Genetic mutations and leukapheresis in acute myeloid leukemia: is there a link?

Acute myeloid leukemia is the most common acute leukemia in adults and up to 20% of patients present with hyperleukocytosis at the onset of the disease. The therapeutic approach involves medical support, cytoreductive treatment, and/or leukapheresis. Despite WBC count greater than 100.000/μL, not all patients develop symptoms. To clarify the role of leukapheresis in the setting of hyperleukocytotic AML, we aimed to find associations between AML morphologic subtypes and molecular alterations on presence or absence of leukostasis symptoms (and hence therapeutic vs prophylactic leukapheresis) and clinical outcomes in the cohort of 41 patients at our single center who underwent leukapheresis for hyperleukocytotic AML. There was a trend for increased WBC count, 30-day mortality, M4-M5 AML subtypes, and number of leukapheresis procedures performed in symptomatic hyperleukocytotic pts. No molecular marker was significantly associated with presence or absence of leukostasis symptoms due to small sample size, though there was a trend for increased NPM1-mutated and NPM1 + FLT3-mutated AML in asymptomatic patients and a greater proportion of symptomatic patients who were negative for all assessed molecular alterations. In conclusion, leukapheresis combined with cytoreductive treatment represents a synergic and efficient approach in the management of hyperleukocytosis especially in symptomatic patients considering the higher mortality independently from the presence of specific clonal markers whose distribution among the two groups may result more considerable with a higher number of patients.