Nice find Hobgoblin.
After pulling the original, the key role of thrombin blockade (they use hirudin) in preventing DIC certainly gives us reason for hope, but I have yet to be convinced this will come as unalloyed good news for efficacy of ATIII in DIC.
The authors take great pains to point out that it is the EXTRAvascular lymphatic dendritic cells that they are indentifying as critical in the process of DIC/sepsis. They go on to point out that INTRAvascular medications will be less effective. The authors note in the original text, "The requirement to block thrombin in the lymphatics for antiinflammatory benefit may explain the limited clinical efficacy of intravenously administered plasma protease inhibitors, such as antithrombin3." The #3 they cite as the basis of this is a very weak paper, but the statement still stands out.
It is not perfectly clear to me why hirudin (admittedly a smaller protein than ATIII) would be effective while they postulate that ATIII would be less so. Perhaps hirudin (even given IV) is present in sufficient quantities in the lymphatic tissue (unlike AT3???) that it inhibits thrombin there where it will have greatest effect.
I'll be in touch with the authors, and pass along further information if it comes to light.
Best,
MTB
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