Psoriatic arthritis (PsA) is a chronic inflammatory arthritis that occurs in patients with skin psoriasis (PsO), with both genders affected equally [
1]. The prevalence of PsO varies from 2 to 3% of the general population, and PsA affects 10–30% of patients with PsO [
2]. PsA is a heterogeneous disease with various manifestations, including peripheral arthritis, enthesitis, dactylitis, axial arthritis, and skin and nail psoriasis. More than half of the patients affected by PsA exhibit progressive erosive arthritis, associated with severe functional impairment [
3]. The pathophysiology of PsA remains to be completely elucidated, but the overexpression of tumor necrosis factor-α (TNF-α) is believed to play a key role in the pathogenic mechanisms linking PsA and PsO [
4]. The PsA synovium shows infiltration with T cells, B cells, and macrophages. Clonally expanded CD8+ T cells are frequently observed in PsA. Plasmacytoid dendritic cells are thought to play a key role in PsO, and there is some evidence that these cells are also involved in PsA. The extensive bone lesions in patients with PsA are consistent with the findings of osteoclastic progenitors in the peripheral blood of these patients, as well as upregulation of the receptor activator of nuclear factor kappa b (NF-κB) ligand (RANKL) in the synovial lining layer. Cytokines produced by T-helper 17 (Th17) cells are likely to be important in PsA, given their prominence in PsO and in other forms of spondylarthritis [
5]. Innate immunity also seems to play a role in the pathogenesis of PsA. Current treatment options for patients with PsA include non-steroidal inflammatory drugs, glucocorticoids, disease-modifying antirheumatic drugs (DMARDs), biologic agents [such as the anti-TNF-α drugs adalimumab, etanercept, golimumab, infliximab, and certolizumab pegol (CZP), and the interleukin (IL)-12/23 inhibitor ustekinumab], and the phosphodiesterase-4 inhibitor apremilast. To date, biologic agents have been suggested to have a more favorable side effect profile than synthetic DMARDs. Anti-TNF-α has shown efficacy in improving peripheral arthritis and psoriasis symptoms, as well as other PsA manifestations, such as enthesitis, dactylitis, axial disease, physical function, quality of life, productivity, and work disability, and by inhibiting radiographic progression.
CZP is a novel TNF inhibitor formed by a humanized Fab fragment (50 kDa) fused to a 40-kDa polyethylene glycol (PEG) moiety (a nontoxic and nonimmunogenic polymer). The lack of the Fc region in CZP prevents activities such as complement fixation and antibody-mediated cytotoxicity. The attachment of the 40-kDa PEG moiety to the Fab fragment markedly increases the half-life of CZP to a value comparable with that of a whole antibody product [
6,
7]. CZP has been shown to improve patient-reported outcomes in rheumatoid arthritis (RA), PsA, and PsO [
8]. The efficacy and safety of CZP as a treatment for PsA were investigated in the RAPID-PsA study [
9], which is the first published trial in PsA to include patients with prior exposure to TNF inhibitors. In Europe, CZP was approved in 2009 for the treatment of active PsA in adults with inadequate response to previous DMARD therapy; it has just recently been approved in Italy. The aim of the study reported here was to evaluate the efficacy, safety, and patient-reported outcomes (PROs) of CZP in real life.