Association ofabnormal fibrin polymerisation with severeliver disease

SUMMARY Thefrequent occurrenceofabnormal fibrin polymerisation inpatients withliver disease hasrecently beenreported. Toinvestigate this further, fibrin polymerisation wasstudied in68patients withcirrhosis orchronic active liver disease. Thirty-three ofthese patients demonstrated impairmentofthis phase ofblood coagulation. Whenother tests ofliver function werecompared inpatients demonstrating this abnormality andthose inwhomfibrin polymerisation was normal, itwas found thattheformer groupdemonstrated significantly reduced albumin concentrations (p< 0-0002), raised bilirubin andaspartate aminotransferase levels (p< 00006and< 0003respectively), andgreater prolongation oftheone-stage prothrombin time(p< 0-001) with more markedreduction infactor VIIlevels (p< 0002) compared withthelatter patients. Itisconcluded that defective fibrin polymerisation occurring inpatients withliver disease indicates thepresenceofseverely impaired hepatocellular function. Thismight account forthegraveprognosis reported incirrhotic patients withabnormal fibrin polymerisation whoalsosuffer bleeding fromgastro-oesophageal varices. Amongthemanyabnormalities ofblood coagulation inpatients withliver disease, delayed conversion offibrinogen tofibrin clot undertheinfluence of thrombin isacommonlaboratory finding. Evidence hasbeenpresented toimplicate a disturbance of fibrin polymerisation inthese patients asacauseof theprolonged thrombin time(VonFelten etal., 1969; Soria etal., 1970; Aiach etal., 1973; Barr etal., 1976; Greenetal., 1976a). Theincidence ofabnormal fibrin polymerisation hasbeenshowntobeashighas50%inadvanced cirrhosis, 47%inchronic liver disease, and100% inpatients withacuteliver failure (Green etal., 1975). This contrasts withits infrequency inobstructive jaundice andsecondary liver disease (Green etal., 1976a). Ithasalsobeenshownthathaemorrhage from