Stress and Rheumatic Diseases

Stress and Rheumatic Diseases
SHORT FEATURES and FACES ARTICLE

In this editorial Afton Hassett and Daniel Clauw, of University of Michigan Medical School, discuss some aspects of the complex interactions between psychological stress and the onset, expression and progression of rheumatic diseases.

The authors mention that some studies in this research area are limited by the use of cross-sectional designs and the pitfalls associated with self-report retrospective data, but they nevertheless highlight some interesting findings found therein. A relatively large study of Vietnam combat veterans with current post-traumatic stress disorder (n = 2,490) suggested an increased risk for autoimmune diseases compared to veterans without post-traumatic stress disorder.

This is further substantiated by studies proposing that early life stressors increase vulnerability to autoimmune disease, and studies describing relationships between psychological stress and poor outcomes, and disease flares in both rheumatoid arthritis and systemic lupus erythematosus. The authors propone that the mechanisms presumed to underlie these associations include stress-related changes in autonomic, neuroendocrine and/or immune system functioning.

Furthermore, work performed to examine how stress modulates symptoms, especially pain, in nonautoimmune rheumatic conditions such as fibromyalgia may also help elucidate the role of stress in symptom expression.

For example, in fibromyalgia, observable changes in the autonomic nervous system or the hypothalamic–pituitary–adrenal axis tone in some individuals may represent a baseline diathesis or risk factor for the subsequent development of chronic pain; alternatively, such changes may manifest due to pain itself or to the indirect effects of pain such as deconditioning secondary to decreased exercise.

The authors conclude stating that ‘when our patients say that stress worsens their disease, they may be correct’, and that there are ‘clearly both immune mechanisms and nonimmune mechanisms that may be responsible for increased disease activity and/or symptom expression during periods of stress’.

Arthritis Res Ther 2010, 12: 123

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