Bleeding and Coagulation Abnormalities in Alcoholic Cirrhotic Liver Disease

Abstract

Coagulation profiles were performed in 30 consecutive alcoholic cirrhotic patients without known infection, malignancy, recent surgery, transfusion or alcoholic intake. Hemorrhagic phenomena were present in 70% and included gastrointestinal bleeding, oozing from venipuncture sites, bruising and epistaxis. All 30 patients had multiple liver function and coagulation abnormalities, the most frequent of which were increases in F [factor] VIII components and decreases in F XI and F VII. Also decreased in .gtoreq. 1/2 of the 30 patients were Fletcher F, F II, F X, prothrombin time (PT), partial thromboplastin time (APTT), thrombin time (TT), reptilase time (RT), antithrombin III and plasminogen. When comparing cirrhotic bleeders with nonbleeders, 4 parameters were significantly different in those with a bleeding tendency: F VII, antithrombin III, plasminogen and albumin. The prolonged APTT was associated in 4 cases with a blocking inhibitor of unknown etiology. The prolonged TT and RT, in the absence of fibrin split products, fibrin monomers, DIC [disseminated intravascular coagulation] or shortened euglobulin lysis time in any patient were suggestive of an abnormal fibrinogen, a dysfibrinogen. In 3 other patients, there was an inhibitor of the TT. Further investigation of the suspected dysfibrinogen in 21 patients by SDS[sodium dodecyl sulfate]-polyacrylamide gel electrophoresis revealed that the MW of the A.alpha., B.beta. and .gamma. polypeptide chains of fibrinogen were not different from normal. Two-dimensional immunoelectrophoresis of the suspected dysfibrinogen was similar to normal in 18 of 21 patients, with loss of the initial shoulder in 3.