Low Serum Ficolin-3 Levels on Admission Are Associated With Poor Outcomes After Severe Traumatic Brain Injury

Complement activation is one of the pathological mechanisms that contribute to the secondary brain injury after traumatic brain injury. Ficolin-mediated lectin pathways of complement activation contribute to the pathogenesis of ischemic stroke and may be additive to complement-independent inflammatory processes. 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 relationship between serum ficolin-3 levels and 1-week mortality, 6-month mortality and 6-month unfavorable outcome (defined as Glasgow Outcome Scale score of 1-3) in patients with severe traumatic brain injury. This study recruited 128 patients and 128 sex- and age- matched healthy controls. Serum ficolin-3 levels on admission were measured by sandwich immunoassays. It was postulated that serum ficolin-3 levels were correlated with Glasgow Coma Scale scores and ficolin-3 was identified as an independent prognostic predictor for 1-week mortality, 6-month mortality and 6-month unfavorable outcome. Thus, it was proposed that lower serum ficolin-3 levels, correlated with injury severity reflected by Glasgow Outcome Scale scores, had the potential to be the useful, complementary tool to predict short- or long- term clinical outcome after severe traumatic brain injury.

Inclusion criteria

• Isolated head trauma
• Postresuscitation Glasgow Coma Scale score of 8 or less.

Exclusion criteria

• Less than 18 years of age
• Admission time > 6 hours
• Previous head trauma
• Neurological disease including ischemic or hemorrhagic stroke
• Use of antiplatelet or anticoagulant medication
• Diabetes mellitus
• Hypertension
• Presence of other prior systemic diseases including uremia, liver cirrhosis, malignancy, and chronic heart or lung disease