Abstract

Psoriatic arthritis (PsA) is a chronic inflammatory arthritis, usually seronegative for rheumatoid factor associated with psoriasis [Taylor et al. 2006; Reece et al. 1999]. Although PsA was first described and classified in the 1970s it is only in more recent times that its serious consequences have been studied and understood more widely, not only among rheumatologists but also in the broader medical community. The clinical phenotype varies widely, which has led to difficulties with classification, diagnosis and therefore predicting prognosis. Initially, PsA was considered a benign disease, one study suggesting only 11% of patients developed erosions over 7 years [Shbeeb et al. 2000]. However, in the same journal it was highlighted that a number of reports suggested a high occurrence of erosions in as many as 46—62% of patients [Veale, 2000]. The incidence of PsA varies from 5.4 to 42% depending on the report. In a Finnish population-based study 46% of patients developed erosions [Kaipiainen-Seppanen, 1996] and in another study 62% of patients worsened and the pattern of disease changed over time [Jones et al. 1994]. Several recent studies, however, suggest PsA is progressive, often disabling and associated with increased mortality [Gladman, 2008]. In a study of early arthritis clinic patients, PsA accounted for 13% of new patients and progressive, erosive damage occurred in almost 50% of patients in the first 2 years [Kane and Pathare, 2005]. In the absence of evidence from randomized clinical trials, methotrexate is generally accepted to be useful for controlling peripheral arthritis, but it has little efficacy in spinal disease [Van Der Horst-Bruinsma et al. 2002]. In a study of early PsA, however, erosive damage appeared to develop even when methotrexate therapy was commenced early [Kane and Pathare, 2005]. This raises the question, should anti-tumour necrosis factor (TNF) agents be introduced early? Remission implies the reversibility of functional impairment, minimal or no progression to joint destruction, and at least a theoretic potential to heal a damaged joint [Emery et al. 2007]. Recent studies suggest remission may now be attainable in rheumatoid arthritis (RA) with the advent of anti-TNF therapy [Breedveld et al. 2004], however RA remission has been defined by different criteria: a Disease Activity Score using 28 joint counts (DAS28) value of 2.6 or lower [Saleem et al. 2006]; imaging — no progression on X-ray/ultrasound/MRI; or American College of Rheumatology (ACR) criteria [Arnett et al. 1988]. Drug-induced remission may be defined as minimal or no clinically detectable disease activity in the presence of continuing drug treatment, which is not stopped or interrupted, but is required to retain the remission state [Goekoop-Ruiterman et al. 2005]. Drug-free remission persists in the absence of medication. In a recent editorial, de Vlam and Lories highlighted that remission may now be a possible goal in PsA [de Vlam and Lories, 2008] and our group have published our latest PsA cohort analysis of remission following TNF therapy [Saber et al. 2010].

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