Abstract
Despite improvements in critical care medicine and the development and aggressive
use of potent broad-spectrum anti-microbial agents, mortality due to severe sepsis
has not changed during the recent years and still comes to 35% to 45%.
For quite a long time our understanding of the pathophysiology of sepsis was mainly
focused on endotoxin and proinflammatory cytokines like tumor necrosis factor or interleukin-1.
Now it is generally accepted that many signs and symptoms of sepsis are not directly
mediated by cytokines but are transmitted through other mediator systems. The coagulation
system comes into play especially when the septic process progresses to malperfusion
and organ failure. Antithrombin III is an important inhibitor of the intrinsic, extrinsic
and common pathway of coagulation. Recently, evidence has been accumulating that there
is an additional anti-inflammatory potential of the drug. Currently there are several
clinical trials ongoing to investigate whether this effect is of clinical relevance
in the treatment of patients with severe sepsis.
Keywords:
Antithrombin (AT III) - severe sepsis - multiple organ failure - clinical trials -
DIC
