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Metabolism of fibrinogen in children with acute lymphoblastic leukaemia
Insights
Fibrinogen metabolism is altered in children with acute lymphoblastic leukemia (ALL), often indicating consumption due to disseminated intravascular coagulation during induction therapy. Accelerated synthesis may persist even in remission.
Area of Science:
- Hematology
- Oncology
- Biochemistry
Background:
- Acute lymphoblastic leukemia (ALL) is a common childhood cancer.
- Fibrinogen is a key protein in blood clotting.
- Understanding fibrinogen kinetics is crucial in managing leukemia complications.
Purpose of the Study:
- To investigate the metabolism and in vivo kinetics of fibrinogen in children with ALL.
- To differentiate fibrinogen turnover during induction therapy versus remission.
Main Methods:
- Utilized homologous 125I-labelled fibrinogen to study metabolism and kinetics.
- Analyzed plasma fibrinogen levels, pool, half-life, and catabolic rates.
- Assessed the effects of heparin and epsilon-aminocaproic acid on fibrinogen turnover.
Main Results:
- During induction therapy, elevated fibrinogen pools and shortened half-lives were observed, suggesting consumption via disseminated intravascular coagulation.
- Heparin administration corrected fibrinogen turnover, supporting the DIC hypothesis.
- In complete remission, fibrinogen levels were mostly normal, but accelerated synthesis was noted in some patients.
Conclusions:
- Fibrinogen consumption is a significant factor in children with ALL undergoing induction therapy.
- Accelerated fibrinogen synthesis may continue in some patients even after achieving remission.
- Further research is needed to elucidate the causes of accelerated fibrinogen synthesis in ALL remission.
Abstract:
The metabolism and in vivo kinetics of fibrinogen were studied using homologous 125I-labelled fibrinogen in 21 children with acute lymphoblastic leukaemia (ALL). Ten patients were undergoing induction therapy, 11 children were in complete remission on maintenance therapy. Results in the patients undergoing induction therapy were: plasma fibrinogen levels were normal in all except one patient, the plasma fibrinogen pool was elevated in six cases, seven patients had a shortened fibrinogen half-life and increased fractional catabolic rate for fibrinogen. The absolute catabolic rate for fibrinogen was elevated in six cases. This shortened fibrinogen half-life together with the correcting effect of heparinisation on the fibrinogen turnover indicated that fibrinogen was consumed by chronic disseminated intravascular coagulation. Inhibition of the fibrinolytic system with epsilon-aminocaproic acid in five patients had no influence on the fibrinogen half-life in three of them but resulted in its prolongation in two patients. All except two children in complete remission had normal fibrinogen levels. Six patients had elevated plasma fibrinogen pools and in all of the cases survival and fractional catabolic rate of fibrinogen were normal. The absolute catabolic rate for fibrinogen was normal in eight, elevated in three of the patients. This observation indicates that fibrinogen synthesis remains accelerated in some cases of ALL in complete remission, but the cause of this is not known.