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

Read more

Summary

Introduction

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]

Methods
Results
Discussion
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call