Immune-mediated hemolytic anemia (IMHA) has a high mortality rate due to thrombosis. Cell-free DNA from hypoxia-induced cell death and neutrophil extracellular trap release may contribute to IMHA hypercoagulability because it activates clot formationand impairs fibrinolysis. Reduced endogenous DNase activity reported in human autoimmune diseases may impair cell-free DNA clearance. We hypothesized that cell-free DNA would be increased in dogs with IMHA, in part due to reduced DNase activity.
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