A cross-sectional study of pain sensitivity, disease-activity assessment, mental health, and fibromyalgia status in rheumatoid arthritis

Abstract

IntroductionPain remains the most important problem for people with rheumatoid arthritis (RA). Active inflammatory disease contributes to pain, but pain due to non-inflammatory mechanisms can confound the assessment of disease activity. We hypothesize that augmented pain processing, fibromyalgic features, poorer mental health, and patient-reported 28-joint disease activity score (DAS28) components are associated in RA.MethodsIn total, 50 people with stable, long-standing RA recruited from a rheumatology outpatient clinic were assessed for pain-pressure thresholds (PPTs) at three separate sites (knee, tibia, and sternum), DAS28, fibromyalgia, and mental health status. Multivariable analysis was performed to assess the association between PPT and DAS28 components, DAS28-P (the proportion of DAS28 derived from the patient-reported components of visual analogue score and tender joint count), or fibromyalgia status.ResultsMore-sensitive PPTs at sites over or distant from joints were each associated with greater reported pain, higher patient-reported DAS28 components, and poorer mental health. A high proportion of participants (48%) satisfied classification criteria for fibromyalgia, and fibromyalgia classification or characteristics were each associated with more sensitive PPTs, higher patient-reported DAS28 components, and poorer mental health.ConclusionsWidespread sensitivity to pressure-induced pain, a high prevalence of fibromyalgic features, higher patient-reported DAS28 components, and poorer mental health are all linked in established RA. The increased sensitivity at nonjoint sites (sternum and anterior tibia), as well as over joints, indicates that central mechanisms may contribute to pain sensitivity in RA. The contribution of patient-reported components to high DAS28 should inform decisions on disease-modifying or pain-management approaches in the treatment of RA when inflammation may be well controlled.

The role of ultrasonography in assessing disease activity in patients with rheumatoid arthritis and associated fibromyalgia

“…Recent studies suggest that central mechanisms of pain play an important role in rheumatoid arthritis and patients exhibit features of fibromyalgia [4,5]. In this context US assessment of disease activity in the presence of low pain thresholds should be studied.…”

“…It seems that an even higher percent of patients with RA may present features of FM and increased pain sensitivity without satisfying diagnostic criteria for FM. These patients have higher patient reported components of the disease activity scores [4]. Wolfe et al evaluated the effect of polysymptomatic distress, a composite measure of fibromyalgianess derived from the 2010 classification criteria for FM, on disease activity measurements in patients with RA [5].…”

Interpretation of DAS28 and its components in the assessment of inflammatory and non-inflammatory aspects of rheumatoid arthritis

“…Swollen joint count (SJC) and ESR are markers of inflammation. However, tender joint counts (TJCs) might be increased in people with centrally augmented pain, and the visual analogue scale for global health (VAS-GH) might be high in people fulfilling fibromyalgia (FM) classification [6,7]. Persistent non-inflammatory pain can result in patients in remission being misclassified as having active inflammatory disease, leading to inappropriate clinical decisions to escalate therapy.…”

Editorial: Synovitis and Pain Sensitization

“…Indeed, augmented central pain processing is associated with more severe pain, and normalization of central pain processing accompanies pain relief after arthroplasty (5,6). However, in inflammatory arthritis models central sensitization develops alongside synovitis (7), and widespread reduced pressure pain thresholds are associated with inflammatory disease activity in rheumatoid arthritis (RA) (8,9). Central sensitization might therefore be mediated by inflammation, rather than its accompanying pain, and widespread augmentation of central pain processing might be driven by circulating factors such as cytokines (10) rather than directly by nociceptive drive.…”