Pollard LC et al. (2006) Fatigue in rheumatoid arthritis reflects pain, not disease activity. Rheumatology 45: 885–889

Fatigue is a common complaint of patients with active rheumatoid arthritis (RA), and it is well-known that treatment with anti-tumor necrosis factor (anti-TNF) agents or disease-modifying antirheumatic drugs (DMARDs) can reduce RA patients' fatigue levels. The results of two studies by Pollard et al. have now shown that the improvements in fatigue that occur with RA therapy depend on improvements in patients' levels of pain and depression, rather than on reductions in disease activity. These results suggest that RA-related fatigue is centrally mediated; the authors speculate that improvements in pain and fatigue reflect interactions between RA therapies and sensory neurons.

The authors performed two cross-sectional studies comprising 238 and 274 patients with RA, respectively. Most patients (81% and 84%) reported clinically relevant fatigue. Regardless of which assessment tools were used to measure fatigue and mental health, the authors found consistent, strong associations between fatigue and pain, and between fatigue and depression.

Fatigue decreased with RA treatment: of the 30 patients who started and maintained anti-TNF therapy over 3 months, and to a lesser extent the 54 who started and continued DMARDs over 6 months, the proportion who reported high fatigue levels fell dramatically (from 87% to 50% with anti-TNF therapy and from 63% to 48% with DMARDs). This effect of RA treatment on fatigue was found to be mainly attributable to improvements in pain; multiple regression analysis indicated that the observed correlation between fatigue levels and disease activity was secondary to the relationship with pain.