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Psoriasis In-Depth

Introduction

Psoriasis is a common chronic, inflammatory, immune-mediated disorder characterized by epidermal hyperproliferation, abnormal keratinocyte differentiation, and complex immunologic and vascular pathologies.¹ It has a strong genetic component and varies in occurrence with geography and race/ethnicity.^1,2 Psoriasis affects approximately 3% of Americans³ and up to 3% of people worldwide.⁴ Psoriasis has traditionally been considered a dermatologic disorder, but recent literature has redefined it as a multisystem disease with a significant immune etiology.^1,5,6

Psoriasis predominantly manifests in the skin and joints.⁵ Dermatologic lesions typically include disfiguring erythematous scaly papules and plaques that can be painful and intensely pruritic.⁵ Moreover, clinical manifestations of psoriasis can have a significant emotional, social and physical impact on patient quality of life.^5,7 Psoriasis is associated with numerous comorbidities,⁶ and data suggest that the longevity of patients with severe forms of psoriasis may be decreased by approximately 4 years.⁸ Both topical and systemic anti-psoriatic therapies are used to manage symptoms of psoriasis, but patient treatment needs are often unmet. In one study, 40% of patients were frustrated with the ineffectiveness of their current therapies and close to one-third felt that treatment was not aggressive enough.⁷ Few patients experience a durable spontaneous remission from symptoms.⁵

The immunologic mechanisms of psoriasis are complex and not well understood. Overactivation of T cells likely leads to their proliferation in the developing psoriatic lesion, where they produce inflammatory signals that cause the trafficking of other immune cells to the affected area.¹ These proinflammatory cytokines include interferon-γ (IFN-γ), interleukin-2 (IL-2) and tumor necrosis factor-α (TNF-α), which likely cause keratinocyte hyperplasia in response to a programmed injury repair response.^1,2 The development of psoriatic skin is supported further by proangiogenic factors.²

Psoriasis can affect most, if not all, cutaneous cell types. Histological micrographs of psoriatic skin reveal hyperproliferation of epidermal keratinocytes and hyperkeratosis, in addition to immunocytes that have trafficked into the perivascular space from twisted blood vessels.² Each of these histological features contribute to the thickening and scaling of the erythematous psoriatic skin.^2,9 The mitotic cycle of basal keratinocytes is so greatly increased that keratinocytes need only 3 to 5 days (compared to 28 to 30 days normally) to move from the basal layer to the cornified layer. This abbreviated maturation time, accompanied by altered differentiation, is apparent in the absence of the granular layer of the epidermis and parakeratosis, which is characterized by nuclei still present in the thickened cornified layer.²

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