Glucocorticoid Effects on Cellular Cytokine Release

Healthy Clinical Trial

Official title:

Glucocorticoid Effects on Cellular Cytokine Release

Clinical Trial Details — Status: Completed

Administrative data

• NCT number: NCT00001415
• Other study ID #: 940146
• Secondary ID: 94-M-0146
• Status: Completed
• Phase: N/A
• First received: November 3, 1999
• Last updated: March 3, 2008
• Start date: May 1994
• Est. completion date: July 2000

Study information

• Verified date: April 1999
• Source: National Institutes of Health Clinical Center (CC)
• Contact: n/a
• Is FDA regulated: No
• Health authority: United States: Federal Government
• Study type: Observational

Clinical Trial 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.

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.

Recruitment information / eligibility

• Status: Completed
• Enrollment: 130
• Est. completion date: July 2000
• Accepts healthy volunteers: Accepts Healthy Volunteers
• Gender: Both
• Age group: N/A and older

Eligibility

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).

Study Design

N/A

Related Conditions & MeSH terms

• Depression
• Depressive Disorder
• Fatigue Syndrome, Chronic
• Fibromyalgia
• Healthy
• Inflammation
• Myofascial Pain Syndromes

Locations

Country	Name	City	State
United States	National Institute of Mental Health (NIMH)	Bethesda	Maryland

Sponsors (1)

Lead Sponsor	Collaborator
National Institute of Mental Health (NIMH)

Country where clinical trial is conducted

United States, 

References & Publications (2)

DeRijk RH, Petrides J, Deuster P, Gold PW, Sternberg EM. Changes in corticosteroid sensitivity of peripheral blood lymphocytes after strenuous exercise in humans. J Clin Endocrinol Metab. 1996 Jan;81(1):228-35. — View Citation

Sternberg EM, Chrousos GP, Wilder RL, Gold PW. The stress response and the regulation of inflammatory disease. Ann Intern Med. 1992 Nov 15;117(10):854-66. Review. — View Citation