Abstract
Biologic drugs have been recently used to treat psoriasis. However, some patients do not respond or lose therapeutic benefit with first-line use of tumor necrosis factor (TNF) antagonists. We report a case of psoriasis vulgaris, that failed to respond to TNF antagonists, infliximab and adalimumab, completely disappeared after treatment with ustekinumab, a therapeutic agent for biologically blocking p40 protein of interleukin (IL) 12 and 23. This report highlights anti-TNF agents only inhibited the TNF-α/inducible nitric oxide synthase (iNOS)-producing dendritic cells (TIP-DCs), but the plasmacytoid-DC-derived psoriatic response was re-initiated. On the other hand, ustekinumab may inhibit both the TIP-DCs and the plasmacytoid-DC-derived inflammatory response.
Highlights
INTRODUCTIONPatients with psoriasis experience a significant reduction in quality of life and psychosocial disability; this emphasizes the need for prompt, effective treatment and long-term disease control [2]
Psoriasis is a common, chronic inflammatory skin disease [1,2]
Long been assumed to be a disorder in T helper type 1 (Th1) cells, recent evidence indicated that psoriasis pathophysiology involves tumor necrosis factor (TNF)-α, inducible nitric oxide synthase-producing dendritic cells (TIP-DCs), and Th17 cells
Summary
Patients with psoriasis experience a significant reduction in quality of life and psychosocial disability; this emphasizes the need for prompt, effective treatment and long-term disease control [2]. Psoriasis has been treated with biologic agents that selectively block specific steps in the inflammatory cascade [2]. Some patients do not respond or lose therapeutic benefit with anti-TNF antagonists [4]. Ustekinumab was recently approved by the National Institute for Health and Clinical Excellence for first-line use or for treatment after failure with an anti-TNF antagonist [4]. We describe a patient with severe psoriasis that was successfully treated with ustekinumab after responding poorly to two TNF antagonists, infliximab and adalimumab
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