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Decreased Nocturnal Levels of Prolactin and Growth Hormone in Women with Fibromyalgia¹

Biobehavioral Nursing and Health Systems (C.A.L., M.J.L., J.R., S.C.R.), Chronic Fatigue Clinic (D.C.), Department of Medicine, Chronic Fatigue Syndrome Cooperative Research Center (D.B.), University of Washington, Seattle, Washington 98195; and University of Illinois College of Nursing (J.L.F.S.), Chicago, Illinois 60612

Address all correspondence and requests for reprints to: Dr. Carol A. Landis, Biobehavioral Nursing and Health Systems, University of Washington, Seattle, Washington 98195.

Fibromyalgia (FM) is a complex syndrome, primarily of women, characterized by chronic pain, fatigue, and sleep disturbance. Altered function of the somatotropic axis has been documented in patients with FM, but little is known about nocturnal levels of PRL. As part of a laboratory study of sleep patterns in FM, we measured the serum concentrations of GH and PRL hourly from 2000–0700 h in a sample of 25 women with FM (mean, 46.9 ± 7.6 yr) and in 21 control women (mean, 42.6 ± 8.1 yr). The mean (±SEM ) serum concentrations (micrograms per L) of GH and of PRL during the early sleep period were higher in control women than in patients with FM [GH, 1.6 ± 0.4 vs. 0.6 ± 0.2 (P < 0.05); PRL, 23.2 ± 2.2 vs. 16.9 ± 2.0 (P < 0.025)]. The mean serum concentrations of GH and PRL increased more after sleep onset in control women than in patients with FM [GH, 1.3 ± 0.4 vs. 0.3 ± 0.2 (P < 0.05); PRL, 16.2 ± 2.4 vs. 9.7 ± 1.5 (P < 0.025)]. Sleep efficiency and amounts of sleep or wake stages on the blood draw night were not different between groups. There was a modest inverse relationship between sleep latency and PRL and a direct relationship between sleep efficiency and PRL in FM. There was an inverse relationship between age and GH most evident in control women. Insulin-like growth factor I levels were not different between the groups. These data demonstrate altered functioning of both the somatotropic and lactotropic axes during sleep in FM and support the hypothesis that dysregulated neuroendocrine systems during sleep may play a role in the pathophysiology of FM.

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