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A coagulation screen has been performed on 12 patients with acute liver failure. Six died and six recovered. All six fatal cases developed a haemorrhagic state with haemostatic failure. An attempt has been made to delineate the various mechanisms for the production of the coagulation defect. The significance of the different haematological parameters in assessing prognosis has been assessed. The study emphasizes the importance of the synthetic ability of the liver in determining survival prospects. A good correlation between the factor-VII level, which is a guide to liver synthesis, and recovery has been shown. The value of a specific factor-VII assay in acute liver failure appears considerable. Where this assay cannot be performed the clot opacity fibrinogen technique provides a reasonable guide to the prognosis. The presence or absence of DIC was not a determinant factor in survival in this series.

Although there have been isolated reports of an acquired abnormal fibrinogen in patients with liver disease, its frequency and clinical significance is not known. In this study 121 consecutive patients with a wide spectrum of hepatic disorders were screened for abnormal fibrin polymerization. A simple colorimetric method using Reptilase was employed. Of 32 patients with proven cirrhosis, 16 (50%) showed abnormal fibrin polymerization. The incidence in decompensated alcoholic cirrhosis was particularly high. The abnormality was also detected in all patients with acute liver failure and seven of 15 with chronic active liver disease. Clinical improvement often correlated with its disappearance. Two patients with primary liver cell tumours demonstrated the abnormal polymerization. In patients with bleeding oesophageal varices the detection of abnormal fibrin polymerization was associated with a poor prognosis. None of the patients with surgical obstructive jaundice (26) or miscellaneous liver disorders (37) had abnormal fibrin polymerization. The occurrence of abnormal fibrin polymerization in liver disease is more frequent than previously suspected and usually signifies severe primary hepatocellular dysfunction. Evidence is presented to support the presence of a primary abnormality of fibrinogen as the cause of impaired fibrin monomer polymerization.

SummaryThe clinical relevance of the e antigen-antibody system was investigated in 61 people persistently positive for hepatitis-B surface antigen, including 22 healthy carriers. The e antigen was not detectable in any of the healthy carriers, whereas it was found in 15 out of 28 patients with chronic aggressive hepatitis and two out of 11 with chronic persistent hepatitis. Its presence therefore indicates chronic liver disease but its absence does not exclude it. It may prove to be a particularly useful prognostic aid in chronic persistent hepatitis, since one of the two patients in whom it was found later developed aggressive hepatitis. In contrast, e antibody is of little diagnostic help, for, though it was found mostly in healthy carriers (18; 820 ), it was also detectable in 9 (230o) of the patients with chronic hepatitis.In 13 (76°' ) of the patients positive for e antigen Dane particles were seen on electron microscopy, but these were also present in 5 (19%) of the patients positive for e antibody. These findings are consistent with other evidence suggesting that e antigen is not a surface component of the Dane particle, but rather an independent soluble protein manufactured by the host in response to infection with the hepatitis-B virus.

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SYNOPSIS Factor VII levels have been measured in 100 patients with liver disease following parenteral vitamin K1 therapy. There was good agreement between specific factor VII measurements and the one-stage prothrombin time apart from six patients with compensated cirrhosis in whom the prothrombin time was prolonged despite the presence of normal factor VII levels. A mean activity of 58 % was found in patients with cirrhosis. Cirrhotic patients with features of hepatic decompensation had a significantly lower mean level of activity (40 %) than the 'contrast' patients with surgical obstruction of the major bile ducts (93 %). Patients with chronic active liver disease had moderate depression of factor VII levels and those with non-cirrhotic alcoholic liver damage had mean activities similar to the contrast group.Factor VII levels could not be correlated with BSP retention but there was a correlation with serum albumin concentration.It is concluded that the prothrombin time using the Quick test with a standardized thromboplastin showing good sensitivity to factor VII, eg, the Manchester reagent (BCT), provides a reliable index of coagulability in chronic liver disease, and specific factor VII assays are not indicated.The liver is the major site of synthesis of many clotting factors (Roberts and Cederbaum, 1972) and it is not unexpected that reduced levels of these have been reported in liver disease (Owren, 1949;Hallen and Nilsson, 1964;Donaldson et al, 1969).Biochemical tests of liver function have traditionally been used to assess and monitor the progress of patients with hepatic disorders. More recently, both broad-spectrum tests of blood clotting, ie, onestage prothrombin time and partial thromboplastin time and specific clotting factor measurements, particularly factor VII assays (Dymock et al, 1975), have proved of additional value in the diagnosis and assessment of liver disease. When measuring factor VII levels most workers have had to rely on combined assays such as the P and P test and Normotest (Hillenbrand and Sherlock, 1973;Henning and Yano, 1973) which are affected by deficiencies of other clotting factors, eg, factors II and X as well as factor VII. However, the availability of a naturally occurring factor VII deficient plasma in beagle dogs (Poller et al, 1971) has provided a standardized specific clotting factor VII assay. Its importance in accurately reflecting the state of hepatic function in