Prader-Willi综合征儿童阻塞性睡眠呼吸暂停严重程度与胰岛素抵抗：SPISE指数作为候选代谢标志物
Obstructive sleep apnoea severity and insulin resistance in children with Prader-Willi Syndrome: the SPISE index as a candidate metabolic marker.
文献信息
| PMID | 42855587 |
|---|---|
| 原文 | 在 PubMed 查看原文 ↗ |
| 发表日期 | 2026 |
| 作者 | Abdurrahman Zarif Güney |
| 作者单位 | Division of Paediatric Pulmonology, Department of Paediatrics, Cerrahpaşa Faculty of Medicine, Istanbul University-Cerrahpaşa, Istanbul, Turkey. |
| 期刊 | European journal of pediatrics |
| SCI 分区 | Q1 |
| IF | 3 |
| 研究类型 | 临床研究 · 临床 |
| 所属专科 | 鼻科 |
中文摘要
未标注： 我们比较了两种胰岛素敏感性替代标志物——单点胰岛素敏感性估计器（SPISE）和HOMA-IR——并评估了它们在经基因确诊的PWS儿童以及有症状的非综合征转诊组（NSR）中与OSA严重程度的关联，这些儿童均有可用的多导睡眠监测（PSG）和空腹生化数据。在这项单中心回顾性横断面研究中，OSA严重程度以阻塞性呼吸暂停-低通气指数（oAHI）、中枢AHI（cAHI）和氧减饱和度指数（ODI）表示，照护者报告的症状以PSQ-SRBD量表表示。多变量模型在PWS组内拟合。在筛选的458份PSG研究中，31名PWS儿童和47名NSR儿童符合纳入标准。PWS组的cAHI更高（p < 0.001），PSQ-SRBD评分略低，尽管oAHI分布相似。在PWS组内，oAHI与SPISE呈负相关（ρ = -0.378，p = 0.036）。在调整年龄、性别、BMI-SDS和生长激素治疗的多变量模型中，较高的oAHI与较低的SPISE相关（B = -0.154，p = 0.015），而与ln(HOMA-IR)的关联为临界显著（B = 0.081，p = 0.0497）。ODI与SPISE相关（ρ = -0.427，p = 0.017），但与HOMA-IR不相关（ρ = 0.319，p = 0.081）。分期分层分析显示，oAHI-SPISE相关性出现在第2和第3期，oAHI-HOMA-IR相关性出现在第3期。
结论： 在PWS儿童中，OSA严重程度与胰岛素敏感性受损标志物相关。SPISE与oAHI和ODI的关联支持将其作为OSA严重程度的候选代谢相关指标进一步研究。这些发现具有假设生成性，需要在更大的独立队列中验证。
已知内容： • OSA在PWS中高度流行。OSA严重程度与成人和非综合征肥胖儿童的胰岛素抵抗相关，但这一关系以及不依赖胰岛素的SPISE指数尚未在PWS中评估。
新发现： • OSA严重程度与PWS儿童的胰岛素敏感性受损标志物相关。• SPISE由血脂和BMI推导，无需空腹胰岛素，在PWS中与oAHI和ODI相关；它作为OSA严重程度的候选代谢相关指标值得进一步研究。
英文摘要
UNLABELLED: We compared two surrogate markers of insulin sensitivity - the single-point insulin sensitivity estimator (SPISE) and HOMA-IR - and evaluated their associations with OSA severity in children with genetically confirmed PWS and a symptomatic non-syndromic referral group (NSR) with available polysomnography (PSG) and fasting biochemical data. In this single-centre retrospective cross-sectional study, OSA severity was indexed by the obstructive apnoea-hypopnoea index (oAHI), central AHI (cAHI) and oxygen desaturation index (ODI), and caregiver-reported symptoms by the PSQ-SRBD scale. Multivariable models were fitted within the PWS group. Of 458 PSG studies screened, 31 children with PWS and 47 NSR met the inclusion criteria. cAHI was higher in PWS (p < 0.001), and PSQ-SRBD scores were slightly lower, despite a similar oAHI distribution. Within the PWS group, oAHI correlated inversely with SPISE (ρ = - 0.378, p = 0.036). In multivariable models adjusted for age, sex, BMI-SDS, and growth hormone therapy, higher oAHI was associated with lower SPISE (B = - 0.154, p = 0.015), whereas the association with ln(HOMA-IR) was borderline (B = 0.081, p = 0.0497). ODI correlated with SPISE (ρ = - 0.427, p = 0.017) but not with HOMA-IR (ρ = 0.319, p = 0.081). Phase-stratified analyses showed oAHI-SPISE correlations in phases 2 and 3 and an oAHI-HOMA-IR correlation in phase 3.
CONCLUSION: In children with PWS, OSA severity was associated with markers of impaired insulin sensitivity. The associations of SPISE with oAHI and ODI support its further investigation as a candidate metabolic correlate of OSA severity. These findings are hypothesis-generating and require validation in larger independent cohorts.
WHAT IS KNOWN: • OSA is highly prevalent in PWS. OSA severity is associated with insulin resistance in adults and in non-syndromic children with obesity, but this relationship and the insulin-independent SPISE index have not been evaluated in PWS.
WHAT IS NEW: • OSA severity was associated with impaired insulin sensitivity markers in children with PWS. • SPISE, derived from lipids and BMI without fasting insulin, was associated with oAHI and ODI in PWS; it merits further investigation as a candidate metabolic correlate of OSA severity.