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PATIENT STORY

A 33-year-old woman presents with uncontrolled psoriasis for 20 years. In addition to the plaque psoriasis (Figure 158-1), she has inverse psoriasis (Figure 158-2). Topical ultrahigh-potency steroids and topical calcipotriene have not controlled her psoriasis. The options for phototherapy and systemic therapy were discussed. The patient chose to try narrowband UVB treatment in addition to her topical therapy.

FIGURE 158-1

Typical plaque psoriasis on the elbow and arm. (Reproduced with permission from Richard P. Usatine, MD.)

FIGURE 158-2

Inverse psoriasis in the inframammary folds of the patient in Figure 158-1. This is not a Candida infection. (Reproduced with permission from Richard P. Usatine, MD.)

INTRODUCTION

Psoriasis is a chronic inflammatory papulosquamous and immune-mediated skin disorder. It is also associated with joint and cardiovascular comorbidities. Psoriasis can present in many different patterns from the scalp to the feet and cause psychiatric distress and physical disabilities. It is crucial to be able to identify psoriasis in all its myriad presentations so that patients receive the best possible treatments to improve their quality of life and avoid comorbidities.

EPIDEMIOLOGY

Psoriasis affects approximately 1% to 8% of the world population.1 In the United States, 3.7% of non-Hispanic white patients have psoriasis compared to 2.0% of African American patients and 1.6% of Hispanic patients.2 Psoriasis affects men and women equally, but occurs earlier in women. While psoriasis can begin at any age, it has two peak incidences: ages 20–29 and 50–59 among women and ages 30–39 and 60–69 among men.1

ETIOLOGY AND PATHOPHYSIOLOGY

Psoriasis is an immune-mediated disease in which T cells play a pivotal role. Evidence suggests that foreign antigens in the skin first trigger antigen-presenting cells to release cytokines, including interleukin (IL)-23 and IL-1β. These cytokines trigger dermal T cells and helper T cells that release more cytokines, including IL-17 and tumor necrosis factor (TNF)-α, promoting keratinocyte hyperproliferation. This inflammatory immune response attracts more immune cells to the skin, which release further cytokines and chemokines. An escalated positive feedback loop results in psoriatic plaques. Greater understanding of the pathophysiology has led to the development of effective treatments targeted at TNF-α, IL-17, and IL-23.

RISK FACTORS

Table 158-1 lists the factors that trigger and exacerbate psoriasis.

TABLE 158-1Factors that Trigger and Exacerbate Psoriasis

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