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Related Experiment Videos

Multiple sclerosis is associated with alterations in hypothalamic-pituitary-adrenal axis function

D Michelson1, L Stone, E Galliven

  • 1Clinical Neuroendocrinology Branch, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892.

The Journal of Clinical Endocrinology and Metabolism
|September 1, 1994
PubMed
Summary
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Multiple sclerosis (MS) patients do not exhibit a hypoactive hypothalamic-pituitary-adrenal (HPA) axis. Studies indicate hypercortisolism in MS, with distinct HPA axis regulation compared to depression.

Area of Science:

  • Neuroendocrinology
  • Immunology
  • Clinical Medicine

Background:

  • A hypoactive hypothalamic-pituitary-adrenal (HPA) axis is linked to inflammatory disease susceptibility in animal models.
  • Early steroid intervention in human optic neuritis reduces subsequent multiple sclerosis (MS) development, suggesting a potential HPA axis role.

Purpose of the Study:

  • To investigate whether patients with established multiple sclerosis (MS) exhibit evidence of a hypoactive HPA axis.
  • To compare the HPA axis response in MS patients to that of matched controls and patients with depression.

Main Methods:

  • Thirteen patients with MS underwent baseline HPA axis assessment and provocative testing with ovine corticotropin-releasing hormone (CRH), arginine vasopressin (AVP), and ACTH.
  • Plasma cortisol and ACTH levels were measured at baseline and after stimulation.

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Main Results:

  • Patients with MS displayed significantly higher baseline plasma cortisol levels compared to controls, indicating hypercortisolism.
  • MS patients showed normal ACTH responses to ovine CRH, unlike blunted responses seen in depression, suggesting different pathophysiology.
  • Blunted ACTH responses to AVP stimulation and normal cortisol responses to ACTH stimulation were observed in MS patients.

Conclusions:

  • The findings do not support a role for hypocortisolism in established MS.
  • The data suggest a mild HPA axis activation in MS, with increased AVP activity, aligning with animal models of chronic inflammatory stress.
  • The hypercortisolism in MS appears to have a different underlying mechanism than that observed in depression.