Characterizing Glycemic Control and Sleep in Adults with Long-Standing Type 1 Diabetes and Hypoglycemia Unawareness Initiating Hybrid Closed Loop Insulin Delivery.
Characterizing Glycemic Control and Sleep in Adults with Long-Standing Type 1 Diabetes and Hypoglycemia Unawareness Initiating Hybrid Closed Loop Insulin Delivery.
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DOI：
10.1155/2021/6611064
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发表时间：
2021
影响因子：
4.3
通讯作者：
Goel N
中科院分区：
文献类型：
--
作者：
Malone SK;Peleckis AJ;Grunin L;Yu G;Jang S;Weimer J;Lee I;Rickels MR;Goel N
由于缺乏低血糖症状识别（低血糖无意识）和葡萄糖反调节功能受损，夜间低血糖对 1 型糖尿病 (T1D) 患者来说会危及生命。这些人还表现出睡眠不安，这可能是由血糖失调引起的。使用混合闭环（HCL）胰岛素输送系统和集成连续血糖监测（CGM）来改善血糖控制是否与该人群的长期睡眠质量有关仍不清楚。本研究的目的是描述患有 1 型糖尿病和低血糖的成人患者开始混合闭环 (HCL) 胰岛素给药后血糖控制和客观睡眠的长期变化。为了实现这一目标，六名成年人（中位年龄 = 58 岁）参加了一项为期 18 个月的持续试验，评估 HCL 的有效性。每 3 个月使用连续血糖监测和腕部加速度计测量血糖控制和睡眠。配对样本 t 检验和 Cohen d 效应大小模拟了血糖和睡眠变化以及这些变化从基线到 9 个月的幅度。从基线到 9 个月，低血糖减少（d = 0.47-0.79），基础胰岛素需求减少（d = 0.48），葡萄糖变异系数更小（d = 0.47），中大效应大小。低血糖意识从基线到 6 个月有所改善，效果中等（Clarke 评分 (d = 0.60)、不稳定性指数 (d = 0.50)、HYPO 评分 (d = 1.06)）。从基线到 9 个月，中大效应大小出现较短的入睡潜伏期（d = 1.53；p < 0.01）、较短的睡眠持续时间（d = 0.79）、较少的总活动计数（d = 1.32）、较短的平均觉醒长度（d = 0.46）以及入睡延迟（d = 1.06）和睡眠中点（d = 0.72）。 HCL 使低血糖发生率在临床上显着减少，并提高了低血糖意识。启动 HCL 后，睡眠表现出延迟开始、觉醒长度和开始潜伏期缩短以及维持高睡眠效率。我们的研究结果为糖尿病治疗技术与睡眠健康之间关系的有限证据提供了补充。该试验已在 ClinicalTrials.gov 注册 (NCT03215914)。
Nocturnal hypoglycemia is life threatening for individuals with type 1 diabetes (T1D) due to loss of hypoglycemia symptom recognition (hypoglycemia unawareness) and impaired glucose counter regulation. These individuals also show disturbed sleep, which may result from glycemic dysregulation. Whether use of a hybrid closed loop (HCL) insulin delivery system with integrated continuous glucose monitoring (CGM) designed for improving glycemic control, relates to better sleep across time in this population remains unknown. The purpose of this study was to describe long-term changes in glycemic control and objective sleep after initiating hybrid closed loop (HCL) insulin delivery in adults with type 1 diabetes and hypoglycemia unawareness. To accomplish this, six adults (median age = 58 y) participated in an 18-month ongoing trial assessing HCL effectiveness. Glycemic control and sleep were measured using continuous glucose monitoring and wrist accelerometers every 3 months. Paired sample t-tests and Cohen's d effect sizes modeled glycemic and sleep changes and the magnitude of these changes from baseline to 9 months. Reduced hypoglycemia (d = 0.47‐0.79), reduced basal insulin requirements (d = 0.48), and a smaller glucose coefficient of variation (d = 0.47) occurred with medium-large effect sizes from baseline to 9 months. Hypoglycemia awareness improved from baseline to 6 months with medium-large effect sizes (Clarke score (d = 0.60), lability index (d = 0.50), HYPO score (d = 1.06)). Shorter sleep onset latency (d = 1.53; p < 0.01), shorter sleep duration (d = 0.79), fewer total activity counts (d = 1.32), shorter average awakening length (d = 0.46), and delays in sleep onset (d = 1.06) and sleep midpoint (d = 0.72) occurred with medium-large effect sizes from baseline to 9 months. HCL led to clinically significant reductions in hypoglycemia and improved hypoglycemia awareness. Sleep showed a delayed onset, reduced awakening length and onset latency, and maintenance of high sleep efficiency after initiating HCL. Our findings add to the limited evidence on the relationships between diabetes therapeutic technologies and sleep health. This trial is registered with ClinicalTrials.gov (NCT03215914).
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5.9
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