Distinguishing rheumatoid arthritis from psoriatic arthritis

Abstract

Rheumatoid arthritis (RA) and psoriatic arthritis (PsA) have key differences in clinical presentation, radiographic findings, comorbidities and pathogenesis to distinguish between these common forms of chronic inflammatory arthritis. Joint involvement is typically, but not always, asymmetric in PsA, while it is predominantly symmetric in RA. Bone erosions, without new bone growth, and cervical spine involvement are distinctive of RA, while axial spine involvement, psoriasis and nail dystrophy are distinctive of PsA. Patients with PsA typically have seronegative test findings for rheumatoid factor (RF) and cyclic citrullinated peptide (CCP) antibodies, while approximately 80% of patients with RA have positive findings for RF and CCP antibodies. Although there is overlap in the pathogenesis of PsA and RA, differences are also present that affect the efficacy of treatment. In PsA, levels of interleukin (IL)-1β, IL-6, IL-17, IL-22, IL-23, interferon-γ and tumour necrosis factor-α (TNF-α) are elevated, and in RA, levels of IL-1, IL-6, IL-22, IL-33, TNF-α, chemokine ligand 11 and chemokine C-X-C motif ligand 13 are elevated. Differences in the pathogenesis of RA and PsA translate into some variances in the specificity and efficacy of therapies.

Keywords: inflammatory disease; psoriatic arthritis; rheumatoid arthritis.

Figure1

Pathogenesisof PsA and RA. Reprinted from Coates et al and Perera et al. IFN, interferon; IL, interleukin; MHC, major histocompatibility complex; PsA, psoriatic arthritis; Pso, psoriasis; RA, rheumatoid arthritis; TCR, T cell receptor; TGF-β, transforming growth factor-β; Th, T helper; TNF-α, tumour necrosis factor-α.