Fibrinogen measurement in liver disease: validation of the functional fibrinogen thromboelastography assay and a novel mathematical predictive model.

BACKGROUND: Fibrinogen is produced in the liver and tends to be reduced in liver cirrhosis. Quantitative and qualitative tests exist to measure fibrinogen. We aimed to validate the functional fibrinogen thromboelastography assay (FF-TEG) and propose a new model to estimate fibrinogen levels via the Clauss method (Clauss) using data from a prothrombin time-derived fibrinogen assay (PT-Fg) in patients with liver cirrhosis. MATERIALS AND METHODS: Clauss, PT-Fg, fibrinogen antigen (Fib-Ag) and FF-TEG were studied in 55 patients with liver cirrhosis (26 with Child-Turcotte-Pugh [CTP]-A disease, 14 with CTP-B and 15 CTP-C) and 20 healthy individuals. RESULTS: The results of all four assays correlated strongly with each other, but gave significantly different mean levels in all cohorts. PT-Fg gave the highest levels whereas the Clauss gave the lowest levels. The FF-TEG performed well with results which were in between the Clauss and the PT-Fg. Significant differences were only observed between CTP-A and CTP-C for the Clauss, PT-Fg and Fib-Ag but not functional fibrinogen level. We devised a simple linear regression model in order to estimate Clauss from the PT-Fg. DISCUSSION: The results of the FF-TEG correlate well with those of routine fibrinogen assays in patients with liver cirrhosis. However, the FF-TEG assay does not discriminate between early and late stages of disease, pointing to a preserved fibrin clot strength in cirrhosis. Through linear regression models, fibrinogen levels can be accurately estimated using the Clauss method based on fibrinogen levels obtained in the cheaper PT-Fg.

Flow cytometry and thromboelastography to assess platelet counts and coagulation in patients with haematological malignancies.

BACKGROUND: Accurate platelet counts (PC) are necessary in order to follow recommendations for prophylactic platelet transfusion. We carried out a study comparing the standard way of counting platelets using a routine analyser and compared it with PC determined by flow cytometry (FC) and haemostatic data obtained with thromboelastography (TEG). MATERIALS AND METHODS: The study was carried out on 24 patients with haematological malignancies, all given one adult dose of platelets. The PC was determined before and after transfusion using an automated blood cell counter and FC. Citrated, "native" whole blood TEG was carried out before and after platelet transfusion to assess global haemostasis. RESULTS: No bleeding was observed in any of the subjects. Thirty-one assessments were performed in the 24 patients. The mean pre-transfusion PC were 9.8 and 13×10(9)/L with the automated counter and FC, respectively with a difference of 3.7 (p=0.0011). Excellent correlation was observed between the two counts (r=0.89; p<0.0001). Mean post-transfusion increments were 23 and 29×10(9)/L for the routine counter and FC, respectively. Using the immunological PC, patients would not have qualified for transfusion in 18.2% of cases since their PC was >20×10(9)/L. TEG showed a shortened reaction time in 69.6% of cases and a normal mean K time of 6.7 min. Only 9% had a low α angle signifying hypocoagulability. The maximum amplitude was reduced in the majority of cases but normal in 25% despite PC<20×10(9)/L. Mean activated partial thromboplastin time, prothrombin time and fibrinogen were normal prior to transfusion. DISCUSSION: Although higher PC as assessed by FC could potentially have an impact on platelet transfusion practices, TEG was sensitive enough to detect PC<10×10(9)/L and some between 10-20×10(9)/L. Whether patients with the latter PC are more prone to bleeding remains to be verified in larger studies.