A comparative evaluation of assays for markers of activated coagulation and/or fibrinolysis: thrombin-antithrombin complex, D-dimer and fibrinogen/fibrin fragment E antigen.
Measurements were made of levels of D-dimer in plasma and serum, thrombin-antithrombin complex (TAT) in plasma and fibrinogen/fibrin fragment E antigen (FgE) in serum in a normal healthy control group and in patients with a range of disorders associated with hypercoagulability. Levels were determined in 31 normal healthy controls, 30 patients with disseminated intravascular coagulation (DIC), 21 patients with deep venous thrombosis (DVT), 27 patients with myocardial infarction (MI), 26 patients with acute leukaemia and 56 patients with liver disease. Considering all subjects, significant correlations were established between the results of all assays. Notably high correlations (r greater than 0.9) were established between plasma and serum levels of D-dimer, between plasma levels of D-dimer and serum levels of FgE, and between serum levels of D-dimer and FgE. All assays showed very high discrimination (sensitivity) between the normal control group and patients with DIC (97-100%), but there were marked differences between the assays in sensitivity for DVT and MI. In general, the FgE assay was more sensitive than the D-dimer assay, whilst both the FgE and D-dimer assays were more sensitive than the TAT assay. The same trends were apparent in the capability of the assays to discriminate between the normal control group and patients with acute leukaemia and liver disease: disorders with an unknown prevalence of activation of coagulation/fibrinolysis. Our results indicated that measurements of fibrinogen/fibrin degradation products (FDPs) in serum were almost unaffected by artefacts. The data further suggested that the broad-spectrum FgE assay was better than the more specific D-dimer assay in detecting clinical hypercoagulability. Our study showed that, in the clinical conditions examined, FDPs were more effective markers of hypercoagulability than TAT.
Boisclair
M D
MD
Department of Haematology, Charing Cross & Westminster Medical School, London.
Lane
D A
DA
Wilde
J T
JT
Ireland
H
H
Preston
F E
FE
Ofosu
F A
FA
D000208:Acute Disease; D000328:Adult; D000941:Antigens / Q000032:analysis; D000990:Antithrombin III / Q000032:analysis; D015415:Biomarkers / Q000097:blood*; D001778:Blood Coagulation Disorders / Q000175:diagnosis*; D001780:Blood Coagulation Tests / Q000379:methods*; D004211:Disseminated Intravascular Coagulation / Q000097:blood; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D005342:Fibrinolysis / Q000502:physiology*; D006801:Humans; D007938:Leukemia / Q000097:blood; D008107:Liver Diseases / Q000097:blood; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood; D010447:Peptide Hydrolases / Q000032:analysis; D013927:Thrombosis / Q000097:blood
D000941:Antigens; D015415:Biomarkers; D005338:Fibrin Fibrinogen Degradation Products; C046193:antithrombin III-protease complex; C036309:fibrin fragment D; C023456:fibrinogen-related antigen; D000990:Antithrombin III; D010447:Peptide Hydrolases