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Published on: October 2, 2019
An evaluation of the neuroendocrine response to sleep in pediatric burn patients
Michele M Gottschlich1, Jane Khoury, Glenn D Warden
1Department of Nutrition, Shriners Hospitals for Children, Cincinnati, OH 45229, USA. mgottschlich@shrinenet.org
Insights
Burn injury disrupts sleep stages and hormone levels. While medications increased dehydroepiandrosterone (DHEA), they didn't significantly alter other hormones or improve sleep quality. Epinephrine and norepinephrine inversely correlated with REM sleep.
Area of Science:
- Burn injury research
- Sleep medicine
- Endocrinology
Background:
- Burn injuries are known to reduce sleep stages, particularly stage 3+4 and REM sleep.
- Previous studies indicate altered endocrine status post-burn.
- This study investigates drug interventions' hormonal effects and their relation to sleep patterns.
Purpose of the Study:
- To evaluate the hormonal effects of zolpidem and haloperidol on endocrine status in pediatric burn patients.
- To examine the relationship between specific hormones and sleep stage distribution after burn injury.
- To understand the impact of sleep deprivation on metabolism and clinical outcomes post-burn.
Main Methods:
- Forty pediatric patients (3-18 years) with severe burns (mean 50.1% TBSA) were enrolled.
- A blinded crossover design assigned patients to zolpidem or haloperidol.
- Polysomnography and hormonal level measurements (epinephrine, norepinephrine, GH, melatonin, DHEA, serotonin, cortisol) were conducted over two weeks.
Main Results:
- Both zolpidem and haloperidol increased dehydroepiandrosterone (DHEA) levels (P < .03).
- No other significant hormonal changes were observed due to medication.
- REM sleep showed a significant inverse correlation with epinephrine (r = -.34, P = .004) and norepinephrine (r = -.45, P = .02).
- Serotonin positively correlated with stage 3+4 (r = 0.24, P = .01) and REM sleep (r = 0.48, P = .01).
Conclusions:
- Drug interventions were insufficient to modulate hormonal response or improve sleep post-burn.
- The inverse correlation between REM sleep and catecholamines suggests a link between hypermetabolism and sleep deprivation.
- Further research is needed to clarify the effects of sleep deprivation on metabolism and clinical outcomes in burn patients.
Introduction:
Previous work demonstrated reduced stage 3+4 and rapid eye movement (REM) sleep following burn injury. This study evaluated the hormonal effects of drug intervention on measures of endocrine status. A secondary objective examined the relationship between hormones and sleep stage distribution.
Methods:
Forty patients 3-18 years of age with a mean percent total body surface area burn of 50.1 +/- 2.9 were randomly assigned to zolpidem or haloperidol utilizing a blinded crossover design. Polysomnography was performed 6 nights, 3/week over 2 weeks. Each week's first night of monitoring was conducted without medication, serving as a baseline. Hormonal levels (epinephrine, norepinephrine, growth hormone, melatonin, dehydroepiandrosterone [DHEA], serotonin, cortisol) were obtained at 0600 h each study day.
Results:
Both drugs were associated with increased DHEA levels (P < .03); no other hormones were affected by medication. Significant inverse correlation was observed between REM sleep and epinephrine (r = -.34, P = .004) and norepinephrine levels (r = -.45, P = .02). A positive relationship existed between serotonin and sleep stage 3+4 (r = 0.24, P = .01) and REM (r = 0.48, P = .01). No other significant associations were identified between hormones and sleep.
Conclusions:
This work characterizes the relationship between sleep deprivation and select endocrine parameters postburn. Drug interventions utilized in this study were either ineffective or insufficient in modulating improved hormonal response. Significance of zolpidem's and haloperidol's effect on serum levels of DHEA is unclear. The inverse correlation of epinephrine with REM may suggest that hypermetabolism associated with burns is partly due to lack of REM sleep. Questions remain regarding the effects of sleep deprivation on metabolism and clinical outcome.
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