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Early Complementopathy After Multiple Injuries in Humans.

Burk, Anne-Maud; Martin, Myriam LU ; Flierl, Michael A; Rittirsch, Daniel; Helm, Matthias; Lampl, Lorenz; Bruckner, Uwe; Stahl, Gregory L; Blom, Anna LU and Perl, Mario, et al. (2012) In Shock 37(4). p.348-354
Abstract
ABSTRACT: After severe tissue injury, innate immunity mounts a robust systemic inflammatory response. However, little is known about the immediate impact of multiple trauma on early complement function in humans. In the present study we 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 [ISS] = 30.3 ± 2.9) was performed. After polytrauma serum was collected as early as possible at the scene, upon admission to the emergency room and 4, 12, 24, 120 and 240... (More)
ABSTRACT: After severe tissue injury, innate immunity mounts a robust systemic inflammatory response. However, little is known about the immediate impact of multiple trauma on early complement function in humans. In the present study we 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 [ISS] = 30.3 ± 2.9) was performed. After polytrauma serum was collected as early as possible at the scene, upon admission to the emergency room and 4, 12, 24, 120 and 240 hours post trauma and analysed for the complement profile. Complement hemolytic activity (CH-50) was massively reduced within the first 24 h after injury, recovered only 5 days after trauma and discriminated between lethal and non-lethal 28-day outcome. Serum levels of the complement activation products C3a and C5a were significantly elevated throughout the entire observation period and correlatedwith the severity of traumatic brain injury and survival. The soluble terminal complement complex SC5b-9 and mannose-binding lectin (MBL) showed a biphasic response after trauma. Key fluid phase inhibitors of complement, such as C4b-binding protein (C4BP) and factor I, were significantly diminished early after trauma.The present data indicate an almost synchronically rapid activation and dysfunction of complement suggesting a trauma-induced "complementopathy" early after injury. These events may participate to the impairment of the innate immune response observed after severe trauma. (Less)
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Contribution to journal
publication status
published
subject
in
Shock
volume
37
issue
4
pages
348 - 354
publisher
BioMedical Press
external identifiers
  • wos:000301681400003
  • pmid:22258234
  • scopus:84858799356
ISSN
1540-0514
DOI
10.1097/SHK.0b013e3182471795
language
English
LU publication?
yes
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27dc59fd-d0bf-463d-a0ed-26d0b1256c06 (old id 2336216)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/22258234?dopt=Abstract
date added to LUP
2012-02-01 22:00:43
date last changed
2017-11-19 04:18:10
@article{27dc59fd-d0bf-463d-a0ed-26d0b1256c06,
  abstract     = {ABSTRACT: After severe tissue injury, innate immunity mounts a robust systemic inflammatory response. However, little is known about the immediate impact of multiple trauma on early complement function in humans. In the present study we 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 [ISS] = 30.3 ± 2.9) was performed. After polytrauma serum was collected as early as possible at the scene, upon admission to the emergency room and 4, 12, 24, 120 and 240 hours post trauma and analysed for the complement profile. Complement hemolytic activity (CH-50) was massively reduced within the first 24 h after injury, recovered only 5 days after trauma and discriminated between lethal and non-lethal 28-day outcome. Serum levels of the complement activation products C3a and C5a were significantly elevated throughout the entire observation period and correlatedwith the severity of traumatic brain injury and survival. The soluble terminal complement complex SC5b-9 and mannose-binding lectin (MBL) showed a biphasic response after trauma. Key fluid phase inhibitors of complement, such as C4b-binding protein (C4BP) and factor I, were significantly diminished early after trauma.The present data indicate an almost synchronically rapid activation and dysfunction of complement suggesting a trauma-induced "complementopathy" early after injury. These events may participate to the impairment of the innate immune response observed after severe trauma.},
  author       = {Burk, Anne-Maud and Martin, Myriam and Flierl, Michael A and Rittirsch, Daniel and Helm, Matthias and Lampl, Lorenz and Bruckner, Uwe and Stahl, Gregory L and Blom, Anna and Perl, Mario and Gebhard, Florian and Huber-Lang, Markus},
  issn         = {1540-0514},
  language     = {eng},
  number       = {4},
  pages        = {348--354},
  publisher    = {BioMedical Press},
  series       = {Shock},
  title        = {Early Complementopathy After Multiple Injuries in Humans.},
  url          = {http://dx.doi.org/10.1097/SHK.0b013e3182471795},
  volume       = {37},
  year         = {2012},
}