Psychological stress triggers the release of tumor necrosis factor(TNF)-α, study findings show, potentially explaining the link between emotions and flare-ups of rheumatoid arthritis (RA).
Numerous anecdotal reports have suggested that psychological stress can aggravate disease activity in RA patients, but the physiologic mechanisms are unclear.
In the present study, Sarosh Motivala and co-workers from the University of California in Los Angeles, USA, hypothesized that acute, experimentally induced psychological stress would increase TNFα levels, as measured by lipopolysaccharide-stimulated monocyte production.
They recruited three groups: 21 RA patients taking TNFα antagonists; 10 RA patients not taking TNFα antagonists; and 20 healthy controls matched for age and gender.
Writing in the journal Arthritis & Rheumatism, the authors reveal that the stress task was associated with increased cardiovascular activity and a surge in adrenocorticotropic hormone and cortisol levels.
Acute stress also induced a marked increase in monocyte production of TNFα in RA patients not taking TNFα antagonists. This effect was not seen in patients taking these drugs or in healthy controls, however.
Motivala et al say that their observations cannot be explained by differences in clinical or other variables and conclude that patients taking TNFα antagonists are protected from the effects of psychological stress on TNFα expression. ,P>"Subsequent work examining how psychological stress affects signal transduction of TNFα would help to explain why RA patients may be particularly prone to flares in disease activity following stress," the authors conclude.
"If future studies corroborate this finding, use of TNFα antagonists may be particularly helpful for those RA patients who are vulnerable to the effects of psychological stress."