Concurrent acute myeloid leukemia and chronic lymphocytic leukemia: A review and clinical insights.

Abstract

e18513 Background: Chronic lymphocytic leukemia (CLL) is the most common indolent lymphoproliferative neoplasm in older adults, frequently associated with immunoglobulin deficiencies and secondary solid tumors. Acute myeloid leukemia (AML), characterized by the rapid proliferation of myeloid blasts, is a distinct hematological malignancy with poor prognosis in elderly patients. The simultaneous occurrence of AML and CLL in a single patient is exceedingly rare and presents unique diagnostic and therapeutic challenges. Recent advancements in genomic and molecular diagnostics have led to an increased number of documented cases. This review aims to evaluate reported cases of concomitant AML and CLL, analyzing clinical features, diagnostic findings, treatment strategies, and outcomes. Methods: A systematic review was conducted using available literature to identify cases of concurrent AML and CLL. Cases were analyzed for demographic data, hematological parameters, cytogenetic and molecular findings, treatments administered, and outcomes. Data from 43 patients with coexisting AML and CLL were included for detailed analysis. Results: The mean age of patients at presentation was 70 years (range 38–82), with a male predominance (70%). Presenting symptoms included fatigue (34%), anemia (21%), and weight loss (14%), while 9% of patients were asymptomatic. Hematological parameters revealed mean hemoglobin levels of 11 g/dL, WBC counts of 40 × 10³/µL, and platelet counts of 30 × 10³/µL. Cytogenetic analysis showed diploid karyotypes in 48% of cases, with deletions of chromosomes 7, 13, and 12 also reported. Molecular findings, although limited, included mutations in, CEBPA ASXL1, TET2, STAG2, and other genes. Treatments varied, with AML patients predominantly receiving 3+7 induction chemotherapy (32%), while CLL treatments included bendamustine-rituximab-venetoclax (13%). Overall mortality was high, with 54% of patients succumbing to disease progression or complications. Long-term follow-up data were scarce, with only 2 patients documented beyond 12 months. Conclusions: The coexistence of AML and CLL is an uncommon but clinically significant phenomenon that is often associated with poor outcomes with more less than 50 % survival over 12 months. The overlapping yet distinct pathophysiology of these diseases suggests mechanisms such as clonal evolution, genetic mutations, and immune dysregulation may play a role. Effective management requires a multifaceted approach, addressing the aggressive nature of AML and the profound immunosuppression linked to CLL. Further research into the underlying mechanisms and treatment strategies is essential to improve outcomes for patients with this dual diagnosis.