The
hemostatic balance in patients with
liver diseases is relatively well preserved due to concomitant alterations in pro- and antihemostatic pathways.
Thrombin generation studies support the notion of
hemostatic competence in
liver diseases, but in such tests alterations in
fibrinogen level and function are not taken into account. We have recently studied structural and functional properties of the
fibrin clot in patients with
liver diseases. Although we have confirmed previous findings that hypersialylation of the
fibrinogen molecule in patients with
liver diseases contributes to a defective
fibrinogen-to-
fibrin conversion, we have found that once the clot has been formed, it has a thrombogenic nature as assessed by permeability assays. These thrombogenic properties of the
fibrin clot in
cirrhosis relate to incompletely characterized intrinsic changes in the
fibrinogen molecule, which may include oxidation and hypersialylation. In addition, in patients with
nonalcoholic fatty liver disease thrombogenic properties of the
fibrin clot are not only due to
liver disease but also to
obesity and the
metabolic syndrome. During
liver transplantation, the clot normalizes and becomes increasingly permeable, and the functional properties of the
fibrin clot are markedly normalized by
fibrinogen concentrate, when added to plasma samples in vitro. These new insights in the functional properties of the
fibrin clot in patients with
liver diseases facilitate a more rational approach to treatment and prevention of both
bleeding and thrombotic complications.