Abstract
Introduction
In patients with chronic and acute liver disease and sepsis, the liver is exposed to a neutrophil-mediated injury and inflammation, which may lead to the release of endogenous heparinoids (e.g. heparan sulphate and dermatan sulphate) from the vascular endothelium into the blood stream1. These substances can cause a heparin-like effect (HLE) by inhibiting activated clotting factor Xa in blood and may, therefore, contribute to the coagulopathy and increased risk of bleeding in these patients2-5. In this regard, it is well known that the liver contains abundant parenchymal deposits of endogenous heparinoids, heparan sulphate being the predominant2,3. Additionally, in patients with acute liver failure, the ability to eliminate circulating HLE substances is likely to be greatly impaired due to the important reduction of liver function. Furthermore, during sepsis, mast cells can release HLE substances. [...]
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