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生物学年龄和年龄加速对老年髋部骨折患者1年死亡率的影响:一项前瞻性队列研究。

The impact of biological age and age acceleration on 1-year mortality rates in elderly hip fracture patients: a prospective cohort study.

作者信息

Randall Zachary D, Barber Helena F, Buesser Katherine E, Obey Mitchel R, Wilson Jenna-Leigh, McAndrew Christopher M, Berkes Marschall B

机构信息

Department of Orthopaedic Surgery, Washington University in St. Louis School of Medicine, Campus Box 8233, 660 Euclid Avenue, St. Louis, 63110, MO, USA.

出版信息

Arch Osteoporos. 2025 Jun 26;20(1):84. doi: 10.1007/s11657-025-01572-x.

Abstract

UNLABELLED

This study examines how biological age, calculated from routine lab tests, predicts 1-year mortality in elderly hip fracture patients better than chronological age. Our findings highlight that increased biological aging is linked to higher mortality, emphasizing its potential for improving preoperative risk assessment.

INTRODUCTION

Geriatric hip fractures cause high morbidity and up to 30% 1-year mortality. Incorporating biological age and age acceleration into traditional assessments may improve predictions of outcomes and guide clinical interventions and perioperative counseling.

METHODS

In this prospective study, patients aged ≥ 50 with low-energy hip fractures had demographic data, chronological age, comorbidities, and nine laboratory parameters collected preoperatively. Biological age was computed per Levine et al. (2018), and age acceleration was defined as the difference between biological and chronological age. Patients were categorized by age acceleration (< 20 vs. ≥ 20 years) and into four subgroups (-15 to 5, 5-20, 20-30, and ≥ 30 years) for survival analysis.

RESULTS

Ninety-one patients were included. Mean chronological age was 76.6 (SD 9.2) years, biological age 90.5 (SD 15.0) years, and age acceleration 13.9 (SD 13.1) years; the mean Charlson Comorbidity Index was 4.1 (SD 3.1). One-year mortality was 25.3%. Those who died had higher CCI (6.0 vs. 3.5; p = 0.001), biological age (102.6 vs. 86.4; p < 0.001), and age acceleration (23.8 vs. 10.7; p < 0.001). Mortality increased from 7.7% in the lowest (-15 to 5 years) to 63.6% in the highest (≥ 30 years) age acceleration bracket. Cox regression-adjusted for ambulation, race, sex, CCI, and smoking-confirmed age acceleration ≥ 20 years as an independent predictor (HR 3.27; 95% CI 1.28-8.38; p = 0.014).

CONCLUSION

Biological age and age acceleration outperform chronological age in predicting 1-year mortality, supporting their role in risk stratification for geriatric hip fracture patients.

摘要

未标注

本研究探讨了根据常规实验室检查计算得出的生物学年龄如何比实际年龄更好地预测老年髋部骨折患者的1年死亡率。我们的研究结果强调,生物学衰老加剧与更高的死亡率相关,突出了其在改善术前风险评估方面的潜力。

引言

老年髋部骨折导致高发病率和高达30%的1年死亡率。将生物学年龄和年龄加速纳入传统评估可能会改善对预后的预测,并指导临床干预和围手术期咨询。

方法

在这项前瞻性研究中,对年龄≥50岁的低能量髋部骨折患者术前收集了人口统计学数据、实际年龄、合并症和九项实验室参数。生物学年龄根据莱文等人(2018年)的方法计算,年龄加速定义为生物学年龄与实际年龄之差。患者按年龄加速(<20岁与≥20岁)分类,并分为四个亚组(-15至5岁、5至20岁、20至30岁和≥30岁)进行生存分析。

结果

纳入91例患者。平均实际年龄为76.6(标准差9.2)岁,生物学年龄为90.5(标准差15.0)岁,年龄加速为13.9(标准差13.1)岁;平均Charlson合并症指数为4.1(标准差3.1)。1年死亡率为25.3%。死亡患者的CCI更高(6.0对3.5;p = 0.001)、生物学年龄更高(102.6对86.4;p < 0.001)以及年龄加速更高(23.8对10.7;p < 0.001)。年龄加速最低组(-15至5岁)的死亡率为7.7%,最高组(≥30岁)为63.6%。经Cox回归调整步行能力、种族、性别、CCI和吸烟情况后,确认年龄加速≥20岁是独立预测因素(风险比3.27;95%置信区间1.28 - 8.38;p = 0.014)。

结论

生物学年龄和年龄加速在预测1年死亡率方面优于实际年龄,支持它们在老年髋部骨折患者风险分层中的作用。

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