Abstract
Objective: Pain sensitization may contribute to pain severity in rheumatoid arthritis (RA), impacting disease activity assessment. We examined whether pain processing mechanisms were associated with disease activity among RA patients with active disease. Methods: The study included 139 subjects enrolled in the Central Pain in Rheumatoid Arthritis cohort. Subjects underwent quantitative sensory testing (QST), including assessment of pressure pain thresholds (PPTs) at multiple sites, conditioned pain modulation, and temporal summation. RA disease activity was assessed using the Clinical Disease Activity Index (CDAI) and its components. We examined cross-sectional associations between QST measures and disease activity using linear regression. Results: Low PPTs (high pain sensitization) at all sites were associated with high CDAI scores (P ≤ 0.03) and tender joint counts (P ≤ 0.002). Associations between PPTs and patient global assessments were also seen at most sites. High temporal summation at the forearm (also reflecting high pain sensitization) was significantly associated with high CDAI scores (P = 0.02), patient global assessment scores (P = 0.0006), evaluator global assessment scores (P = 0.01), and tender joint counts (P = 0.02). Conversely, conditioned pain modulation (a measure of descending inhibitory pain pathways) was associated only with tender joint count (P = 0.03). Conclusion: High pain sensitization is associated with elevations in disease activity measures. Longitudinal studies are underway to elucidate the cause–effect relationships between pain sensitization and inflammatory disease activity in RA.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 197-204 |
| Number of pages | 8 |
| Journal | Arthritis Care and Research |
| Volume | 70 |
| Issue number | 2 |
| DOIs | |
| State | Published - Feb 2018 |
Funding
Supported by the NIH/National Institute of Arthritis and Musculoskeletal and Skin Diseases (grants R01-AR-064850, P60-AR-47785, and R01-AR-062506), Harvard Catalyst/The Harvard Clinical and Translational Science Center (NIH UL1-TR-001102), Harvard University and its affiliated academic health care centers, the Rheumatic Diseases Research Core Center (P30-AR-053503), and the Camille Julia Morgan Arthritis Research and Education Fund. Dr. Lee has received grant support from Pfizer and owns stock in Express Scripts. Dr. Bolster has received research support from Amgen and Eli Lilly. Dr. Clauw has received consulting fees from Eli Lilly, Nuvo, Cerephex, Tonix, Abbott, Forest Labs, Johnson & Johnson, Merck, Purdue Pharma, Sam-mumed, Zynerba, Astellas Pharma, Williams & Connolly LLP, and Therevance (less than $10,000 each) and from Pfizer (more than $10,000), and has received research support from Pfizer, Cypress Biosciences, Forest, Merck, Nuvo, and Cerephex. The authors thank the study coordinators at all of the sites, including Cassandra Corrigan, Agnes Zak, and Dee Luo (Brigham and Women's Hospital); Malini Moni and Grazyna Purwin (Johns Hopkins University); Alieysa Patel and Melanie Woods (University of Michigan); Joyce Goggins (Boston University); and Laurie Hope and Kelly Reckley (University of Pittsburgh). The authors also acknowledge all of the referring physician and patient participants.
ASJC Scopus subject areas
- Rheumatology