Sleep disturbances, daytime sleepiness and quality of life in adults with growth hormone deficiency

Low energy and fatigue are frequent complaints in subjects with GH deficiency (GHD). Since interrelations between sleep and GH regulation are well documented, these complaints could partly reflect alterations of sleep quality. Therefore we sought to determine objective and subjective sleep quality and daytime sleepiness in adult GHD patients compared to age, gender and BMI-matched controls, and in a subset of these GHD patients undergoing recombinant human GH (rhGH) therapy compared to placebo. Thirty patients, aged 19-74 yr, with untreated GHD (primary pituitary defects confirmed or likely in 26 patients, hypothalamic origin in 4 patients), and 30 healthy controls individually matched for gender, age and body mass index were enrolled in the study. Patients with associated pituitary hormonal deficiencies were on appropriate replacement therapy. Polygraphic sleep recordings were performed at baseline and after 4 months on recombinant human GH or placebo. Subjective sleep quality and quality of life were evaluated by means of the Pittsburgh Sleep Quality Index (PSQI) and Quality of Life-Assessment for GHD in Adults (QoL-AGHDA). Irrespective of etiology, GHD patients had a PSQI score above the clinical cut-off for poor sleep and lower QoL-AGHDA scores than controls, with tiredness being the most affected domain. Patients with pituitary GHD spent more time in slow-wave sleep (SWS) and had a higher intensity of SWS than their controls. Amongst these patients, older individuals obtained less total sleep than controls and their late sleep was more fragmented. Contrasting with pituitary GHD, the 4 patients with hypothalamic GHD had lower intensity of SWS than their controls. Thirteen patients were reevaluated after 4 months rhGH and 4 months placebo. Compared to placebo, SWS duration was decreased in younger patients after rhGH, and a trend for a decrease in SWS intensity was observed in the whole group. PSQI scores decreased, while QoL ratings improved. In conclusion, GHD is associated with sleep disorders that may be caused by specific hormonal alterations, as well as with poor subjective sleep quality and daytime sleepiness. Disturbed sleep is likely to be partly responsible for increased tiredness, a major component of QoL in GHD. Partial reversal of the sleep alterations was observed after 4 months of rhGH treatment, which was paralleled by an improvement in QoL and reports of tiredness, as well as subjective sleep quality

Effects of insufficient sleep on pituitary-adrenocortical response to CRH stimulation in healthy men

Study Objectives: Severe sleep restriction results in elevated evening cortisol levels. We examined whether this relative hypercortisolism is associated with alterations in the pituitary-adrenocortical response to evening corticotropin-releasing hormone (CRH) stimulation. Methods: Eleven subjects participated in 2 sessions (2 nights of 10 hours vs. 4 hours in bed) in randomized order. Sleep was polygraphically recorded. After the second night of each session, blood was sampled at 20-minute intervals from 09:00 to 24:00 for adrenocorticotropic hormone (ACTH) and cortisol measurements, and perceived stress was assessed hourly. Ovine CRH was injected at 18:00 (1 μg/kg body weight). Results: Prior to CRH injection, baseline ACTH, but not cortisol, levels were elevated after sleep restriction. Relative to the well-rested condition, sleep restriction resulted in a 27% decrease in overall ACTH response to CRH (estimated by the incremental area under the curve from 18:00 to 24:00; p = .002) while the cortisol response was decreased by 21% (p = .083). Further, the magnitude of these decreases was correlated with the individual amount of sleep loss (ACTH: rSp = -0.65, p = .032; cortisol: rSp = -0.71, p = .015). The acute post-CRH increment of cortisol was reduced (p = .002) without changes in ACTH reactivity, suggesting decreased adrenal sensitivity. The rate of decline from peak post-injection levels was reduced for cortisol (p = .032), but not for ACTH. Scores of perceived stress were unaffected by CRH injection and were low and similar under both sleep conditions. Conclusions: Sleep restriction is associated with a reduction of the overall ACTH and cortisol responses to evening CRH stimulation, and a reduced reactivity and slower recovery of the cortisol response.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Erratum to: Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (Autophagy, 12, 1, 1-222, 10.1080/15548627.2015.1100356

non present