Abstract
BackgroundFicolin-mediated activation of the lectin pathway of complement contributes to the complement-independent inflammatory processes of traumatic brain injury. Lower serum ficolin-3 levels have been demonstrated to be highly associated with unfavorable outcome after ischemic stroke. This prospective observatory study was designed to investigate the relationships between serum ficolin-3 levels and injury severity and clinical outcomes after severe traumatic brain injury.MethodsSerum ficolin-3 levels of 128 patients and 128 healthy controls were measured by sandwich immunoassays. An unfavorable outcome was defined as Glasgow Outcome Scale score of 1–3. Study endpoints included mortality at 1 week and 6 months and unfavorable outcome at 6 months after head trauma. Injury severity was assessed by Glasgow Coma Scale score. Multivariate logistic models were structured to evaluate the relationships between serum ficolin-3 levels and study endpoints and injury severity.ResultsCompared with the healthy controls, serum ficolin-3 levels on admission were statistically decreased in patients with severe traumatic brain injury. Serum ficolin-3 levels were independently correlated with Glasgow Coma Scale scores. Ficolin-3 was also identified as an independent prognostic predictor for 1-week mortality, 6-month mortality, and 6-month unfavorable outcome. Under receiver operating characteristics curves, ficolin-3 has similar prognostic predictive values for all study endpoints compared with Glasgow Coma Scale scores.ConclusionsIt was proposed that lower serum ficolin-3 levels, correlated with injury severity, had the potential to be the useful, complementary tool to predict short- or long-term clinical outcomes after severe traumatic brain injury.
Highlights
Ficolin-mediated activation of the lectin pathway of complement contributes to the complementindependent inflammatory processes of traumatic brain injury
In agreement with previous reported data regarding acute ischemic stroke and aneurysmal subarachnoid hemorrhage [41, 42], the decreased serum ficolin-3 levels were found within 6 h after Severe traumatic brain injury (STBI) in the current study
This study demonstrated that the decreased serum ficolin-3 levels were highly associated with trauma severity reflected by Glasgow Coma Scale (GCS) scores
Summary
Ficolin-mediated activation of the lectin pathway of complement contributes to the complementindependent inflammatory processes of traumatic brain injury. Lower serum ficolin-3 levels have been demonstrated to be highly associated with unfavorable outcome after ischemic stroke. This prospective observatory study was designed to investigate the relationships between serum ficolin-3 levels and injury severity and clinical outcomes after severe traumatic brain injury. Low Glasgow Coma Scale (GCS) scores are associated highly with poor clinical outcomes of STBI patients [7,8,9]. The C1 complex initiates the classical pathway upon recognition of immune complexes and dying host cells [19]. Various studies have revealed novel findings on the wide-ranging involvement of complement in neural development, synapse elimination, and maturation of neural networks, as well as the progression of pathology in a range of acute and chronic neurodegenerative disorders [23,24,25,26]
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