Hypothalamic–pituitary–adrenal axis perturbations in patients with fibromyalgia

Authors

  • Leslie J. Crofford M.D,

    Corresponding author
    1. National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), NIH, Bethesda, Maryland
    Current affiliation:
    1. Cleveland clinic Foundation, Cleveland, ohio
    • Department of Internal Medicine, Division of Rheumatology, University of Michigan, 200 Zina Pitcher Place, R4570 Kresge I, Ann Arbor, MI 48109-0531
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  • Stanley R. Pillemer Md: Niams, NIH;,

    1. (current address: Cleveland Clinic Foundation, Cleveland, Ohio)
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  • Konstantine T. Kalogeras Md: Niams, NIH,

    1. (current address: Cleveland Clinic Foundation, Cleveland, Ohio)
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  • Joseph M. Cash Md: Niams, NIH,

    1. (current address: Cleveland Clinic Foundation, Cleveland, Ohio)
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  • David Michelson M.D,

    1. National Institute of Mental Health (NIMH), NIH
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  • Mitchel A. Kling Md: Nimh, NIH,

  • Esther M. Sternberg Md: Nimh, NIH,

  • Philip W. Gold Md: Nimh, NIH,

  • George P. Chrousos MD, PhD,

    1. National Institute of Child Health and Human Development, NIH
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  • Ronald L. Wilder Md, Phd: Niams, NIH


Abstract

Objective. To examine basal and stimulated hypothalamic–pituitary–adrenal (HPA) axis and related hormone levels, including adrenocorticotropin (ACTH), cortisol, arginine vasopressin (AVP), and neuropeptide Y (NPY), in patients with fibromyalgia (FM).

Methods. Basal and ovine corticotropin-releasing hormone (oCRH)–stimulated HPA axis function were assessed in 12 patients with FM and in age- and sex-matched normal subjects. Basal plasma AVP levels and AVP release after postural change were assessed, and plasma NPY levels were measured in the same samples.

Results. Patients with FM had low 24-hour urinary free cortisol, but normal peak and elevated trough plasma cortisol levels, compared with normal subjects. The net integrated ACTH response to oCRH in FM was not significantly different from that in normal subjects, but tended toward an exaggerated response. There was a significant decrease in net integrated cortisol response to oCRH in FM patients, indicating adrenal hyporesponsiveness. AVP levels were not significantly different between FM patients and control subjects, but variability was greater among the FM patients. Plasma NPY levels were significantly lower in FM patients than in normal subjects.

Conclusion. These data support the view that HPA axis function is perturbed in patients with FM. Further study is required to ascertain the cause of HPA axis perturbations and their relationship to symptoms in patients with FM.

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