Chapter 13: Acute Myeloid Leukaemia

Acute Myeloid Leukaemia malignant cells crowd the bone marrow and blood, leading to the failure of normal blood production, which clinically manifests as severe anaemia, life-threatening infections due to low white cell counts, and significant bleeding risks from a lack of platelets. Diagnosis is typically confirmed when blast cells represent at least twenty percent of the marrow or blood, though the presence of specific genetic abnormalities can confirm the disease even with lower counts. The classification of these disorders follows the World Health Organization guidelines, categorizing cases based on recurrent genetic mutations, associations with previous toxic therapies, and lineage-specific morphological features like monocytic or erythroid differentiation. Identifying the genomic landscape is essential, as mutations in genes like FLT3, NPM1, and DNMT3A, or chromosomal translocations such as the t(15;17) found in acute promyelocytic leukaemia, are primary determinants of both the treatment strategy and the patient's prognosis. Clinical investigations utilize advanced techniques including flow cytometry for immunophenotyping, cytogenetics for karyotype analysis, and molecular assays to detect minimal residual disease, which helps monitor treatment effectiveness. Standard medical management for fit individuals involves intensive induction chemotherapy—frequently the "3+7" regimen of daunorubicin and cytarabine—designed to achieve complete remission, followed by consolidation therapy or stem cell transplantation for those at higher risk of relapse. Special attention is paid to acute promyelocytic leukaemia, a subtype characterized by severe bleeding tendencies that is uniquely responsive to differentiation-inducing agents like all-trans retinoic acid and arsenic trioxide. While medical advancements have greatly improved the cure rates for younger patients, the disease remains a significant challenge for the elderly, who often face poorer outcomes due to co-morbidities and inherent disease resistance.