Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Comment
. 2005 Oct;63(4):363-5.
doi: 10.1111/j.1365-2265.2005.02361.x.

Post-SARS sickness syndrome manifestations and endocrinopathy: how, why, and so what?

George P Chrousos  1 , Gregory Kaltsas
Affiliations
Comment

Post-SARS sickness syndrome manifestations and endocrinopathy: how, why, and so what?

George P Chrousos et al. Clin Endocrinol (Oxf). 2005 Oct.
No abstract available

PubMed Disclaimer

Figures

Figure 1
Figure 1
(a) Activation of the immune and inflammatory response of any aetiology leads to peripheral production and/or circulation of proinflammatory agents, which, through endocrine or neural afferent signals, stimulate a central nervous system (CNS) inflammatory cascade, cause manifestations of the sickness syndrome and spur the hypothalamic–pituitary–adrenal (HPA) axis at all levels. Note the involvement of NF‐κB, a major proinflammatory transcription factor in both CNS and peripheral inflammation. On the other hand, the activated HPA axis, through its end‐hormone, cortisol, and its receptor (GR), inhibits CNS and peripheral inflammation, as well as its own activity. (b) The presence of increased proinflammatory cytokines and other agents in the vicinity of peripheral somatic and autonomic afferent nerves decreases the pain and fatigue threshold of an individual and hence produces hyperalgesia and fatigue. This is further accentuated by post‐stress hypocortisolism and diminished by cortisol elevations or administration. iCRH, immune corticotropin‐releasing hormone; Sms, somatostatin; TLR, Toll‐like receptor.
See this image and copyright information in PMC

Comment on

References

    1. Leow, M.K.‐S. , Kwek, D.S.‐K. , Ng, A.W.‐K. , Ong, K.‐C. , Kaw, G.J.‐L. & Lee, L.S.‐U. (2005) Hypocortisolism in survivors of severe acute respiratory syndrome (SARS). Clinical Endocrinology, 63, 197–202. - PMC - PubMed
    1. Chrousos, G.P. & Harris, A.G. (1998) Hypothalamic–pituitary–adrenal axis suppression and inhaled corticosteroid therapy. Part I. General principles. Neuroimmunodulation, 5, 277–287. - PubMed
    1. Demitrack, M. , Dale, J. , Straus, S. , Laue, L. , Listwak, S. , Kruesi, M. , Chrousos, G.P. & Gold, P.W. (1991) Evidence of impaired activation of the hypothalamic–pituitary–adrenal axis in patients with chronic fatigue syndrome. Journal of Clinical Endocrinology and Metabolism, 73, 1224–1234. - PubMed
    1. Laue, L. , Peck, G. , Gallucci, W.T. , Loriaux, D.L. & Chrousos, G.P. (1991) Adrenal androgen secretion in postadolescent cystic acne: increased adrenocortical function without hypersensitivity to ACTH. Journal of Clinical Endocrinology and Metabolism, 73, 380–384. - PubMed
    1. Chrousos, G.P. & Gold, P.W. (1992) The concepts of stress and stress system disorders: overview of physical and behavioral homeostasis. Journal of the American Medical Association, 267, 1244–1252. - PubMed

MeSH terms