Liver disease can be acute or chronic and can be accompanied by a severe loss of liver function. Ultimately, liver function can deteriorate to such an extent that a liver transplant will be required. The course of serious liver diseases is different for each individual because there are several factors that influence the speed of the disease process. This thesis focuses on the development of thrombosis, or a dangerous blood clot, as a complication of liver disease, but also as a factor that can contribute to the worsening of the disease. Thrombosis can develop anywhere in the body, but we now know that this can also happen in the liver itself. This can then lead to an accelerated disease process because the supply of oxygen and nutrients is cut off in the smaller liver blood vessels. Thrombosis within the liver is likely caused by damage to the liver and the inflammatory response resulting from this damage. The liver also produces many of the proteins involved in the development of thrombosis. The coagulation balance is disturbed in patients with liver disease and these changes in the blood coagulation system are likely to contribute to thrombosis in the liver. Liver failure thus appears to be able to accelerate itself through a tendency to develop thrombosis in the liver. However, we do not know exactly what changes in the coagulation system are behind this, in whom they will occur and, above all, what we can do about it. This thesis has helped unravel some of these mechanisms. We also describe how similar changes in the blood coagulation system can increase the risk of thrombosis in a number of other diseases and procedures, such as lung transplantation. We provide advice from which others can develop therapies. This could be, for example, a new anticoagulant therapy that can slow down the disease process by preventing thrombosis.