Leukaemias — Overview

This is a classification/comparison hub — see ALL, AML, CML, and CLL for full detail on each subtype.

A malignant condition in which immature leukocytes lose the ability to mature, abnormally proliferate, and don’t die — leading to progressive expansion of blast cells that replaces normal blood elements with malignant cells.

Leukaemia is classified as acute or chronic — by the percentage of blasts in peripheral blood/bone marrow, not just rate of onset — and by cell line: myeloid (granulocytes: neutrophils, eosinophils, basophils) or lymphoid (B-cells and T-cells). Acute leukaemias have greater than 20% blasts on peripheral smear or bone marrow; chronic leukaemias have less than 20% blasts and a more indolent course. A handful of favourable cytogenetic subtypes (e.g. t(15;17) PML-RARA, t(8;21), inv(16)) are treated as acute regardless of blast count.

The four most common types: acute myeloid leukaemia (33%), chronic lymphocytic leukaemia (35%), chronic myeloid leukaemia (14%), acute lymphoblastic leukaemia (10%), other (8%).

Myelodysplastic syndromes are bone marrow failure without a significant proportion of blast cells (< 20%) — around 40–60% of cases evolve into AML. See Myelodysplastic Syndrome.

Diagnostic workup

• FBC + peripheral blood smear — first-line; cytopenias, blasts, or Auer rods (AML) prompt urgent haematology referral.
• Bone marrow aspirate/biopsy — the gold standard for blast percentage, morphology, and cellularity.
• Flow cytometry (immunophenotyping) — identifies lineage (myeloid vs B-/T-lymphoid) and maturation stage from surface markers; also used to track measurable residual disease during treatment.
• Cytogenetics/molecular panel — Philadelphia chromosome (BCR-ABL1) and other translocations carry direct therapeutic and prognostic implications across subtypes.

Community management of chronic leukaemias

Oral targeted therapy (tyrosine kinase inhibitors for CML, BTK/BCL-2 inhibitors for CLL) has shifted most chronic leukaemia care from hospital-based chemotherapy to outpatient/community follow-up, giving GPs an ongoing role in monitoring and adherence support.

• Adherence matters directly to disease control — patients taking imatinib who are less than 85% adherent are over 17 times more likely to lose control of their disease; interruptions to ibrutinib similarly worsen progression-free survival in CLL.
• Drug interactions — all agents in this class are major CYP3A4 substrates; check for interacting drugs at every review.
• Cardiovascular risk — GPs support monitoring/management of smoking, hypertension, dyslipidaemia and obesity, which several TKIs and BTK inhibitors worsen.
• CLL without active/symptomatic disease (progressive cytopenias, unexplained fever, night sweats, weight loss, disabling lethargy) is watched without treatment — no survival benefit to early intervention.
• Contraception/fertility: TKIs and BTK/BCL-2 inhibitors are teratogenic (pregnancy category C/D); discuss with the treating haematologist before conception.

Comparison table

Feature	Acute lymphoblastic	Acute myeloid	Chronic lymphocytic	Chronic myeloid
Peak age of incidence	Childhood	Any age	Middle/old age	Adulthood
White cell count	High in 50%, normal/low in 50%	High in 60%, normal/low in 40%	High in 98%	High in 100%
Differential WCC	Many lymphoblasts	Many myeloblasts	Small lymphocytes	Entire myeloid series
Anaemia	Severe in >90%	Severe in >90%	Mild in ~50%	Mild in 80%
Platelets	Low in >80%	Low in >90%	Low in 20–30%	High in 60%, low in 10%
Lymphadenopathy	Common	Occasional	Common	Infrequent
Splenomegaly	60%	50%	Usual, moderate	Usual, severe
Other features	CNS involvement common without prophylaxis	CNS rarely involved; Auer rods sometimes seen	Occasional haemolytic anaemia, hypogammaglobulinaemia	Low leukocyte alkaline phosphatase; Philadelphia chromosome-positive in >90%