The role of stress in rheumatic diseases

In the present issue of Arthritis Research & Therapy, de Brouwer and colleagues review the literature pertaining to experimental studies targeting acute-phase reactivity in the stress-response systems of patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) [1]. The authors included only studies employing experimental stressors (psychosocial, cognitive, exercise, and sensory/pain induction) to evaluate physiological responses at three levels - the autonomic nervous system (ANS), the hypothalamic-pituitary-adrenal (HPA) axis, and the immune system - in patients with RA and SLE.Sixteen studies were identified [1]. The authors found inconsistent results regarding experimentally induced stress and the ANS and HPA axis baseline levels and reactivity, but found some evidence for alterations in immune functioning in patients compared with controls. They noted that the most consistent finding in response to experimentally induced stress was an increase in the number of natural killer cells, but this may not be surprising because natural killer cell trafficking is very sensitive to stress hormones such as catecholamines. The authors note, however, that many of the studies possessed methodological problems of their own. Most studies were underpowered (that is, small sample sizes) and some failed to control for potential confounders such as medication use, age, sex, psychiatric comorbidity, stress coping/appraisal and abuse history. In patients with rheumatologic illness, the presence of depression and a history of abuse are relatively common and have been associated with alterations in the stress-response and immune systems [2,3].The results from the present review of the effects of stress in RA and SLE suggest that the findings in these disorders are congruent with a broader literature including both animal models and clinical studies of other rheumatic disorders. A number of different types of stress have been shown to induce arthritis in animal mod