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Traumatic Brain Injury (TBI) is a significant cause of mortality and morbidity worldwide. However, the literature on determining its severity and predicting prognosis is insufficient. This study aimed to examine the differences in metabolite levels between trauma patients with severe TBI and orthopedic trauma patients without brain injury.
Traumatic Brain Injury (TBI) is a significant cause of mortality and morbidity worldwide, particularly in young people. TBI is a complex metabolic process associated with an energy crisis resulting from multiple mechanisms, including ischemia, diffusion hypoxia, and mitochondrial dysfunction. Because metabolic derangement is a fundamental component of TBI pathophysiology, these metabolic changes may provide prognostic information and guide treatment. Additionally, the release of brain-specific metabolites (i.e., small molecules with a molecular mass below 500 Da) into the systemic circulation may provide insights into blood-brain barrier (BBB) dysfunction, a fundamental process in TBI. Metabolomic profiling studies are introductory and valuable for elucidating this metabolic process.
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| Label | Type | Description | Intervention Names |
|---|---|---|---|
| TBI | Patients aged 18-65 years with a diagnosis of severe TBI based on clinical or National Institute for Health and Care Excellence (NICE) criteria (post-traumatic imaging) | ||
| Non_TBI | Patients aged 18-65 years who had a traumatic injury without TBI |
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| Measure | Description | Time Frame |
|---|---|---|
| metabolomic analysis | Venous blood samples are taken from the participants after the injury. Samples will be analysed using LC/MS. All relevant metabolomes and their respective metabolic pathways will be evaluated using the "KEGG Pathway database". | Day 1 |
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Inclusion Criteria:
Exclusion Criteria:
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Trauma patients with or without TBI, aged between 18 and 65 years, who applied to Aksaray UniversityTraining and Research Hospital will be included in the study.
| Name | Role | Phone | Extension | |
|---|---|---|---|---|
| Hazal Ekin AYTUĞ, Consultant anesthesiologist | Contact | +905078448449 | drekinguran@gmail.com |
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| Facility | Status | City | State | ZIP | Country | Contacts |
|---|---|---|---|---|---|---|
| Aksaray University | Recruiting | Aksaray | Ankara | 06810 | Turkey (Türkiye) |
| PubMed Identifier | Type | Citation | Retractions |
|---|---|---|---|
| 37481590 | Result | Banoei MM, Lee CH, Hutchison J, Panenka W, Wellington C, Wishart DS, Winston BW; Canadian biobank, database for Traumatic Brain Injury (CanTBI) investigators, the Canadian Critical Care Translational Biology Group (CCCTBG), the Canadian Traumatic Brain Injury Research, Clinical Network (CTRC). Using metabolomics to predict severe traumatic brain injury outcome (GOSE) at 3 and 12 months. Crit Care. 2023 Jul 22;27(1):295. doi: 10.1186/s13054-023-04573-9. | |
| 38556884 |
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| ID | Term |
|---|---|
| D000070642 | Brain Injuries, Traumatic |
| ID | Term |
|---|---|
| D001930 | Brain Injuries |
| D001927 | Brain Diseases |
| D002493 | Central Nervous System Diseases |
| D009422 | Nervous System Diseases |
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venous blood sample for metabolomic analysis
| Result |
| Zhou M, Liu YW, He YH, Zhang JY, Guo H, Wang H, Ren JK, Su YX, Yang T, Li JB, He WH, Ma PJ, Mi MT, Dai SS. FOXO1 reshapes neutrophils to aggravate acute brain damage and promote late depression after traumatic brain injury. Mil Med Res. 2024 Mar 31;11(1):20. doi: 10.1186/s40779-024-00523-w. |
| 37845610 | Result | Fedoruk RP, Lee CH, Banoei MM, Winston BW. Metabolomics in severe traumatic brain injury: a scoping review. BMC Neurosci. 2023 Oct 16;24(1):54. doi: 10.1186/s12868-023-00824-1. |
| D006259 |
| Craniocerebral Trauma |
| D020196 | Trauma, Nervous System |
| D014947 | Wounds and Injuries |