Journalartikel

Jahr der Veröffentlichung: 2000

Seiten: 989-98+

Zeitschrift: Rheumatic Disease Clinics of North America

Bandnummer: 26

Heftnummer: 4

ISSN: 0889-857X

eISSN: 1558-3163

DOI Link: https://doi.org/10.1016/S0889-857X(05)70180-0

Verlag: Elsevier

Abstract: 
A large body of data from a number of different laboratories worldwide has demonstrated a general tendency for reduced adrenocortical responsiveness in Chronic Fatigue Syndrome (CFS). It is still not clear if this is secondary to abnormalities leading to decreased activity of corticotropin-releasing hormone (CRH)- or arginine vasopressin (AVP)-producing hypothalamic neurons. primary hypofunction of the CRH neurons has been described on the basis of genetic and environmental influences. Ether pathways could secondarily influence hypothalamic-pituitary-adrenal (PIPA) axis activity, however. For example, serotonergic and noradrenergic input acts to stimulate HPA axis activity Deficient serotonergic activity in CFS has been suggested by some of the studies as reviewed here. In addition, hypofunction of sympathetic nervous system function has been described and could contribute to abnormalities of central components of the HPA axis.

Harvard-Zitierstil: Neeck, G. and Crofford, L. (2000) Neuroendocrine perturbations in fibromyalgia and chronic fatigue syndrome, Rheumatic Disease Clinics of North America, 26(4), pp. 989-98+. https://doi.org/10.1016/S0889-857X(05)70180-0

APA-Zitierstil: Neeck, G., & Crofford, L. (2000). Neuroendocrine perturbations in fibromyalgia and chronic fatigue syndrome. Rheumatic Disease Clinics of North America. 26(4), 989-98+. https://doi.org/10.1016/S0889-857X(05)70180-0