Early Complementopathy After Multiple Injuries in Humans
Burk AM et al. – The present data indicate an almost synchronical rapid activation and dysfunction of complement, suggesting a trauma–induced complementopathy early after injury. These events may participate in the impairment of the innate immune response observed after severe trauma.
In the present study, the authors hypothesized that multiple trauma results in immediate activation, consumption, and dysfunction of the complement cascade and that the resulting severe “complementopathy” may be associated with morbidity and mortality.
Therefore, a prospective multicenter study with 25 healthy volunteers and 40 polytrauma patients (mean injury severity score=30.3±2.9) was performed.
After polytrauma, serum was collected as early as possible at the scene, on admission to the emergency room (ER), and 4, 12, 24, 120, and 240h post-trauma and analyzed for the complement profile.
Complement hemolytic activity (CH-50) was massively reduced within the first 24h after injury, recovered only 5days after trauma, and discriminated between lethal and nonlethal 28-day outcome.
Serum levels of the complement activation products C3a and C5a were significantly elevated throughout the entire observation period and correlated with the severity of traumatic brain injury and survival.
The soluble terminal complement complex SC5b-9 and mannose-binding lectin showed a biphasic response after trauma.
Key fluid-phase inhibitors of complement, such as C4b-binding protein and factor I, were significantly diminished early after trauma.
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