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炎症的生化标志物与髋部骨折患者的死亡率增加有关:比斯加普生物库。

Biochemical markers of inflammation are associated with increased mortality in hip fracture patients: the Bispebjerg Hip Fracture Biobank.

机构信息

Department of Clinical Biochemistry, Hvidovre Hospital, Kettegård Alle 30, 2650, Hvidovre, Denmark.

Department of Orthopedic Surgery, Bispebjerg Hospital, Bispebjerg Bakke 23, 2400, Copenhagen NV, Denmark.

出版信息

Aging Clin Exp Res. 2019 Dec;31(12):1727-1734. doi: 10.1007/s40520-019-01140-7. Epub 2019 Feb 1.

DOI:10.1007/s40520-019-01140-7
PMID:30707355
Abstract

PURPOSE

The purpose of this study was to examine the possible association between mortality following a hip fracture and known biochemical markers of inflammation.

METHODS

The study population was identified using two local databases from Bispebjerg Hospital (Copenhagen, Denmark): the Hip Fracture Database containing all patients admitted to the hospital with a fractured hip from 1996 to 2012 and the Hip Fracture Biobank, containing whole blood, serum and plasma taken in relation to admission on a subgroup of patients from the Hip Fracture Database, consecutively collected over a period of 2.5 years from 2008 to 2011. The following biochemical markers of inflammation were included: C-reactive protein (CRP), the soluble urokinase plasminogen activating receptor (suPAR), ferritin and transferrin. The association between the blood markers and mortality was examined using Cox proportional hazards models. Hazard ratios (HR) were expressed per quartile increase in the biochemical markers.

RESULTS

A total of 698 patients were included, 69 (9.9%) died within 30 days after sustaining a hip fracture. The HR for 30-day mortality was significantly increased with increasing quartiles of suPAR, CRP and ferritin and with decreasing quartiles of transferrin.

CONCLUSION

This study shows that 30-day mortality after a hip fracture is associated with elevated levels of suPAR, CRP and ferritin as well as with lower levels of transferrin. This excess inflammatory response is likely caused by muscle damage associated with the hip fracture. However, this needs to be further clarified.

摘要

目的

本研究旨在探讨髋部骨折后死亡率与已知炎症生化标志物之间的可能关联。

方法

该研究人群通过丹麦比斯加弗医院的两个本地数据库确定:髋部骨折数据库包含了 1996 年至 2012 年期间因髋部骨折住院的所有患者,髋部骨折生物库包含了与数据库中一部分患者入院相关的全血、血清和血浆,这些患者是从数据库中连续选取的,采集时间为 2008 年至 2011 年的 2.5 年期间。纳入了以下炎症的生化标志物:C 反应蛋白(CRP)、可溶性尿激酶型纤溶酶原激活物受体(suPAR)、铁蛋白和转铁蛋白。使用 Cox 比例风险模型检查血液标志物与死亡率之间的关联。风险比(HR)表示每个生化标志物四分位增加的倍数。

结果

共纳入 698 例患者,69 例(9.9%)在髋部骨折后 30 天内死亡。suPAR、CRP 和铁蛋白四分位增加,以及转铁蛋白四分位降低与 30 天死亡率的 HR 显著增加相关。

结论

本研究表明,髋部骨折后 30 天死亡率与 suPAR、CRP 和铁蛋白水平升高以及转铁蛋白水平降低相关。这种炎症反应过度可能是由髋部骨折引起的肌肉损伤引起的。但这需要进一步澄清。

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