Skip to Main Content

INTRODUCTION

  • 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, including psoriatic arthritis.

PATHOPHYSIOLOGY

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

  • 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. 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, IL-1) cause epidermal hyperplasia and dermal inflammation.

CLINICAL PRESENTATION

  • Skin lesions in plaque psoriasis (psoriasis vulgaris) 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 on 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 anti-inflammatory drugs [NSAIDs], antimalarials, β-adrenergic blockers, fluoxetine, and withdrawal of corticosteroids), times of stress, and seasonal changes.

  • Potential comorbidities include psoriatic arthritis, depression, anxiety, hypertension, obesity, diabetes mellitus, Crohn disease, and alcoholism.

  • Psoriatic arthritis develops in about 30% of patients with plaque psoriasis. It most commonly presents as polyarticular peripheral arthritis but can vary widely with peripheral and/or axial, monoarticular, or polyarticular patterns.

DIAGNOSIS

  • 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.

TREATMENT

  • 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.

  • See Figures 17-1 and 17-2 for psoriasis treatment algorithms based on disease severity.

FIGURE 17-1

Treatment algorithm for mild-to-moderate psoriasis.

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.