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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Authors

Mirco Nacoti - Paediatric Intensive Care Unit, "Papa Giovanni XXIII" Hospital, Bergamo

Diego Cantù - Department of Perioperative Medicine and Intensive Care, "San Gerardo" Hospital, Monza

Daniele Bonacina - Paediatric Intensive Care Unit, "Papa Giovanni XXIII" Hospital, Bergamo

Federico Lussana - Haematology and Bone Marrow Transplant Unit, "Papa Giovanni XXIII" Hospital, Bergamo

Ezio Bonanomi - Paediatric Intensive Care Unit, "Papa Giovanni XXIII" Hospital, Bergamo

Marina Marchetti - Division of Immunohaematology and Transfusion Medicine and Haemostasis and Thrombosis Centre, "Papa Giovanni XXIII" Hospital, Bergamo, Italy

Anna Falanga - Division of Immunohaematology and Transfusion Medicine and Haemostasis and Thrombosis Centre, "Papa Giovanni XXIII" Hospital, Bergamo, Italy

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