Recent advances in the field of genetics, immunology and molecular biology have improved our understanding of underlying disease mechanisms in psoriatic arthritis (PsA) implicating pathways of innate as well as adaptive immunity. Some of the incriminated pathogenic mechanisms such as cytokine actions associated with TH17-driven effector pathways have also been targeted by new therapeutic agents. Thus, pivotal phase III studies have demonstrated effectiveness of IL-12/IL-23 inhibition by ustekinumab leading to its approval for PsA treatment. Trial programs for additional biologics targeting either IL-17A directly such as the anti-cytokine antibodies secukinumab and ixekizumab or its respective receptor such as the anti-IL-17RA antibody brodalumab are ongoing with preliminary encouraging results. Moreover, the armentarium for PsA treatment has also broadend by the recent approval of the TNF-blocking agent certolizumab. In addition, new results from a large phase III trial program of the orally applicable small-molecule apremilast, a phosphodiesterase inhibitor, have demonstrated its safety and effectiveness in PsA and psoriatic skin disease. The achieved progress in PsA reflected by an increased number of available pharmacotherapeutic options is flanked by attempts to further improve treatment results by the adaptation of treat to target strategies. Respective recommendations have been recently published by an international task force of experts and are supported by data available from the TICOPA study in the UK showing that the use of early and intensive treatment in PsA in routine clinical care leads to an improved clinical and radiographic outcome
Disclosure of Interest H. Burkhardt Grant/Research support from: Abbvie, Pfizer, Roche, Consultant for: Abbvie, BMS, Janssen-Cilag, Pfizer, UCB, Conflict with: Abbvie, BMS,Chugai, GSK, Pfizer, MSD, UCB
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