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Review
Distinguishing rheumatoid arthritis from psoriatic arthritis
  1. Joseph F Merola1,
  2. Luis R Espinoza2 and
  3. Roy Fleischmann3
  1. 1 Department of Dermatology, Medicine and Rheumatology, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
  2. 2 Section of Rheumatology, LSU Health Sciences Center at New Orleans, New Orleans, Louisiana, USA
  3. 3 Department of Medicine, University of Texas Southwestern Medical Center, Metroplex Clinical Research Center, Dallas, Texas, USA
  1. Correspondence to Dr Joseph F Merola; jfmerola{at}bwh.harvard.edu

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.

  • psoriatic arthritis
  • rheumatoid arthritis
  • inflammatory disease

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Footnotes

  • Contributors All authors contributed equally to the content of the paper.

  • Funding Technical assistance with editing, figure preparation, and styling of the manuscript for submission was provided by Oxford PharmaGenesis Inc. and was funded by Novartis Pharmaceuticals Corporation.

  • Funding Technical assistance with editing, figure preparation and styling of the manuscript for submission was provided by Oxford PharmaGenesis, Inc., and was funded by Novartis Pharmaceuticals Corporation.

  • Disclaimer The authors were fully responsible for all content and editorial decisions and received no financial support or other form of compensation related to the development of this manuscript.

  • Competing interests JFM is a consultant for Biogen Idec, AbbVie, Eli Lilly, Novartis, Pfizer, Janssen, UCB, Samumed, Science 37, Celgene, Sanofi Regeneron, Merck and GSK; speaker for AbbVie; an investigator for Biogen Idec, Pfizer, Sanofi Regeneron, Incyte and Novartis; licensed outcome measure to AbbVie and Lilly. LRE has no competing interests to disclose. RF has consulted and served as an investigator for AbbVie, Acea, Amgen, Augurex, BMS, Boehringer Ingelheim, Celgene, Genentech, GSK, Janssen, Eli Lilly, EMD Merck Serono, Novartis, Pfizer, Samumed, Roche, Sanofi Genzyme and UCB.

  • Patient consent Not required.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Data sharing statement No additional data are available.

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