A new accepted manuscript reported that patients with rheumatoid arthritis experienced reduced pain sensitivity after 12 weeks of treatment with disease-modifying antirheumatic drugs.
The study included 182 patients with active rheumatoid arthritis (RA) who initiated or switched disease-modifying antirheumatic drug (DMARD) therapy. Pain sensitivity was assessed using quantitative sensory testing, which measured pressure pain thresholds (PPTs), temporal summation (TS), and conditioned pain modulation (CPM) at baseline and 12 weeks.
Statistically significant increases in PPTs were observed at the wrists (mean change, 0.39 kgf), thumbnails (0.51 kgf), and trapezius muscles (0.38 kgf), indicating reduced pain sensitivity. No significant changes were observed in PPTs at the knees or in TS and CPM, which reflect central nervous system pain processing.
During the same period, disease activity—as measured by the 28-joint Disease Activity Score with C-reactive protein (DAS28-CRP)—decreased by a mean of 1.04 points. Patients also showed reductions in tender joint count (mean change, –4.34), swollen joint count (–2.56), CRP level (–2.97 mg/L), and patient global assessment (–1.32 on a 0–10 scale).
In multivariable analyses, each 1-point decrease in DAS28-CRP was associated with a 0.34 to 0.47 kgf increase in PPTs at the wrists, knees, and thumbnails after adjustment for age, sex, body mass index, RA symptom duration, DMARD type, and study site. These findings support an association between reduced inflammation and improvements in peripheral pain sensitivity, according to the authors, led by Burcu Aydemir, PhD, of Northwestern University Feinberg School of Medicine in Chicago, Illinois.
Participants who achieved remission or low disease activity (DAS28-CRP <3.2) demonstrated statistically significant increases in PPTs at all anatomical sites. In contrast, no significant changes in PPTs were observed among those who remained in moderate to high disease activity. TS and CPM values were not associated with disease activity changes in either group.
Among the DAS28-CRP components, reductions in tender joint count were most strongly associated with increases in PPTs across multiple sites. Changes in CRP levels were not significantly associated with changes in PPTs.
These results suggest that DMARD therapy may reduce peripheral pain sensitivity but has limited short-term impact on central pain mechanisms. The absence of changes in TS and CPM may reflect the brief study duration or the persistence of central sensitization in some patients with RA.
The study population had a mean age of 55 years, was predominantly female (84%), and had a mean RA duration of 10 years. Participants were recruited from 4 academic centers and received a range of DMARD types, including conventional synthetic DMARDs, tumor necrosis factor inhibitors, and other biologic or targeted synthetic agents.
The authors concluded that while reductions in inflammation are associated with improvements in certain pain measures, additional strategies may be necessary to address persistent central pain mechanisms in RA.
The authors reported no conflicts of interest in the accepted manuscript.
Source: Arthritis & Rheumatology