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Chronic fatigue immune dysfunction syndrome: neuroendocrine alterations

Hasan Basri İzgi, Seher Sofuoğlu, Akif Asdemir.

Abstract
Chronic fatigue immune dysfunction syndrome (CFIDS) is a heterogenous
problem with an ambiguous origin and characterized by a severe
disabling physical and mental fatigue that is exacerbating by minor
strain. There has been a great deal of interest in neuroendocrinology on
this challenging syndrome and neuroendocrinologic data obtained so
far will be reviewed in this paper.
Many studies had been performed to investigate the function of the
hypothalamic-pituitary-adrenal (HPA) axis in CFIDS but the results are
quite conflicting. Overall evidence of those neuroendocrinologic studies
and hormonal treatment will be discussed in this article.
Many of the HPA axis studies indicate a reduced cortisol output and
symptom production are correlated in at least some CFIDS patients.
There is some evidence for heightened negative feedback and
changes in glucocorticoid receptor function for impaired ACTH and
cortisol responses. Furthermore, a mutation in the gene which controls
the production of corticosteroid-binding globulin (CBG) which is
associated with complete loss of function of CBG was identified recently
in CFIDS. However, there is no consensus on a specific dysfunction of
HPA axis in CFIDS. There is also some evidence suggesting alterations
in GH and HPT axis or DHEA function and abnormal serotonergic
activity in CFIDS. Serotonergic responses to stimulation were also found
to be inversely correlated with basal cortisol concentrations, and CFIDS
patients had reduced baseline cortisol and enhanced serotonergic
responses, opposite to depressed patients. In the phase of subacute,
acute or chronic phase of CFIDS many variables may affect endocrine
system such as sleep disturbances, inactivity-deconditioning,
psychiatric comorbidity, medication, ongoing stress due to CFIDS itself
and grade or stage which the patient is in.
To obtain clearer data of etiopathological relevance of endocrine
alterations in CFIDS, it seems to be important to perform future
studies, in the cohort of high-risk subjects and patients recovered
from CFIDS. These kinds of strategies may provide valuable
information to identify whether the neuroendocrine abnormalities in
CFIDS are an epiphenomena or trait markers and to find new facilities
for therapeutical interventions.

Key words: Chronic fatigue immune dysfunction syndrome, neuroendocrine, hypothalamo-pituitary-adrenal axis, adrenal gland, adrenal steroids, serotonin



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