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Joint tenderness and ultrasound inflammation in DMARD-naïve patients with early rheumatoid arthritis
  1. Nina Paulshus Sundlisater1,
  2. Anna-Birgitte Aga1,
  3. Inge Christoffer Olsen2,
  4. Hilde Berner Hammer1,3,
  5. Till Uhlig1,3,
  6. Désirée van der Heijde1,4,
  7. Tore K Kvien1,3,
  8. Espen A Haavardsholm1,3,
  9. Siri Lillegraven1
  1. 1 Division of Rheumatology and Research, Diakonhjemmet Hospital, Oslo, Norway
  2. 2 Clinical Trial Unit, Oslo University Hospital, Oslo, Norway
  3. 3 Faculty of Medicine, University of Oslo, Oslo, Norway
  4. 4 Rheumatology, Leiden University Medical Center, Leiden, Zuid-Holland, The Netherlands
  1. Correspondence to Dr Nina Paulshus Sundlisater, Division of Rheumatology and Research, Diakonhjemmet Hospital, Oslo, Norway; ninasundlisater{at}gmail.com

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Tender joint count is part of most composite disease activity scores and treatment targets in rheumatoid arthritis (RA).1 Joint tenderness could represent not only synovial inflammation in the absence of clinical swelling but also factors such as erosive damage and pain sensitisation.2 Ultrasound examination can add information to the clinical evaluation of inflammation.

Joint tenderness did not reflect inflammatory activity when assessed by ultrasound in patients with established RA3 but might be more related to inflammation in early arthritis.4 5 We aimed to explore joint tenderness in DMARD-naïve patients with early RA and assess whether this finding was associated with ultrasound inflammation in the absence of swelling.

The analyses were performed using baseline data from the ARCTIC trial,6 which included assessment of joint tenderness by Ritchie Articular Index and a 44-swollen joint count. The Ritchie Articular Index grades joint tenderness 0–3, with certain joints being treated as a single unit, for example, the metacarpal-phalangeal (MCP) joints. In the ultrasound examination, 32 joints were all dorsally scored semiquantitatively 0–3 for power Doppler (PD), with an ultrasound atlas for reference.6 The wrists were predefined as the joint area of interest since they are commonly involved in RA and were assessed both clinically and by ultrasound. Additionally, in these joints, scoring of tenderness by Ritchie Articular Index could correspond to the more commonly used tender joint count. The presence of ultrasound inflammation was defined as …

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Footnotes

  • Handling editor Josef S Smolen

  • Contributors All authors were involved in drafting the letter or revising it critically for important intellectual content and approved the final manuscript to be submitted and agreed to be accountable for all aspects of the work. Conception and design of the ARCTIC study: A-BA, ICO, HBH, TU, DvdH, TKK, SL and EAH. Acquisition of data: A-BA, HBH, TU and EAH. Analysis and interpretation of data: NPS, A-BA, ICO, HBH, TU, DvdH, TK, SL and EAH. EAH and SL are shared last authors.

  • Funding The ARCTIC study has received grants from the Norwegian Research Council, the South-East Health Region in Norway, the Norwegian Rheumatism Association, the Norwegian Women’s public Health Association and unrestricted grant support from AbbVie, Pfizer, MSD, Roche and UCB. The funders of the study had no role in study design, data collection, data analysis, data interpretation or writing of the report. The corresponding author had full access to all the data in the study and had final responsibility for the decision to submit for publication.

  • Competing interests Dr NPS reports grants from The South-Eastern Norway Regional Health Authority, during the conduct of the study; Dr Aga reports personal fees from Abbvie, personal fees from Eli Lilly, personal fees from Novartis, personal fees from Pfizer, outside the submitted work; Dr ICO has nothing to disclose; Dr NBH reports personal fees from AbbVie, personal fees from Novartis, personal fees from Lilly, outside the submitted work; Dr TU reports personal fees from Lilly, personal fees from Novartis, outside the submitted work; Dr DvdHv reports personal fees from AbbVie, Amgen, Astellas, AstraZeneca, Bayer, BMS, Boehringer Ingelheim, Celgene, Cyxone, Daiichi, Eisai, Galapagos, Gilead, Glaxo-Smith-Kline, Janssen, Lilly, Merck, Novartis, Pfizer, Regeneron, Roche, Sanofi, Takeda, UCB Pharma, outside the submitted work; and Director Imaging Rheumatology BV; Dr TKK reports personal fees from Amgen, personal fees from Celltrion, personal fees from Egis, personal fees from Evapharma, personal fees from Ewopharma, personal fees from Hikma, personal fees from Oktal, personal fees from Sandoz, personal fees from Sanofi, personal fees from Abbvie, personal fees from BMS, personal fees from MSD, personal fees from Pfizer, grants from UCB, personal fees from Biogen, personal fees from Eli Lilly, personal fees from Gilead, personal fees from Mylan, personal fees from Novartis, outside the submitted work; Dr EAH reports grants from The Research Council of Norway, grants from The South-Eastern Norway Regional Health Authority, during the conduct of the study; personal fees from Pfizer, from AbbVie, personal fees from Celgene, personal fees from Novartis, personal fees from Janssen, personal fees from Gilead, personal fees from Eli-Lilly, personal fees from UCB, outside the submitted work; Dr SL reports grants from The South-Eastern Norway Regional Health Authority, grants from The Research Council of Norway, grants from Norwegian Women’s Public Health Association, grants from Norwegian Rheumatism Association, grants from AbbVie, grants from UCB Pharma, grants from Pfizer Inc, grants from MSD Norway, grants from Roche Norway, during the conduct of the study.

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

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