Abstract and Introduction
Psoriasis is a chronic immune-mediated inflammatory disease with epidermal hyperplasia that affects 2–3% of the population. Interleukin (IL)-17 signaling has a central role in its pathogenesis. Brodalumab is a monoclonal antibody that neutralizes IL-17 receptor type A. Brodalumab is highly effective in the reversal of psoriatic phenotype and gene expression patterns.
An immune-mediated disease, psoriasis affects approximately 120 million people or 2% of the population.[1,2] The most common form of the disease, psoriasis vulgaris, accounts for 80% of all cases. Psoriasis is increasingly recognized as more than a skin disease and may be associated with a constellation of comorbidities including psoriatic arthritis, stroke, heart failure, obesity, hypertension, and diabetes. Severe psoriasis is considered an independent risk factor for cardiovascular mortality and psychiatric disorders including depression, anxiety, and suicidal tendency from physical and mental distress. Even patients with limited psoriatic involvement often report a substantial negative impact on their daily quality of life (QoL).
For people with moderate-to-severe plaque psoriasis (17% of all psoriasis patients), topical medications usually provide unsatisfactory results. Advances in the understanding of cytokines in psoriasis have led to the development of more efficacious therapeutic options including biological agents targeting tumor necrosis factor (TNF)-α, interleukin (IL)-23, and IL-17. Current pathogenic models indicate dysfunctional IL-17 signaling may play a pivotal inflammatory role in the pathophysiology of psoriasis.[3,7]
Skin Therapy Letter. 2017;22(1) © 2017 SkinCareGuide.com