The Value of Factor VIII Levels in Acquired Hypofibrinogenemia

Abstract

Acquired hypofibrinogenemia can result from either severe hepatic disease or disseminated intravascular coagulation (DIC). Differentiation between these two entities in the laboratory can be difficult because of similar reductions in certain coagulation factors. In addition, both pathologic events may be present in the same patient. The purpose of this investigation was to study the coagulation mechanisms in 35 patients with acquired hypofibrinogenemia (< 150 mg. per 100 ml.). Of these, 14 had DIC, 18 had hepatic disorders, and three had combinations of hepatic disease and DIC. Similar reductions in Factors II and V were found in the DIC and hepatic-disease cases. Although the platelet counts and fibrin split products values (FSP’s) tended to be normal with hepatic disease, and abnormal with DIC, many patients had thrombocytopenia and/or elevated FSP’s for reasons other than DIC. Factor VIII levels were 404 ± 18 per cent with hepatic disease and 31 ± 14 per cent with DIC (normal range 50–150%), clearly different in the two groups. Since fibrinogen, Factor II and Factor V are synthesized by the liver and are consumed with DIC, the similar results are explainable. Factor VIII has been reported to be produced by the reticuloendothelial system, but more recent evidence suggests that the liver may play a major role in its synthesis. The data suggest that if the liver is involved in Factor VIII production it probably is not totally from the hepatocyte. The data show that Factor VIII levels can be used to distinguish DIC from hepatic disease in acquired hypofibrinogenemic states.