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Defective fibrin crosslinking in acute leukemia
Thrombosis and Haemostasis
|December 29, 1984
Summary
Fibrin crosslinking is often impaired in acute leukemia patients, even with normal Factor XIII levels. This suggests other factors beyond Factor XIII deficiency contribute to coagulation abnormalities in leukemia.
Area of Science:
- Hematology
- Coagulation Science
- Oncology
Background:
- Acute leukemia frequently presents with secondary coagulation abnormalities.
- Fibrin crosslinking is a critical step in hemostasis, ensuring clot stability.
- Factor XIII (FXIII) plays a key role in fibrin stabilization.
Purpose of the Study:
- To investigate fibrin crosslinking patterns in patients with acute leukemia.
- To assess the correlation between Factor XIII activity and fibrin crosslinking.
- To identify potential causes of impaired fibrin crosslinking in acute leukemia.
Main Methods:
- Assay of fibrin crosslinking in 22 acute leukemia patients.
- Evaluation of alpha- and gamma-chain polymerization.
- Correlation analysis of transamidating activity of Factor XIII with fibrin crosslinking patterns.
Main Results:
- Fibrin crosslinking was normal in 9 patients.
- Impaired polymerization of alpha-chains was observed in 10 patients.
- Impaired polymerization of both alpha- and gamma-chains occurred in 3 patients.
- A weak correlation was found between Factor XIII activity and fibrin crosslinking.
- Incomplete fibrin crosslinking occurred at FXIII levels exceeding those needed for normal plasma.
Conclusions:
- Fibrin crosslinking abnormalities are common in acute leukemia.
- Factor XIII deficiency alone does not fully explain impaired fibrin crosslinking.
- Other unidentified factors likely contribute to fibrin crosslinking defects in acute leukemia.
- Further research is needed to elucidate the mechanisms behind these defects.