Haemostatic abnormalities in patients with liver disease associated with viral hepatitis.

Clinical and laboratory findings were studied in 56 patients with liver disease (10 acute hepatitis, 10 fulminant hepatitis and 36 cirrhosis). Spontaneous bleeding occurred in 19 patients (8 fulminant hepatitis, 11 cirrhosis) and another 8 cirrhotic patients had variceal bleeding. There were 22 deaths (36%), 12 of these patients had spontaneous bleeding. Depletion of antithrombin III (AT III) occurred in fulminant hepatitis (mean +/- S.D. = 27 +/- 16%) and cirrhosis (49 +/- 23%) but thrombin-antithrombin III complexes (TAT) were significantly higher in the former (45 +/- 22 vs 8.6 +/- 7.0 ng/ml; p = 0.006). Within subgroups of cirrhosis (with or without spontaneous bleeding or with variceal bleeding), there were no significant differences in levels of AT III or TAT. Of all patients, those with spontaneous bleeding had persistently lower AT III levels but had variable changes of other coagulation parameters (PT, PTT, TT, FDP, fibrinogen and platelet counts). This study showed that coagulopathic consumption is an important cause of AT III deficiency in fulminant hepatitis but not in cirrhosis. Serial changes in AT III levels correlated with bleeding risk in patients with liver disease.