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Glucocorticoid Effects on Cellular Cytokine Release
This study has been completed.
Study NCT00001415   Information provided by National Institutes of Health Clinical Center (CC)
First Received: November 3, 1999   Last Updated: March 3, 2008   History of Changes

November 3, 1999
March 3, 2008
May 1994
 
 
 
Complete list of historical versions of study NCT00001415 on ClinicalTrials.gov Archive Site
 
 
 
Glucocorticoid Effects on Cellular Cytokine Release
Glucocorticoid Effects on Cellular Cytokine Release

A variety of hormones and immune system processes are responsible for how the body responds to illness. This study concentrates on how the hormone cortisol effects the release of immune system factors called cytokines.

Cortisol is a hormone produced in the adrenal glands as a response to stimulation from the pituitary gland. Abnormal levels of cortisol have been seen in several diseases such as depression and multiple sclerosis.

Cytokines are factors produced by certain white blood cells. They act by changing the cells that produce them (autocrine effect), altering other cells close to them (paracrine), and effecting cells throughout the body (endocrine effect). Cytokines are important in controlling inflammation processes.

In this study researchers would like to determine if changes in levels of hormones in the blood are associated with changes in cytokine levels. In addition, researchers would like to learn more about how cytokines respond to hormones in certain diseases.

Many of the biochemical alterations observed in people suffering from major depression are changes in the concentrations and activity of components of the generalized stress response. These include the principal hypothalamic stimulus of pituitary-adrenal activation (corticotropin releasing hormone) and the locus ceruleus/norepinephrine system. The current study attempts to provide a clearer picture of the stability of changes during the acute illness, the treatment phase and the recovery process. We particularly wish to determine whether abnormalities in HPA axis perturbability in the well-state can be demonstrated, and if so how these are related to the acutely-ill state, since this information could provide a quantifiable phenotypic marker for depression.

 
Observational
 
  • Depressive Disorder
  • Fatigue Syndrome, Chronic
  • Fibromyalgia
  • Healthy
  • Inflammation
 
 

*   Includes publications given by the data provider as well as publications identified by National Clinical Trials Identifier (NCT ID) in Medline.
 
Completed
130
July 2000
 

Healthy volunteers.

Depressed patients.

Fibromyalgia patients.

Chronic fatigue patients.

Subjects must not have been treated with steroids for more than two weeks during the previous year.

Subjects must not be on chronic medications.

Subjects must not have known medical problems or any condition which interferes with their immune system's ability to respond to infections (talk with your physician if you are not sure about a particular situation).

Both
 
Yes
Contact information is only displayed when the study is recruiting subjects
United States
 
NCT00001415
 
940146, 94-M-0146
National Institute of Mental Health (NIMH)
 
 
National Institutes of Health Clinical Center (CC)
April 1999

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP