Abstract

Psoriasis is a common chronic immunologic condition of the skin and nails that affects approximately 2% of the population and is characterized by red elevated plaques with silvery scale. Various forms exist, of which, chronic plaque psoriasis is most common, occurring in 90% of patients.1 Other less common forms, including guttate, pustular, inverse, and erythrodermic, may appear spontaneously or evolve from plaque psoriasis. Psoriatic arthritis exists in around 20% to 30% of patients suffering from moderate to severe psoriasis.2 In recent years, the importance of T helper 17 cells and associated pathologic enhanced expression of the cytokine interleukin-17A (IL-17A) were discovered to be integral to the pathogenesis of psoriasis and psoriatic arthritis.1 Novel biologic therapies, such as secukinumab and ixekizumab, are monoclonal antibodies that selectively bind to and inhibit IL-17A, whereas brodalumab binds to the IL-17RA receptor. These drugs were found in clinical trials to be highly effective in treating patients with moderate-to-severe plaque psoriasis and psoriatic arthritis.3 Currently, only secukinumab from this class has received Health Canada and US Food and Drug Administration approval for treatment of moderate-to-severe psoriasis, whereas ixekizumab and brodalumab are still under clinical development.∗ Secukinumab has also recently received US Food and Drug Administration approval for treatment of psoriatic arthritis and ankylosing spondylitis but is not currently indicated for the treatment of pustular psoriasis. We report a case of severe chronic plaque psoriasis in a patient who had pustular psoriasis and new onset of psoriatic arthritis after discontinuation of brodalumab therapy.

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