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单核细胞与高密度脂蛋白胆固醇比值在临床定义的以目击呼吸暂停为特征的儿童睡眠呼吸障碍表型中的研究

Monocyte-to-HDL cholesterol ratio in a clinically defined pediatric sleep-related breathing disorder phenotype characterized by witnessed apnea.

临床研究鼻科IF 1.7Q2

文献信息

中文摘要

目的: 单核细胞与高密度脂蛋白胆固醇比值(MHR)是炎症-代谢平衡的复合标志物。本研究评估了临床定义的以目击呼吸暂停或呼吸停顿为特征的睡眠呼吸障碍(SRBD)表型儿童的MHR。
材料与方法: 这项回顾性病例对照研究纳入74例临床定义的SRBD儿童和70例对照。由于多导睡眠监测(PSG)并非系统可用,研究组未被归类为PSG确诊的阻塞性睡眠呼吸暂停。组间比较采用Holm校正。进行了年龄和性别校正的logistic回归及ROC分析。基于MHR、单核细胞和HDL的模型采用DeLong检验进行比较,MHR模型进行了bootstrap内部验证。
结果: 研究组MHR更高[13.84(11.57-16.48)vs 10.15(8.78-12.07);Holm校正p < 0.001],且在年龄和性别校正后仍与组别相关(校正OR = 1.315,95% CI:1.173-1.474;p < 0.001)。加入MHR使AUC从0.563增至0.777(DeLong p < 0.001);乐观校正后AUC为0.762。MHR在单标志物模型中AUC最高,但与基于单核细胞和HDL的模型相比,Holm校正后差异无统计学意义。
结论: MHR在该儿童SRBD表型中升高,并在年龄和性别之外提供了额外信息。其潜在价值可能在于将炎症和代谢信息整合为一个易于计算的指数,而非优于其组成部分。MHR应被视为补充性研究生物标志物,而非诊断性检测。

英文摘要

OBJECTIVE: The monocyte-to-high-density lipoprotein cholesterol ratio (MHR) is a composite marker of inflammatory-metabolic balance. This study evaluated MHR in children with a clinically defined sleep-related breathing disorder (SRBD) phenotype characterized by witnessed apnea or respiratory pauses.
MATERIALS AND METHODS: This retrospective case-control study included 74 children with clinically defined SRBD and 70 controls. Because polysomnography (PSG) was not systematically available, the study group was not classified as PSG-confirmed obstructive sleep apnea. Group comparisons used Holm correction. Age- and sex-adjusted logistic regression and ROC analyses were performed. MHR-, monocyte-, and HDL-based models were compared using DeLong tests, and the MHR model underwent bootstrap internal validation.
RESULTS: MHR was higher in the study group [13.84 (11.57-16.48) vs 10.15 (8.78-12.07); Holm-adjusted p < 0.001] and remained associated with group membership after age and sex adjustment (adjusted OR = 1.315, 95% CI: 1.173-1.474; p < 0.001). Adding MHR increased the AUC from 0.563 to 0.777 (DeLong p < 0.001); the optimism-corrected AUC was 0.762. MHR had the highest AUC among single-marker models, but differences versus monocyte- and HDL-based models were not significant after Holm correction.
CONCLUSION: MHR was elevated in this pediatric SRBD phenotype and added information beyond age and sex. Its potential value may lie in integrating inflammatory and metabolic information into one readily calculated index rather than in superiority over its components. MHR should be regarded as a complementary research biomarker, not a diagnostic test.