[Pathogenesis and laboratory diagnosis of venous thrombosis]

Due to the increasing number of elderly as well as chronically-ill patients, venous thrombosis assumes an increasing role as a typical complication of many courses of disease. Postoperatively, in patients without anticoagulation, fibrinogen tests show venous thrombosis in the lower extremities in up to 50% but not all were clinically relevant. Prophylactic treatment has markedly lowered the manifestation of deep venous thrombosis. Nevertheless, in current epidemiologic studies, the prevalence of thrombotic disease is three-fold higher (1:7,500) than that of bleeding diseases (1:20,000).

Congenital deficiency or congenital dysfunction of inhibitors of activated clotting factors have provided insight into the functional principles of limited proteolysis. Unequivocal causes of recurrent thrombosis are deficiency or dysfunction of AT III, protein C, protein S or plasminogen (Figure 1). Dysfibrinogenemia, in about 10% of the patients, leads to a tendency to thrombosis. Unclarified remains the relevance of lowered values for factor XII, heparin-cofactor II (HC II) and histidine-rich glycoprotein (HRG) (Table 1). Congenital disorders usually manifest themselves in the early adulthood. For the clinical manifestation of venous thrombosis, imbalance between pro-coagulatory and inhibitor factors are of importance, therefore the compensatory capabilities of other protease inhibitors, for example, alpha-2-macroglobulin should be taken into consideration. In acquired lowering of hemostasis factors, the balance in the plasma protein cascade should be assessed (Figure 1).(ABSTRACT TRUNCATED AT 250 WORDS)