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Inflammatory correlates of the Patient Global Assessment of Disease Activity vary in relation to disease duration and autoantibody status in patients with rheumatoid arthritis
  1. Serena Bugatti1,2,
  2. Ludovico De Stefano1,2,
  3. Bernardo D’Onofrio1,2,
  4. Andrea Nicrosini1,2,
  5. Eleonora Mauric1,2,
  6. Michele di Lernia1,2,
  7. Garifallia Sakellariou2,3,
  8. Ennio Giulio Favalli4,5,
  9. Antonio Manzo1,2,
  10. Roberto Caporali4,5,
  11. Carlomaurizio Montecucco1,2
  1. 1 Division of Rheumatology, Fondazione IRCCS Policlinico San Matteo, Pavia, Italy
  2. 2 Department of Internal Medicine and Therapeutics, Università di Pavia, Pavia, Italy
  3. 3 Maugeri Clinical Research Institutes IRCCS Pavia, Pavia, Italy
  4. 4 Department of Rheumatology, Gaetano Pini-CTO, Milano, Italy
  5. 5 Department of Clinical Sciences and Community Health, University of Milan, Milano, Italy
  1. Correspondence to Professor Serena Bugatti, Division of Rheumatology, Fondazione IRCCS Policlinico San Matteo, 27100 Pavia, Italy; serena.bugatti{at}unipv.it

Abstract

Objective To investigate the associations between the Patient Global Assessment (PGA) and measures of disease activity in patients with rheumatoid arthritis (RA) in relation to disease duration and autoantibody status.

Methods 1412 patients from three independent cohorts were studied: a prospective cohort of 810 patients with early RA followed up for 24 months; a cross-sectional cohort of 210 patients with established RA in low disease activity; a cross-sectional cohort of 401 patients with established RA in moderate-to-high disease activity. Correlations of the PGA were analysed by Pearson’s coefficients and multivariable linear regression at baseline and at months 6, 12 and 24 in the overall populations and after stratification for autoantibody subgroup and remission status (Boolean remission, PGA near remission and non-remission).

Results In patients with early RA in non-remission, swollen joints correlated independently with the PGA; the correlation became progressively weaker but persisted at all time points in autoantibody-positive patients (adjusted r=0.30–0.12) but lost significance after month 12 in autoantibody-negative patients. Swollen joints independently correlated with the PGA also in near remission until month 12 (adjusted r=0.18–0.16) in autoantibody-positive patients. No independent correlations of inflammatory variables were instead found in patients with established RA irrespective of disease activity and autoantibody status.

Conclusions In the early phases of RA, particularly in autoantibody-positive patients, inflammatory variables directly correlate with the PGA across different disease activity states. The optimal cut-off values of the PGA capable of identifying absence of disease should be better explored in relation to disease duration and autoantibody status.

  • Early Rheumatoid Arthritis
  • Inflammation
  • Anti-Citrullinated Protein Antibodies
  • Patient Reported Outcome Measures
  • Rheumatoid Factor

Data availability statement

Data are available upon reasonable request. Data relevant to the study are included in the article. Deidentified participant rough data are available from the corresponding author (serena.bugatti@unipv.it) upon reasonable request.

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Data availability statement

Data are available upon reasonable request. Data relevant to the study are included in the article. Deidentified participant rough data are available from the corresponding author (serena.bugatti@unipv.it) upon reasonable request.

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Footnotes

  • Handling editor Josef S Smolen

  • SB and LDS contributed equally.

  • Contributors SB, LDS and CM conceived the work, accept full responsibility for the conduct of the study, had access to the data and controlled the decision to publish. SB and LDS contributed to the analysis and interpretation of data and drafted the manuscript. BD'O, AN, MdL, EM and GS contributed to the acquisition and the analysis of data and revised the manuscript critically. EGF, AM, RC and CM contributed to the interpretation of data and revised the manuscript critically for important intellectual content. All the authors provided final approval of the version to be published.

  • Funding This study was supported by fundings from the IRCCS Policlinico San Matteo Foundation, Pavia, Italy.

  • Competing interests SB reports grant/research support from Pfizer and personal fees from AbbVie, Bristol-Myers Squibb, Eli Lilly, Galapagos, Pfizer and Sanofi. GS reports personal fees from AbbVie, Bristol-Myers Squibb and Galapagos. EGF reports personal fees from AbbVie, Bristol-Myers Squibb, Celltrion, Ely Lilly, Galapagos, Janssen, Novartis, Pfizer, Roche and Sandoz. RC reports personal fees from AbbVie, Accord, Bristol-Myers Squibb, Celltrion, Ely Lilly, Fresenius-Kabi, Galapagos, Janssen, Novartis, Pfizer, Roche and Sandoz. CM reports personal fees from AbbVie, Bristol-Myers Squibb, Eli Lilly, Galapagos, Pfizer, Roche and Sanofi.

  • Patient and public involvement Patients and/or the public were not involved in the design, conduct, reporting or dissemination plans of this research.

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