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Glucocorticoid Effects on Cellular Cytokine Release

This study has been completed.
Information provided by National Institutes of Health Clinical Center (CC)

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Descriptive Information Fields
Brief Title  Glucocorticoid Effects on Cellular Cytokine Release
Official Title  Glucocorticoid Effects on Cellular Cytokine Release
Brief Summary

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.

Detailed Description

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.

Study Phase
Study Type  Observational
Study Design 
Primary Outcome Measure 
Secondary Outcome Measure 
Condition  Depressive Disorder
Fatigue Syndrome, Chronic
Fibromyalgia
Healthy
Inflammation
Intervention 
MEDLINE PMIDs 8550757,   1416562
Links
Recruitment Information Fields
Recruitment Status  Completed
Enrollment  130
Start Date  May 1994
Completion Date July 2000
Eligibility Criteria 

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).

Gender Both
Ages
Accepts Healthy Volunteers Yes
Contacts ††
Location Countries  United States
Administrative Information Fields
NCT ID  NCT00001415
Organization ID 940146
Secondary IDs †† 94-M-0146
Study Sponsor  National Institute of Mental Health (NIMH)
Collaborators ††
Investigators 
Information Provided By National Institutes of Health Clinical Center (CC)
Verification Date April 1999
First Received Date  November 3, 1999
Last Updated Date March 3, 2008

 †    Required WHO trial registration data element.
††   WHO trial registration data element that is required only if it exists.




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