RESEARCH - Enhanced reactivity to pain in patients with RA

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Research article

Arthritis Research & Therapy 2009, 11:R61doi:10.1186/ar2684

Published: 4 May 2009

Enhanced reactivity to pain in patients with rheumatoid arthritis

R , Ajay D Wasan , Clifton O Bingham III , Joan Bathon

, A Haythornthwaite , T and Gayle G Page

Abstract (provisional)

Introduction

Maladaptive physiological responses to stress appear to play a role in

chronic inflammatory diseases such as rheumatoid arthritis (RA).

However, relatively little stress research in RA patients has involved

the study of pain, the most commonly reported and most impairing

stressor in RA. In the present study, we compared psychophysical and

physiological responses to standardized noxious stimulation in 19 RA

patients and 21 healthy controls.

Methods

Participants underwent a single psychophysical testing session in

which responses to a variety of painful stimuli were recorded, and

blood samples were taken at multiple time points to evaluate the

reactivity of cortisol, interleukin-6 (IL-6), and tumor necrosis

factor-alpha (TNF-alpha) to the experience of acute pain.

Results

The findings suggest that RA patients display a fairly general

hyperalgesia to mechanical and thermal stimuli across several body

sites. In addition, while serum cortisol levels did not differ at

baseline or following pain testing in patients relative to controls,

the RA patients tended to show elevations in serum IL-6, and

demonstrated enhanced pain-reactivity of serum levels of TNF-alpha

compared to the healthy controls (P< .05).

Conclusions

These findings highlight the importance of pain as a stressor in RA

patients, and add to a small body of literature documenting amplified

responses to pain in RA. Future studies of the pathophysiology of RA

would benefit from the consideration of acute pain levels when

comparing RA patients to other groups, and future trials of analgesic

interventions in RA patients may benefit from evaluating the effects

of such interventions on inflammatory activity.

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http://arthritis-research.com/content/pdf/ar2684.pdf

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