Coagulation disorders in liver diseasesK76,-

Since the liver is the synthesis organ of many coagulation parameters, disorders of the coagulation system occur in acute and chronic liver diseases. Both the factors of coagulation and anticoagulation are affected.

In the case of acute damage to the liver, e.g. fulminant hepatitis or intoxication (bulbous leaf fungus), a drop in factor VII is initially seen, as this has the shortest half-life.

In the case of chronic liver damage, there is a uniform decrease in practically all parameters with the exception of factor VIII, which is often elevated. There are disturbances in the liver cell metabolism, whereby sufficient coagulation factors are still produced quantitatively. However, these are associated with a significant reduction in activity.

In addition to the coagulatory factors, there is a reduction in the inhibitors of coagulation, such as antithrombin III, protein C, antiplasmin and plasminogen. Thus, in most cases there is a hemostatic balance between coagulation factors and coagulation inhibitors, with regard to function, however, at a significantly lower level. In the course of liver damage, systemic hypocoagulability often occurs, often with consumption reactions, since small disturbances, such as infections or bleeding, stimulate this equilibrium in the direction of the consumption reaction.
In addition to the quantitative reduction, the quality of the factors also changes, so that dysprothrombinaemia or dysfibrinogenaemia can occur, which leads to a disturbed polymerization of the alpha chains. At the same time, a factor XIII deficiency occurs, as a result of which the polymerisation of the fibrinogen cleavage products cannot be stabilised.
In chronic liver failure, the production of alpha-2-antiplasmin is disrupted, resulting in a reduction in the binding of alpha-2-antiplasmin to fibrin. As a result, the plasminogen is less inhibited and fibrinolysis gains the upper hand. In these disturbed control loops, there is an increase in t-PA and its activity, which further increases fibrinolysis. Subclinical consumption coagulopathy thus occurs, which can be recognised by an increase in fibrin cleavage products.
In addition to the disturbances of the plasma factors, there is also a disturbance of the platelet function. Thrombopenia occurs, especially in portal hypertension in liver cirrhosis due to increased platelet sequestration in the spleen. An important cause of a disturbance of platelet function is direct toxic disorders, e.g. caused by alcohol or drugs.