Published in Nature this paper offers an updated look at the pathophysiology of septic shock-DIC. From GTC's standpoint of view the most important portion of the paper implicated the involvement of certain dendridic lymphnoid cell in the conversion of mild sepsis into the malignant frequently fatal version. The dendridic cells posses surface receptor sites called PARs. PAR stands fo protease receptor site. The most important PAR is PAR1 which responds to thrombin. Thrombin generated either intra vascularly or extrinsically reacts with the dendrites' PAR1s to enhance the mobility of the dendrite enabling it to migrate out of the lymphnode and eventually enter the circulation. Thrombin also triggers (from the dendrite), the secretion of Sphingo 1 phosphate a complex lipid with many actions (few of them good for you)...which increases intravascular coagulation and inflamation and triggers multi systems organ failure.
This puts Thrombin at the scene of the crime and suggests a pathophysiological mechanism by which Atryn might block the process....