Acute Leukaemia
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Direct answer
Auer rods in the cytoplasm of blasts prove acute myeloid leukaemia (AML) and exclude acute lymphoblastic leukaemia (ALL), where blasts instead stain positive for TdT and PAS. AML dominates in adults and is subtyped by defining genetics — t(8;21), inv(16), and above all t(15;17) in acute promyelocytic leukaemia, which is treated with all-trans retinoic acid (ATRA) and carries a DIC emergency at presentation. ALL is the commonest childhood malignancy, peaks at ages 2-5 years, and is cured in a high proportion of children with paediatric-inspired protocols.
What you must remember
- Diagnosis requires at least 20 per cent blasts in marrow or blood (WHO criterion; the 2022 classification allows lower counts with defining AML genetics).
- Auer rods = AML; they are azurophilic needle-shaped primary granule aggregates, classic in promyelocytic (M3) and myelomonoblastic types.
- t(15;17) PML-RARA: acute promyelocytic leukaemia presents with DIC and microangiopathic haemolysis; ATRA plus arsenic trioxide differentiates the promyelocytes and is curative without conventional chemotherapy in many patients.
- FAB favourites: M2 t(8;21) RUNX1-RUNX1T1; M4 eos t(16;16) or inv(16) CBFB-MYH11 with abnormal eosinophils; M5 monocytic with gum hypertrophy and skin infiltration (chloromas in M2/MS are granulocytic sarcomas).
- ALL blasts: TdT nuclear positivity, PAS block positivity, CD10 (common B-ALL); T-ALL presents as an anterior mediastinal mass with a high count in adolescent boys.
- Philadelphia chromosome-positive ALL (BCR-ABL1) carries the worst prognosis in children and mandates tyrosine kinase inhibitor addition.
- Tumour lysis syndrome: hyperkalaemia, hyperphosphataemia, hypocalcaemia and hyperuricaemia after treatment of high-burden disease (Burkitt-type ALL, AML M5); prevent with hydration and allopurinol or rasburicase.
- Classic smear clue: ALL in a child shows very high counts with mature neutrophils nearly absent ("gap"), no Auer rods, and lymphadenopathy with bone tenderness.
How to work through a suspected acute leukaemia
Picture a six-year-old with two weeks of fever, pallor and gum bleeding: total count 18,000 with 80 per cent blasts, haemoglobin 6 g per dL, platelets 20,000. Step one is morphology — look deliberately for Auer rods. None are seen, so myeloid lineage is not established by smear alone. Step two is cytochemistry: myeloperoxidase negativity and PAS block positivity with nuclear TdT on flow cytometry lock in B-lymphoblastic leukaemia, CD10 positive. Step three is risk assignment: age 1-9 years, count below 50,000, no CNS disease at presentation and favourable cytogenetics define standard risk, which carries the best outlook in all of paediatric oncology.
Now contrast a 38-year-old with pancytopenia and intractable bleeding from venepuncture sites. The smear shows hypergranular promyelocytes with bundles of Auer rods (faggot cells). This is APL: send coagulation profile immediately because DIC, not the blast count, kills these patients early. Start ATRA without waiting for genetic confirmation once morphology is suspicious, add arsenic trioxide, and transfuse platelets and cryoprecipitate to keep fibrinogen above 150 mg per dL. Confirm t(15;17) by RT-PCR; monitor PML-RARA transcript for minimal residual disease, since molecular relapse precedes haematological relapse by weeks.
For every acute leukaemia, the marrow report should give blast percentage, lineage by flow cytometry, and cytogenetics/molecular markers, because therapy is now risk-adapted rather than one-size-fits-all.
Where students slip
The recurring exam error is treating "blasts" as a diagnosis. Both leukaemias and the blast crisis of CML produce blasts; the discriminators are Auer rods, TdT, myeloperoxidase and the clinical setting. A second slip is calling every gum hypertrophy leukaemic: monocytic AML (M5) is the classical cause, but scurvy and drug reactions can mimic it — the marrow settles the issue. Third, candidates forget that the emergency in APL is coagulopathy, so the best answer to "first step in management" is ATRA with blood product support, not waiting for genetics. Finally, remember that chloroma (granulocytic sarcoma) can precede marrow disease and on biopsy may be misread as lymphoma unless myeloperoxidase staining is requested.
Frequently asked questions
What is the significance of Auer rods and in which leukaemia are faggot cells seen?
Auer rods prove myeloid differentiation and therefore AML; faggot cells — bundles of Auer rods — are characteristic of acute promyelocytic leukaemia, FAB M3.
Which acute leukaemia presents with DIC at onset, and what is the specific treatment?
Acute promyelocytic leukaemia with t(15;17); treatment is all-trans retinoic acid with arsenic trioxide, with aggressive platelet and cryoprecipitate support for the coagulopathy.
Which markers confirm B-lymphoblastic leukaemia?
Nuclear TdT positivity with CD10, CD19 and CD79a on flow cytometry, and block-type PAS positivity on cytochemistry.
Which AML subtype shows abnormal marrow eosinophils?
AML with inv(16) or t(16;16), the CBFB-MYH11 fusion, historically M4Eo, which has a relatively favourable prognosis.
Why does gum hypertrophy point to a specific FAB type?
Monocytic AML (M5) preferentially infiltrates gingival tissue, so gum hypertrophy with blasts should prompt myeloid rather than lymphoblastic work-up.
What laboratory tetrad defines tumour lysis syndrome?
Hyperkalaemia, hyperphosphataemia, hypocalcaemia and hyperuricaemia, occurring after rapid lysis of a high tumour burden.