Disseminated intravascular coagulation (DIC) occurrence and coagulation profile appear to be associated with the cytogenetics and mutations in acute leukemia, according to results from a retrospective study published in Blood Cells, Molecules and Diseases.
Researchers analyzed the characteristics of coagulopathy in cytogenetically and molecularly distinct acute leukemias in 211 adult patients with de novo, nonacute promyelocytic leukemia (non-APL) acute myeloid leukemia (AML), 105 newly diagnosed patients with B-cell acute lymphoblastic leukemia (B-ALL), and 83 patients with APL AML. Occurrence of DIC was measured using criteria from the International Society of Thrombosis and Haemostasis (ISTH).
In patients diagnosed with DIC, signiﬁcant diﬀerences in distribution of ISTH DIC scores were found between those with APL AML and those with non-APL AML (P =.001), those with APL and those with B-ALL (P =.002), and those with non-APL AML and those with B-ALL (P =.009).
A normal karyotype with NPM1 mutations or FLT3-ITD mutations was independently associated with the development of DIC in non-APL AML, characterized by signiﬁcant prothrombin time prolongation and signiﬁcantly elevated D-dimer. The P210 BCR-ABL1 transcript was found to be a strong predictor of hypoﬁbrinogenemia in patients with B-ALL, according to multivariate analysis. However, the researchers also noted that the Philadelphia chromosome negatively aﬀected elevated D-dimer.
The inv(16) karyotype also emerged as a statistically significant predictor of DIC in multivariate analysis.
The researchers noted that severe hypoﬁbrinogenemia occurred in the absence of elevated D-dimer in some patients with B-ALL who were not diagnosed with DIC. In addition, the s210 BCR-ABL1 transcript was identified as a potential risk factor for bleeding, as it correlated with thrombocytopenia and hypoﬁbrinogenemia.
- Guoa Z, Chen X, Tan Y, Xu Z, Xu L. Coagulopathy in cytogenetically and molecularly distinct acute leukemias at diagnosis: Comprehensive study. Blood Cells Mol Dis. 2020;81:102393.