Abnormal stress responses suspected of worsening RA

Janis Kelly

January 18, 2005

Jan 18, 2005

Regensburg, Germany - Stress that is minor and brief normally enhances immune response, while sustained major stress leads eventually to immune suppression. Some patients with inflammatory rheumatoid diseases may lack the adaptive response that cools things down when stress turns chronic. Dr Rainer H Straub (University Hospital, Regensburg, Germany) and colleagues report in the January 2005 issue of Arthritis & Rheumatism that rheumatoid arthritis (RA) patients have abnormal hormonal and sympathetic nervous system responses, causing a functional loss of sympathetic nerve fibers in inflamed synovial tissue and uncoupling the cortisol and norepinephrine branches of the stress axes [ 1 ].


Patients have underlying defects in stress responses

Straub tells rheuma wire that RA and juvenile idiopathic arthritis (JIA) patients appear to have abnormalities in the stress axes, as a result of which sustained stress may increase inflammatory responses rather than decreasing them, perhaps because the stress axes are not able to generate the normal long-term responses.

Stress axes that are chronically stimulated do not work anymore.

"Stress axes that are chronically stimulated do not work anymore," Straub says.

Straub reviewed several cross-sectional studies on stress and immune responses in RA and JIA. Minor stress was defined as acute minor stress over a few hours ("daily hassles"). Major stress was defined as lasting over days or weeks, such as caring for a handicapped family member.

The reviewers found that:

  • Cortisol has both immunostimulatory and immunosuppressant activity, and effective treatment with glucocorticoids mimics the levels reached during sustained major stress.

  • In chronic inflammation, RA patients had inadequate cortisol secretion, increased sympathetic tone at rest, but inadequate response during stress.

  • Responsiveness of the hypothalamo-pituitary axis (HPA) in RA patients is diminished in relation to ongoing inflammation.

  • In RA and JIA patients, norepinephrine does not have its normal immunosuppressive effects on macrophages, neutrophils, and natural killer (NK) cells and in fact has a proinflammatory effect.

  • RA and JIA patients have increased baseline sympathetic tone and local loss of sympathetic nerve fibers, both of which increase inflammatory responses.

The authors hypothesize that sustained stress may increase inflammation in these patients because their stress axes are unable to generate adequate long-term responses.


Turn down the stress to cool the joints?

If so, this suggests several therapeutic approaches. "First," Straub says, "disease activity must be reduced to normalize responses."

Straub would like to see carefully controlled studies of mild exercise training that does not hurt the joints (eg, swimming, bicycling) to see how the stress axes change under mild exercise.


Source

  1. Straub RH, Dhabhar FS, Bijlsma JWJ et al. How psychological stress via hormones and nerve fibers may exacerbate rheumatoid arthritis. Arthritis Rheum 2005; 52:16-26.


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