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Psychosom Med. 2009 Nov;71(9):932-6
Authors: Hiramoto T, Oka T, Yoshihara K, Kubo C
OBJECTIVE: To investigate if pyrogenic cytokines mediated psychological stress-induced hyperthermic response in a patient with psychogenic fever. Despite many case reports on psychogenic fever, the mechanism responsible for how psychological stress increases core body temperature (Tc) in humans is not yet known.
CASE PRESENTATION: A 13-year-old girl with fever (>38 degrees C) of unknown causes was referred to our department because psychogenic fever was suspected. To determine if the fever was actually induced by psychological stress, we conducted a 60-minute stress interview.
Her baseline oral temperature was 36.60 degrees C and it began to increase immediately after commencement of the interview, reaching a maximum of 37.42 degrees C 20 minutes after the end of the interview.
The plasma level of prostaglandin E(2) and the serum interleukin-6 level were increased 90 minutes after the interview.
Serum levels of interleukin-1alpha, interleukin-1beta, and macrophage inflammatory protein-1alpha were all less than their minimum detectable level throughout the observation period.
We also measured the patient’s thermal preference by immersing her hands in warm (40 degrees C) and cold (20 degrees C) water. Her preference changed from cold to warm only during the increasing phase of oral temperature.
CONCLUSIONS: This case report shows that a stress interview actually increased Tc in a patient with psychogenic fever. This study suggests that, although pyrogenic cytokines are not involved, the stress interview-induced increase in Tc was an active hyperthermia under the control of the brain, as is infection-induced fever.
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Norepinephrine – the primary signal for stress – can increase thermogenesis. One mechanism is by increasing the production of seleno-deiodinase enzymes. These cleave iodine from T4 to form T3, the active form of thyroid hormone.
CNS microglial production of pro-inflammatory cytokines under stress may be another important mechanism. However, this may not be reflected in peripheral cytokine measurements. Thus the question to be posed would be: do the brain and periphery constitute two separate compartments for cytokine production? [yes].
Interestingly, the study did, at lease, measure an increase in serum IL-6 level, indicating an increase in immune system signaling activity.