Psychological coping with daily life stressors induces endocrine respo
nses by the central and autonomic nervous systems (CNS, ANS) as well a
s steroid hormone secretion by the hypothalamus-pituitary-adrenal axis
. The adrenocortical hormones together with the catecholamines maintai
n peripheral homeostasis and regulate cardiovascular, metabolic and im
mune functions during stress reactions. Active coping with intermitten
t stressors is related to sympathetic nervous system (SNS)-adrenomedul
lary arousal and to adrenocortical hormone suppression. This is presum
ed to result in a strong, positive response, emotional stability and e
nhancement of the immune system, so-called 'positive stress reaction'.
During passive, long-term coping, SNS arousal is assumed to be associ
ated with adrenocortical (cortisol) stimulation and immune suppression
, so-called 'negative stress reaction'. The consequences include psych
osomatic disorders and cardiovascular, gastrointestinal and/or immune
diseases. Clinical data on adrenocortical hormone measurements in pati
ents with immune diseases, such as systemic lupus erythematosus (SLE),
rheumatoid arthritis (RA) and ulcerative colitis (UC), indicate, howe
ver, that the levels of cortisol and dehydro-epiandrosterone sulphate
(DHEAS) are reduced or normal, compared to those of other categories o
f patients and healthy subjects. Furthermore, the basal cortisol level
s have also been found to be reduced in children with recurrent psycho
somatic abdominal pain (RAP). These data seem to be in contraposition
to the generally assumed role of the adrenocortical pathway in the evo
lution of stress-induced diseases. Studies to assess whether there is
a relationship between long-term 'negative' stress reactions and the l
ow adrenocortical hormone levels are lacking, but are needed.