Table 2 Hemostatic characteristics and mechanisms between “DIC”/DIC and EA-VMTD-associated hepatic coagulopathy
Acute “DIC” (per current concept*) | EA-VMTD-associated hepatic coagulopathy | DIC of APL | |
|---|---|---|---|
Clinical settings | Critical illnesses (e.g., sepsis; trauma) | Critical illnesses (e.g., sepsis; trauma) | APL |
Thrombosis form | Claim to be fibrin clots* by some, but are microthrombi by pathology | Microthrombi | Fibrin clots |
Pathogenesis | Fibrinogenesis* | Microthrombogenesis | Fibrinogenesis |
Hemostatic path | TF path activation* | Lone activation of ULVWF path | Aberrant TF path activation |
Coagulation study | |||
Platelet count | Low | Often low | Low (due to leukemia) |
PT | Prolonged | Prolonged | Prolonged |
aPTT | Prolonged | Prolonged | Prolonged |
FVIII | Supposedly markedly ↓ (due to consumption) | Markedly ↑ (due to endothelial release) | Markedly ↓ (due to consumption) |
FV | Supposedly ↓ (due to consumption) | Moderately ↓ (due to live necrosis) | Decreased (due to consumption) |
FVII | Supposedly normal (because not consumed) | Markedly ↓ (due to liver disease) | Normal |
Fibrinogen | Supposedly ↓ (due to consumption) | Markedly ↑ (due to release in early liver damage) Markedly ↓ (due to liver failure in late stage) | Decreased (due to consumption) |
ULVWF/VWF | Supposedly normal (due to no participation) | Markedly ↑ (due to endothelial exocytosis) | Negative (due to no endotheliopathy) |
D-dimer/FDP | Positive (due to “fibrinolysis*”) | Positive (due to fibrinogenolysis in liver damage) | Positive (due to fibrinolysis) |
Clinical syndrome | Supposedly consumption coagulopathy*, but this disease with the above Lab findings does not exist in real patient. (Please see text for COVID-19 interpretation) | EA-VMTD (i.e., DIT) with hepatic coagulopathy | Consumption coagulopathy of APL |
Correct diagnosis | Does not exist, but it should be → → →→ | EA-VMTD with HC | True DIC (fibrin clot disease) |