Angiopoietin-2, marker and mediator of endothelial activation with prognostic significance early after trauma?

MT Ganter, MJ Cohen, K Brohi, BB Chesebro… - Annals of …, 2008 - journals.lww.com
MT Ganter, MJ Cohen, K Brohi, BB Chesebro, KL Staudenmayer, P Rahn, SC Christiaans
Annals of surgery, 2008journals.lww.com
Objective: To measure plasma levels of angiopoietin-1 (Ang-1), angiopoietin-2 (Ang-2), and
vascular endothelial growth factor (VEGF) early after trauma and to determine their clinical
significance. Background: Angiopoietins and VEGF play a central role in the physiology and
pathophysiology of endothelial cells. Ang-2 has recently been shown to have pathogenetic
significance in sepsis and acute lung injury. Little is known about the role of angiopoietins
and VEGF early after trauma. Methods: Blood specimens from consecutive major trauma …
Objective:
To measure plasma levels of angiopoietin-1 (Ang-1), angiopoietin-2 (Ang-2), and vascular endothelial growth factor (VEGF) early after trauma and to determine their clinical significance.
Background:
Angiopoietins and VEGF play a central role in the physiology and pathophysiology of endothelial cells. Ang-2 has recently been shown to have pathogenetic significance in sepsis and acute lung injury. Little is known about the role of angiopoietins and VEGF early after trauma.
Methods:
Blood specimens from consecutive major trauma patients were obtained immediately upon arrival in the emergency department and plasma samples assayed for Ang-1, Ang-2, VEGF, markers of endothelial activation, protein C pathway, fibrinolytic system, and complement. Base deficit was used as a measure of tissue hypoperfusion. Data were collected prospectively.
Results:
Blood samples were obtained from 208 adult trauma patients within 30 minutes after injury before any significant fluid resuscitation. Plasma levels of Ang-2, but not Ang-1 and VEGF were increased and correlated independently with severity of injury and tissue hypoperfusion. Furthermore, plasma levels of Ang-2 correlated with markers of endothelial activation, coagulation abnormalities, and activation of the complement cascade and were associated with worse clinical outcome.
Conclusions:
Ang-2 is released early after trauma with the degree proportional to both injury severity and systemic hypoperfusion. High levels of Ang-2 were associated with an activated endothelium, coagulation abnormalities, complement activation, and worse clinical outcome. These data indicate that Ang-2 is a marker and possibly a direct mediator of endothelial activation and dysfunction after severe trauma.
Lippincott Williams & Wilkins