Abstract:
The liver is the main organ that synthesises blood coagulation factors. Damage to liver function in a normoxic environment will affect the synthesis of blood coagulation factors and cause bleeding and other diseases. Hypoxic environment (high altitude) and the presence and aggravation of underlying diseases (cardiogenic, pulmonary and blood system diseases) can cause hypoxia in liver tissue. Hypoxic liver disease is defined as the lack of blood supply to the liver (preload failure) or severe congestion (afterload failure), which causes ischemia, hypoxia and even necrosis of hepatocytes in the central area of the liver. In terms of liver-derived diseases, non-alcoholic fatty liver disease, alcoholic liver injury, liver fibrosis, cirrhosis, ischemia-reperfusion liver injury and other liver diseases all have liver tissue hypoxia. The common feature of these diseases is first manifested in the liver itself, and liver tissue hypoxia is caused by the imbalance of metabolic supply and demand. The body will experience changes in the level of coagulation factors under chronic hypoxia. For example, if residents in high-altitude areas live in a low-oxygen environment for a long time, the body will have compensatory changes in blood cell counts, such as increased levels of red blood cells and hemoglobin, resulting in thick and sticky blood; stagnation, thrombosis or microthrombus formation in a hypercoagulable state; prolongation of prothrombin time and partially activated prothrombin time; and abnormal expression of secondary partial coagulation factors. Thus, the blood coagulation function of patients with liver disease and whether liver-derived diseases will affect the expression of coagulation factors need to be determined. This article describes the mechanism of hypoxic liver injury in various liver-derived diseases and the changes in blood coagulation factors after hypoxic liver injury.
Key words:
Hypoxia /
Liver injury /
Mechanism /
Coagulation factors