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The armoury of biological agents available to treat rheumatoid arthritis (RA) has expanded greatly over the last 15 years, but treatment options for psoriatic arthritis (PsA) have failed to keep pace. Therapy with disease modifying anti-rheumatic drugs (DMARDs), such as methotrexate and leflunomide, remain first-line agents despite a paucity of randomised controlled trial evidence.1 There is a good evidence base for the efficacy of TNFα inhibition (TNFi), both as monotherapy and in combination with methotrexate, from a number of studies.2–5 The use of TNFi has the additional benefit of efficacy in treating spinal symptoms where conventional DMARDs show little efficacy.6 Five TNFi agents are now approved for use in PsA patients in Europe, and all show equivalent efficacy in the treatment of joint disease.1 ,7–9
PsA is the second most common inflammatory arthropathy and represents a considerable disease burden for patients and the healthcare system. Therefore, the relative paucity of alternative agents in the treatment of PsA compared with RA represents a significant challenge. Moreover, PsA is not a benign disease, as evidenced by radiological progression and disability.10 In one study of PsA patients attending an early arthritis clinic, treatment with conventional DMARDs for 2 years achieved good disease control, however as many as 50% of PsA patients developed significant bone erosions in that time.11
Our understanding of the pathogenesis of PsA has significantly advanced in recent years, and this has led to the identification of various targets of the inflammatory process observed in PsA.12 It has been clear for some time that in psoriasis (PsO) and PsA, there is a complex interaction of environmental and genetic factors that must lead to a sustained and persistent inappropriate inflammatory response. The relationship between skin and joint disease has been the focus of a …
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