Study of the formation of fibrin clot in cirrhotic patients. An approach to study of acquired dysfibrinogenemia
ABSTRACT Alterations in the coagulation system are common in patients with liver disease. We have examined the importance of the species and chains of fibrinogen in 3 groups of cirrhotic patients. The study of the gelation of fibrinogen in cirrhotic patients shows that the lag time increases in 80.3% of them and that the maximum gelation rate is altered in 51% of these plasmas. Also it is observed that 80% of the plasmas from cirrhotic patients have a percentage (23.3 ± 7.7%) of unpolymerized α chain, after highly cross-linked fibrin formation. These alterations, in lag time and in the maximum gelation rate, have no significant correlation with the situation of the fibrinolytic system in these patients.The study of isolated fibrinogen from cirrhotic patients and normal subjects plasma, shows that there are no objetive alterations in the percentage of fibrinogen species, the amount of sialic acid or the ratio of polypeptide chains.
- [Show abstract] [Hide abstract]
ABSTRACT: Prothrombin time-derived measurement of fibrinogen (PTd) has already been described. Activated partial thromboplastin time-derived measurement of fibrinogen (aPTTd) has not yet been clearly defined. Using an MDA II coagulometer (Organon Teknika, Durham, North Carolina, USA), we have therefore compared fibrinogen levels determined with Clauss, PTd, and aPTTd assays and an enzyme immunoassay (EIA) in 172 samples. Of these, 47 were from pre-operative controls, 18 from patients with liver disease, 28 from patients with hyperfibrinogenaemia, 33 from patients treated with vitamin K antagonists, 22 from patients treated with unfractionated heparin and 24 from haemophilic patients. Within the normal range, interassay and intra-assay variations were comparable. For control samples, PTd, aPTTd and Clauss assays were well correlated, without any systematic error. EIA was also correlated but values were slightly higher (mean of difference = 0.24). Pathological samples showed an overestimation of fibrinogen when using PTd measurements in patients treated with vitamin K antagonists, as well as when using aPTTd measurements in patients presenting with factor VIII and factor IX deficiencies. These results indicate that, despite expected financial savings, aPTTd fibrinogen measurements should not be used without restriction. PTd and aPTTd fibrinogen determinations are provided without any additional cost. Their comparison with Clauss fibrinogen results may constitute a validation tool or have additional diagnostic utility (e.g. identifying polymerization abnormalities in case of dissimilar results).Blood Coagulation and Fibrinolysis 02/2002; 13(1):61-8. · 1.25 Impact Factor
- [Show abstract] [Hide abstract]
ABSTRACT: Dysfibrinogenemia is a coagulation disorder caused by a variety of structural abnormalities in the fibrinogen molecule that result in abnormal fibrinogen function. It can be inherited or acquired. The inherited form is associated with increased risk of bleeding, thrombosis, or both in the same patient or family. Traditionally, dysfibrinogenemia is diagnosed by abnormal tests of fibrin clot formation; the thrombin time and reptilase time are the screening tests, and the fibrinogen clotting activity-antigen ratio is the confirmatory test. The inherited form is diagnosed by demonstrating similar laboratory test abnormalities in family members, and if necessary by analysis of the fibrinogen protein or fibrinogen genes in the patient. The acquired form is diagnosed by demonstrating abnormal liver function tests and by ruling out dysfibrinogenemia in family members. This article reviews the laboratory testing of dysfibrinogenemia and presents an algorithm for sequential test selection that can be used for diagnosis.Archives of pathology & laboratory medicine 05/2002; 126(4):499-505. · 2.78 Impact Factor