Blood biomarkers to identify patients with different intracranial lesion combinations after traumatic brain injury
Introduction: There is a lack of studies examining the most promising blood biomarkers for traumatic brain injury (TBI) in relation to gross pathology types. Research question: To examine whether the admission levels of blood biomarkers can discriminate patients with different combinations of trauma...
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Elsevier
2025-01-01
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| Series: | Brain and Spine |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S2772529425000141 |
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| author | Pia Koivikko Ari J. Katila Riikka SK. Takala Iftakher Hossain Teemu M. Luoto Rahul Raj Mari Koivisto Olli Tenovuo Kaj Blennow Peter Hutchinson Henna-Riikka Maanpää Mehrbod Mohammadian Virginia F. Newcombe Jean-Charles Sanchez Jussi Tallus Mark van Gils Henrik Zetterberg Jussi P. Posti |
| author_facet | Pia Koivikko Ari J. Katila Riikka SK. Takala Iftakher Hossain Teemu M. Luoto Rahul Raj Mari Koivisto Olli Tenovuo Kaj Blennow Peter Hutchinson Henna-Riikka Maanpää Mehrbod Mohammadian Virginia F. Newcombe Jean-Charles Sanchez Jussi Tallus Mark van Gils Henrik Zetterberg Jussi P. Posti |
| author_sort | Pia Koivikko |
| collection | DOAJ |
| description | Introduction: There is a lack of studies examining the most promising blood biomarkers for traumatic brain injury (TBI) in relation to gross pathology types. Research question: To examine whether the admission levels of blood biomarkers can discriminate patients with different combinations of traumatic intracranial findings from patients with negative computed tomography (CT) scans. Material and methods: One hundred thirty patients with all severities of TBI were studied. Seventy-five had CT-positive and 55 CT-negative findings. CT-positive patients were divided into three clusters (CL) using the Helsinki CT score: focal lesions (CL1), mixed lesions (CL2) and mixed lesions + intraventricular haemorrhage (CL3). CT scans were obtained upon admission and blood samples taken within 24 h from admission. S100 calcium-binding protein B (S100B), glial fibrillary acidic protein (GFAP), heart fatty-acid binding protein (H-FABP), neurofilament light (NF-L), interleukin-10 (IL-10), total-tau (t-tau), and β-amyloids 1–40 (Aβ40) and 1–42 (Aβ42) were analysed from plasma samples. CT-negative cluster was used as control. Results: GFAP, Aβ40 and Aβ42 levels differed between the clusters, but not significantly. NF-L and t-tau discriminated CL1 from CT-negative cluster with AUCs of 0.737 and 0.771, respectively. NF-L, t-tau and GFAP discriminated CL2 from CT-negative cluster with AUCs of 0.839, 0.781 and 0.840, respectively. All biomarkers analysed were able to discriminate CL3 and CT-negative cluster. Discussion and conclusion: All studied biomarkers distinguished the most severely injured cluster, CL3, from CT-negative cluster. The results may reflect the severity of TBI but also show that biomarkers have a variable ability to identify patients with combinations of intracranial traumatic lesions in the examined time window. |
| format | Article |
| id | doaj-art-4295cea7a198485ca07b92f2ffe616eb |
| institution | Kabale University |
| issn | 2772-5294 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Brain and Spine |
| spelling | doaj-art-4295cea7a198485ca07b92f2ffe616eb2025-02-09T05:01:42ZengElsevierBrain and Spine2772-52942025-01-015104195Blood biomarkers to identify patients with different intracranial lesion combinations after traumatic brain injuryPia Koivikko0Ari J. Katila1Riikka SK. Takala2Iftakher Hossain3Teemu M. Luoto4Rahul Raj5Mari Koivisto6Olli Tenovuo7Kaj Blennow8Peter Hutchinson9Henna-Riikka Maanpää10Mehrbod Mohammadian11Virginia F. Newcombe12Jean-Charles Sanchez13Jussi Tallus14Mark van Gils15Henrik Zetterberg16Jussi P. Posti17Perioperative Services, Intensive Care Medicine, and Pain Management, Turku University Hospital and University of Turku, Kiinamyllynkatu 4-8, Rakennus 11 A 5, FI20520, Turku, Finland; Anaesthesiology, Intensive Care, Emergency Care and Pain Medicine, University of Turku, Kiinamyllynkatu 4-8, Rakennus 11 A 5, FI20520, Turku, Finland; Corresponding author. Perioperative Services, Intensive Care Medicine, and Pain Management, Turku University Hospital and University of Turku, Kiinamyllynkatu 4-8, Rakennus 11 A 5, FI20520, Turku, Finland.Perioperative Services, Intensive Care Medicine, and Pain Management, Turku University Hospital and University of Turku, Kiinamyllynkatu 4-8, Rakennus 11 A 5, FI20520, Turku, Finland; Anaesthesiology, Intensive Care, Emergency Care and Pain Medicine, University of Turku, Kiinamyllynkatu 4-8, Rakennus 11 A 5, FI20520, Turku, FinlandPerioperative Services, Intensive Care Medicine, and Pain Management, Turku University Hospital and University of Turku, Kiinamyllynkatu 4-8, Rakennus 11 A 5, FI20520, Turku, Finland; Anaesthesiology, Intensive Care, Emergency Care and Pain Medicine, University of Turku, Kiinamyllynkatu 4-8, Rakennus 11 A 5, FI20520, Turku, FinlandTurku Brain Injury Center, Turku University Hospital, Hämeentie 11, FI20521, Turku, Finland; Neurocenter, Department of Neurosurgery, Turku University Hospital, Hämeentie 11, FI20521, Turku, Finland; Department of Clinical Neurosciences, Neurosurgery Unit, University of Cambridge, Addenbrooke's Hospital, Hills Road, CB2 0QQ, Cambridge, United KingdomDepartment of Neurosurgery, Tampere University Hospital and Tampere University, PL 2000, FI33521, Tampere, FinlandDepartment of Neurosurgery, Helsinki University Hospital and University of Helsinki, Haartmaninkatu 4, PL 320, FI00029, HUS, Helsinki, FinlandDepartment of Biostatistics, University of Turku and Turku University Hospital, Medisiina A, FI20014, Turku, FinlandTurku Brain Injury Center, Turku University Hospital, Hämeentie 11, FI20521, Turku, Finland; Neurocenter, University of Turku, Hämeentie 11, FI20521, Turku, FinlandDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, S-431 80, Mölndal, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, S-431 80, Mölndal, Sweden; Paris Brain Institute, ICM, Pitié-Salpêtrière Hospital, Sorbonne University, 47 Boulevard de l’Hôpital, CS 21 414-75646, Paris Cedex 13, France; Neurodegenerative Disorder Research Center, Division of Life Sciences and Medicine, and Department of Neurology, Institute on Aging and Brain Disorders, University of Science and Technology of China and First Affiliated Hospital of USTC, Hefei, 230026, ChinaDepartment of Clinical Neurosciences, Neurosurgery Unit, University of Cambridge, Addenbrooke's Hospital, Hills Road, CB2 0QQ, Cambridge, United KingdomNeurocenter, Department of Neurosurgery, Turku University Hospital, Hämeentie 11, FI20521, Turku, Finland; Neurocenter, University of Turku, Hämeentie 11, FI20521, Turku, FinlandTurku Brain Injury Center, Turku University Hospital, Hämeentie 11, FI20521, Turku, Finland; Neurocenter, University of Turku, Hämeentie 11, FI20521, Turku, FinlandDivision of Anaesthesia, Department of Medicine, University of Cambridge, Addenbrooke's Hospital, Hills Road, CB2 0QQ, Cambridge, United KingdomDepartment of Specialities of Internal Medicine, Faculty of Medicine, University of Geneva, 1 Michel Servet, 1211, Geneva, SwitzerlandNeurocenter, University of Turku, Hämeentie 11, FI20521, Turku, Finland; Department of Radiology, Turku University Hospital, Hämeentie 11, FI20521, Turku, FinlandFaculty of Medicine and Health Technology, Tampere University, Kalevantie 4, FI33100, Tampere, FinlandDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, S-431 80, Mölndal, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, S-431 80, Mölndal, Sweden; Department of Neurodegenerative Disease, UCL Institute of Neurology, Queen Square, London, WC1E 6BT, United Kingdom; UK Dementia Research Institute at UCL, London, WC1E 6BT, United Kingdom; Hong Kong Center for Neurodegenerative Diseases, Clear Water Bay, Units 1501-1502, 1512-1518, 15/F Building 17W, 17 Science Park W Ave, Science Park, Hong Kong, 0000, China; Wisconsin Alzheimer's Disease Research Center, University of Wisconsin School of Medicine and Public Health, University of Wisconsin-Madison, 600 Highland Avenue, MC 2420, Madison, WI, 53792-2420, USATurku Brain Injury Center, Turku University Hospital, Hämeentie 11, FI20521, Turku, Finland; Neurocenter, Department of Neurosurgery, Turku University Hospital, Hämeentie 11, FI20521, Turku, FinlandIntroduction: There is a lack of studies examining the most promising blood biomarkers for traumatic brain injury (TBI) in relation to gross pathology types. Research question: To examine whether the admission levels of blood biomarkers can discriminate patients with different combinations of traumatic intracranial findings from patients with negative computed tomography (CT) scans. Material and methods: One hundred thirty patients with all severities of TBI were studied. Seventy-five had CT-positive and 55 CT-negative findings. CT-positive patients were divided into three clusters (CL) using the Helsinki CT score: focal lesions (CL1), mixed lesions (CL2) and mixed lesions + intraventricular haemorrhage (CL3). CT scans were obtained upon admission and blood samples taken within 24 h from admission. S100 calcium-binding protein B (S100B), glial fibrillary acidic protein (GFAP), heart fatty-acid binding protein (H-FABP), neurofilament light (NF-L), interleukin-10 (IL-10), total-tau (t-tau), and β-amyloids 1–40 (Aβ40) and 1–42 (Aβ42) were analysed from plasma samples. CT-negative cluster was used as control. Results: GFAP, Aβ40 and Aβ42 levels differed between the clusters, but not significantly. NF-L and t-tau discriminated CL1 from CT-negative cluster with AUCs of 0.737 and 0.771, respectively. NF-L, t-tau and GFAP discriminated CL2 from CT-negative cluster with AUCs of 0.839, 0.781 and 0.840, respectively. All biomarkers analysed were able to discriminate CL3 and CT-negative cluster. Discussion and conclusion: All studied biomarkers distinguished the most severely injured cluster, CL3, from CT-negative cluster. The results may reflect the severity of TBI but also show that biomarkers have a variable ability to identify patients with combinations of intracranial traumatic lesions in the examined time window.http://www.sciencedirect.com/science/article/pii/S2772529425000141BiomarkersComputed tomographyTraumatic brain injury |
| spellingShingle | Pia Koivikko Ari J. Katila Riikka SK. Takala Iftakher Hossain Teemu M. Luoto Rahul Raj Mari Koivisto Olli Tenovuo Kaj Blennow Peter Hutchinson Henna-Riikka Maanpää Mehrbod Mohammadian Virginia F. Newcombe Jean-Charles Sanchez Jussi Tallus Mark van Gils Henrik Zetterberg Jussi P. Posti Blood biomarkers to identify patients with different intracranial lesion combinations after traumatic brain injury Brain and Spine Biomarkers Computed tomography Traumatic brain injury |
| title | Blood biomarkers to identify patients with different intracranial lesion combinations after traumatic brain injury |
| title_full | Blood biomarkers to identify patients with different intracranial lesion combinations after traumatic brain injury |
| title_fullStr | Blood biomarkers to identify patients with different intracranial lesion combinations after traumatic brain injury |
| title_full_unstemmed | Blood biomarkers to identify patients with different intracranial lesion combinations after traumatic brain injury |
| title_short | Blood biomarkers to identify patients with different intracranial lesion combinations after traumatic brain injury |
| title_sort | blood biomarkers to identify patients with different intracranial lesion combinations after traumatic brain injury |
| topic | Biomarkers Computed tomography Traumatic brain injury |
| url | http://www.sciencedirect.com/science/article/pii/S2772529425000141 |
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