Understanding the Pathophysiology of Psoriasis

Understanding the Pathophysiology of Psoriasis Posted By:
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Psoriasis is a chronic, inflammatory, recurrent, immune-mediated disease that affects more than 8 million people in the United States. It can occur at any age, but is common in adults, with a median age of onset of 28 years. The skin lesions of psoriasis appear as sharply demarcated, erythematous patches and plaques, surrounded or covered in silvery scales. It is most commonly distributed on the scalp, elbows, and knees, but can occur anywhere—including the nails. About 30% of patients with psoriatic skin disease are at risk for developing psoriatic arthritis.

The pathogenesis of psoriasis is not completely understood but appears to be influenced by genetic and immune-mediated components. This is supported by the successful treatment of psoriasis with immune-mediating, biologic medications. Triggered by environmental stimuli, there is an immune cellular response where T cells are activated by interleukin (IL)-12 and IL-23 secreted by antigen presenting cells in the skin. Ultimately, a hyperactive inflammatory process ensues with a large production of various cytokines such as tumor necrosis factor and IL-17 that alter epidermal hyperproliferation, differentiation, and angiogenesis—producing the cutaneous findings seen in this disease.

In order to offer your patients with psoriasis the most efficacious treatment for their disease, it is important to understand what is currently known about the pathophysiology. To date, there are more than 10 medications approved by the US Food and Drug Administration for the treatment of psoriatic disease, with each targeting a specific cytokine in the inflammatory cascade.

More about these agents to come in my next post this week.

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Filed under: Dermatology

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