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Inhibition of fibrin monomer polymerisation by myeloma immunoglobulin
M J O'Kane1, G B Wisdom, Z R Desai
1Clinical Chemistry Laboratory, Belfast City Hospital, N Ireland.
Insights
This study found that a specific paraprotein in a patient with myelomatosis interfered with blood clot formation by inhibiting fibrin monomer polymerization. Treatment reduced the paraprotein, normalizing coagulation.
Area of Science:
- Hematology
- Oncology
- Biochemistry
Background:
- Multiple myeloma (myelomatosis) is a cancer of plasma cells.
- Patients with multiple myeloma can exhibit bleeding or clotting disorders.
- The role of specific paraproteins in coagulation abnormalities requires further investigation.
Observation:
- A 64-year-old man diagnosed with myelomatosis presented with abnormal blood clotting, including bulky clot formation and prolonged clotting times.
- Coagulation tests revealed significantly prolonged thrombin time, prothrombin time, and reptilase time.
- The patient's serum contained a high concentration of IgG lambda paraprotein.
Findings:
- The patient's plasma showed a reduced rate of fibrin monomer polymerization compared to controls.
- Purified paraprotein inhibited the polymerization of purified fibrin monomer in a dose-dependent manner.
- These findings indicate that the paraprotein directly interfered with fibrin formation by inhibiting polymerization.
Implications:
- Paraproteins in multiple myeloma can cause significant coagulation disturbances by directly impacting fibrin formation.
- Understanding these mechanisms is crucial for managing bleeding and thrombotic risks in myeloma patients.
- Successful chemotherapy led to decreased paraprotein levels and normalization of coagulation parameters, highlighting the reversibility of this complication.
Abstract:
Myelomatosis was diagnosed in a 64 year old man on the basis of a serum paraprotein band (type IgG lambda, 42 g/l), plasma cell infiltration of bone marrow, and multiple lytic lesions evident on skull x ray picture. Blood specimens taken into plain glass tubes showed bulky gelatinous clot formation with minimal clot retraction. Coagulation tests were significantly abnormal with an increase in thrombin time, prothrombin time, and reptilase time. The possibility that the paraprotein was interfering with fibrin production was investigated. The rate of fibrin monomer polymerisation (measured turbidometrically) was reduced in patient plasma compared with control plasma. Although purified fibrin monomer prepared from the patient's fibrinogen polymerised normally, the addition of purified paraprotein caused a dose dependent reduction in the rate of polymerisation. These results suggest that the paraprotein was impairing fibrin formation by inhibiting fibrin monomer polymerisation. After chemotherapy the paraprotein concentration decreased and the coagulation results returned to normal.
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