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Disease activity flares and pain flares in an early rheumatoid arthritis inception cohort; characteristics, antecedents and sequelae


McWilliams DF1,2,3, Rahman S1,2,3, James RJE1,4, Ferguson E1,3,4, Kiely PDW5, Young A6, Walsh DA1,2,3,7. BMC Rheumatol. 2019 Nov 18;3:49. doi: 10.1186/s41927-019-0100-9. eCollection 2019.

Author Information

1 Pain Centre Versus Arthritis, University of Nottingham, Clinical Sciences Building, City Hospital, Nottingham, NG5 1PB UK.

2 Division of ROD, University of Nottingham, Clinical Sciences Building, City Hospital, Nottingham, NG5 1PB UK.

3 NIHR Biomedical Research Centre, University of Nottingham, Clinical Sciences Building, City Hospital, Nottingham, NG5 1PB UK.

4 School of Psychology, University of Nottingham, Nottingham, UK.

5 Department of Rheumatology, St George's University Hospitals NHS Foundation Trust, London, UK.

6 University of Hertfordshire, Hatfield, UK.

7 Department of Rheumatology, Sherwood Forest Hospitals NHS Foundation Trust, Sutton-in-Ashfield, UK.



RA flares are common and disabling. They are described in terms of worsening inflammation but pain and inflammation are often discordant. To inform treatment decisions, we investigated whether inflammatory and pain flares are discrete entities.


People from the Early RA Network (ERAN) cohort were assessed annually up to 11 years after presentation (n = 719, 3703 person-years of follow up). Flare events were defined in 2 different ways that were analysed in parallel; DAS28 or Pain Flares. DAS28 Flares satisfied OMERACT flare criteria of increases in DAS28 since the previous assessment (≥1.2 points if active RA or ≥ 0.6 points if inactive RA). A ≥ 4.8-point worsening of SF36-Bodily Pain score defined Pain Flares. The first documented episode of each of DAS28 and Pain Flare in each person was analysed. Subgroups within DAS28 and Pain Flares were determined using Latent Class Analysis. Clinical course was compared between flare subgroups.


DAS28 (45%) and Pain Flares (52%) were each common but usually discordant, with 60% of participants in DAS28 Flare not concurrently in Pain Flare, and 64% of those in Pain Flare not concurrently in DAS28 Flare. Three discrete DAS28 Flare subgroups were identified. One was characterised by increases in tender/swollen joint counts (14.4%), a second by increases in symptoms (13.1%), and a third displayed lower flare severity (72.5%). Two discrete Pain Flare subgroups were identified. One occurred following low disease activity and symptoms (88.6%), and the other occurred on the background of ongoing active disease and pain (11.4%). Despite the observed differences between DAS28 and Pain Flares, each was associated with increased disability which persisted beyond the flare episode.


Flares are both common and heterogeneous in people with RA. Furthermore our findings indicate that for some patients there is a discordance between inflammation and pain in flare events. This discrete flare subgroups might reflect different underlying inflammation and pain mechanisms. Treatments addressing different mechanisms might be required to reduce persistent disability after DAS28 and Pain Flares.