Pain is an almost inevitable consequence of RA: research into better ways of treating the disease will therefore improve outcomes in terms of pain. The introduction of biologic therapies has revolutionized our treatment: future research should continue to identify new components of the immune response that might be amenable to targeted therapy. This is already happening to some extent: B cells, IL-1, IL-6, IL-10, adhesion molecules and co-stimulatory molecules are all being investigated as potential targets for inhibition. New biologic drugs should maximize efficacy whilst minimizing toxicity, especially infection. Data on the long-term effects of these drugs should continue to be collected, for example using national registries such as the BSR Biologics Database. Cost is currently a limiting factor in use of biologics and novel (cheaper) ways of making such drugs would potentially allow extension of their use. Finally, identifying those patients likely to respond to a particular drug would be of great value in reducing the time and money lost by using expensive therapies that are subsequently found to be ineffective in that individual. Genetic study of response to drugs (pharmacogenomics) will offer the potential to, for example, identify whether one particular individual is more likely to respond to anti-TNF whist another may respond to anti-B cell and a third to anti-IL-10.
Many patients describe flares of RA, with exacerbation of all symptoms including pain, after stressful events such as bereavement or divorce. The relationship between mood, stress and the immune response is another potential area of research. Early work suggests that abnormalities in the hypotha-lamic-pituitary-adrenal axis may provide a link between psychosocial stress and disease activity in RA.
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