A Gonadotropin-Releasing Hormone Agonist Model Demonstrates That Nocturnal Hot Flashes Interrupt Objective Sleep
A Gonadotropin-Releasing Hormone Agonist Model Demonstrates That Nocturnal Hot Flashes Interrupt Objective Sleep
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DOI：
10.5665/sleep.3244
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发表时间：
2013-12-01
期刊：
影响因子：
5.6
通讯作者：
White, David
中科院分区：
文献类型：
--
作者：
Joffe, Hadine;Crawford, Sybil;White, David
目标：女性经常报告睡眠中断，伴有潮热和盗汗（或血管舒缩症状，VMS）。尽管女性报告 VMS 会唤醒她们，但多导睡眠图 (PSG) 研究并未一致支持这一论点。 设计：我们使用促性腺激素释放激素激动剂 (GnRHa) 模拟更年期，以研究 VMS 是否会增加觉醒和入睡后觉醒 (WASO)。在使用 GnRHa 4 周之前和之后测量 VMS、血清雌二醇和家庭 PSG（两次治疗前，两次治疗后）。使用回归模型来确定增加 VMS 频率对觉醒和 WASO 的影响（客观和主观测量）。参与者：29 名健康女性（平均 27.3 岁）。地点：学术医疗中心。干预措施：长效 GnRHa（亮丙瑞林 3.75 毫克）。结果：GnRHa 快速且均匀地抑制血清雌二醇。 69% 的女性报告称持续存在 VMS。夜间 VMS 的数量与睡眠障碍的程度直接相关。每增加一个夜间 VMS，PSG 测量的 WASO 较基线增加 62%（P = 0.007），觉醒次数增加 3%（P = 0.05），%N1 睡眠增加 6%（P = 0.02）。夜间 VMS 还与感知 WASO（312%；P = 0.02）、觉醒（16%；P = 0.007）、失眠严重程度指数（P = 0.03）和匹兹堡睡眠质量指数（P = 0.03）分数增加以及感知睡眠效率降低（P = 0.01）相关。客观记录的夜间 VMS 与 PSG 测量的 WASO 相关（r(s) = 0.45，P = 0.02）。结论：该更年期模型表明，夜间血管舒缩症状与睡眠碎片化增加相关。这些发现与血管舒缩症状对多导睡眠图测量的睡眠中断的特定贡献一致，表明夜间血管舒缩症状会中断更年期的睡眠。
Objectives: Sleep interruption is often reported by women with hot flashes and night sweats (or vasomotor symptoms, VMS). Although women report that VMS awaken them, polysomnography (PSG) studies have not consistently supported this contention.Design: We mimicked menopause using a gonadotropin-releasing hormone agonist (GnRHa) to investigate whether VMS increase awakenings and wake after sleep onset (WASO). VMS, serum estradiol, and at-home PSGs (two pretreatment, two posttreatment) were measured before and after 4 weeks on GnRHa. Regression models were used to determine the effect of increasing VMS frequency on awakenings and WASO, as measured objectively and subjectively.Participants: Twenty-nine healthy women (mean 27.3 y).Setting: Academic medical center.Interventions: Depot GnRHa (leuprolide 3.75-mg).Results: Serum estradiol was rapidly and uniformly suppressed on GnRHa. Persistent VMS were reported by 69% of women. The number of nighttime VMS correlated directly with the degree of sleep disturbance. Each additional reported nighttime VMS was associated with a 62% increase from baseline in PSG-measured WASO (P = 0.007), a 3% increase in awakenings (P = 0.05), and 6% increase in %N1 sleep (P = 0.02). Nighttime VMS were also associated with increased perceived WASO (312%; P = 0.02), awakenings (16%; P = 0.007), Insomnia Severity Index (P = 0.03), and Pittsburgh Sleep Quality Index (P = 0.03) scores, and decreased perceived sleep efficiency (P = 0.01). Objectively recorded nighttime VMS correlated with PSG-measured WASO (r(s) = 0.45, P = 0.02).Conclusions: This menopause model demonstrates that nighttime vasomotor symptoms correlate with increased sleep fragmentation. These findings are consistent with a specific contribution of vasomotor symptoms to polysomnography-measured sleep interruption suggesting that nighttime vasomotor symptoms interrupt sleep in the setting of menopause.