Debbie Norring-Agerskov1,2,3, Lise Bathum4, Ole B Pedersen5, Bo Abrahamsen6,7, Jes B Lauritzen8,9, Niklas R Jørgensen10,7, Henrik L Jørgensen4,9. 1. Department of Clinical Biochemistry, Hvidovre Hospital, Kettegård Alle 30, 2650, Hvidovre, Denmark. Debbie.agerskov@gmail.com. 2. Department of Orthopedic Surgery, Bispebjerg Hospital, Bispebjerg Bakke 23, 2400, Copenhagen NV, Denmark. Debbie.agerskov@gmail.com. 3. Odense Patient Data Explorative Network, University of Southern Denmark and Odense University Hospital, J.B. Winsløws Vej 9A, 5000, Odense C, Denmark. Debbie.agerskov@gmail.com. 4. Department of Clinical Biochemistry, Hvidovre Hospital, Kettegård Alle 30, 2650, Hvidovre, Denmark. 5. Department of Clinical Immunology, Næstved Sygehus, Ringstedgade 61, 4700, Næstved, Denmark. 6. Department of Medicine, Holbæk Hospital, Smedelundsgade 60, 4300, Holbæk, Denmark. 7. Odense Patient Data Explorative Network, University of Southern Denmark and Odense University Hospital, J.B. Winsløws Vej 9A, 5000, Odense C, Denmark. 8. Department of Orthopedic Surgery, Bispebjerg Hospital, Bispebjerg Bakke 23, 2400, Copenhagen NV, Denmark. 9. Department of Clinical Medicine, University of Copenhagen, Blegdamsvej 3B, 2200, Copenhagen N, Denmark. 10. Department of Clinical Biochemistry, Rigshospitalet Glostrup, Valdemar Hansens Vej 13, 2600, Glostrup, Denmark.
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.
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.
Entities:
Keywords:
Hip fracture; Inflammatory markers; Mortality; Prognosis
Authors: Carmen Sánchez-Castellano; Sagrario Martín-Aragón; Paloma Bermejo-Bescós; Nieves Vaquero-Pinto; Carmen Miret-Corchado; Ana Merello de Miguel; Alfonso José Cruz-Jentoft Journal: J Cachexia Sarcopenia Muscle Date: 2020-01-08 Impact factor: 12.910