Psoriasis occurring during anti-TNF-α therapy: causal effect or unrelated?

Abstract

The introduction of biologic agents, such as tumor necrosis factor (TNF) inhibitors, has transformed our therapeutic approach to rheumatic diseases in recent years. Anti-TNF-α therapy has shown a significant reduction in disease activity in a variety of inflammatory joint conditions, such as rheumatoid arthritis, ankylosing spondylitis, juvenile idiopathic arthritis and psoriatic arthritis [1–3]. In addition, TNF-α antagonists have been effectively used for the treatment of other inflammatory conditions, such as Crohn’s disease, Adamantiades-Behcet’s syndrome and refractory plaque-type psoriasis [4–6]. At present, there are three TNF-blocking agents that are used in rheumatology: two monoclonal anti-TNF-α antibodies (infliximab and adalimumab) and one soluble TNF-α receptor (etanercept). With the expanded use of these agents in clinical practice, outside the setting of randomized clinical trials, an increasing number of cutaneous adverse reactions have been observed [7,8]. Severe cutaneous reactions, such as urticaria, erythema multiforme, cutaneous lupus erythematosus, necrotizing vasculitis, dermatomyositis and lymphomatoid papulosis-like and bullous skin lesions have been described, either in anecdotal case reports or in larger prospective studies [7–10]. One of the most striking reactions has been the development of psoriatic or psoriasiform eruptions in patients without a previous history of psoriasis following the administration of TNF-α inhibitors [11–19]. This contradicts the documented efficacy of these agents in plaque-type psoriasis by virtue of their role in decreasing the activity of proinflammatory mediators in psoriatic inflammation [101]. Although there is an open debate as to whether the development of these psoriasiform lesions is triggered by anti-TNF-α treatment or whether it is a coincidental manifestation of a previously ‘latent’ psoriasis, the accumulating evidence in the literature suggests that psoriasis can occur with TNF-α inhibition and that its early recognition and treatment can spare the patient from substantial morbidity, without necessarily discontinuing a beneficial treatment for the underlying inflammatory condition.