Acquired Dysfibrinogenemia Secondary to Multiple Myeloma

Institute of Hematology and Blood Transfusion, Praha, Czech Republic.
Acta Haematologica (Impact Factor: 1.12). 11/2008; 120(2):75-81. DOI: 10.1159/000160182
Source: PubMed


Abnormal coagulation properties indicative of a dysfibrinogen were found in the plasma of a 72-year-old male with multiple myeloma (IgGkappa, stage IIIA). The patient had high paraprotein concentration (85.75 g/l) and prolonged thrombin time (76.8 s), activated partial thromboplastin time (39.5 s), prothrombin time (23.5 s) and reptilase time (72.0 s). The fibrinogen level was increased. The fibrin polymerization induced by both thrombin and reptilase was impaired. Scanning electron microscopy revealed abnormal clot morphology. After six months of treatment, the paraprotein level decreased (19.48 g/l) and coagulation normalized as well as fibrin polymerization and fibrin clot morphology. It was found that the paraprotein interacts with the gamma-chain of fibrinogen. Acquired dysfibrinogenemia associated with multiple myeloma was diagnosed in the 72-year-old patient.

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    • "M-protein free light chains and heavy chains do not inhibit polymerization (Coleman et al, 1972; Teng et al, 2007). Some M-proteins show specificity for fibrin gamma chain, although convincing evidence of autoantibody specificity is lacking (Kotlin et al, 2008). Rarely, symptomatic acquired coagulopathies are due to M-protein autoantibody behaviour targeting specific proteins including thrombin (Colwell et al, 1997), and factor VIII (FVIII) (Liebman, 2000). "
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