorders such as Crohn disease and multiple sclerosis.

  • Psoriatic arthritis involves both psoriatic lesions and inflammatory arthritis-like symptoms. Distal interphalangeal joints and adjacent nails are most commonly involved, but knees, elbows, wrists, and ankles may be affected.

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DIAGNOSIS

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  • Diagnosis is based on physical examination findings of characteristic lesions. Skin biopsies are not diagnostic of psoriasis.

  • Classification of psoriasis as mild, moderate, or severe is based on BSA and Psoriasis Area and Severity Index (PASI) measurements. A 2011 European classification system defines severity of plaque psoriasis as either mild or moderate-to-severe.

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TREATMENT

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  • Goals of Treatment: Minimize or eliminate skin lesions, alleviate pruritus, reduce frequency of flare-ups, treat comorbid conditions, screen for and manage lifestyle factors that may trigger exacerbations, avoid adverse treatment effects, provide cost-effective treatment, provide appropriate counseling (eg, stress reduction), and maintain or improve quality of life.

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