Acute Lymphoblastic Leukaemia in Adults
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Direct answer
Acute lymphoblastic leukaemia in adults is a clonal malignancy of lymphoid precursors, and it behaves more aggressively than the childhood form. Immunophenotype (B-lineage or T-lineage) and the Philadelphia chromosome t(9;22) shape the regimen. Ph-positive disease needs a tyrosine kinase inhibitor added to chemotherapy, and CNS-directed prophylaxis forms a core part of the plan for every patient.
What you must remember
- Lineage: B-lineage disease is the commoner type; CD19 and CD10 mark B-lineage, while cytoplasmic CD3 marks T-lineage, which often presents with a mediastinal mass.
- Philadelphia chromosome: t(9;22) produces the BCR-ABL1 fusion gene; it is found in a substantial minority of adults and carries a worse prognosis without targeted therapy.
- Induction: vincristine, corticosteroid, an anthracycline and asparaginase form the backbone, with intensity matched to risk group and the aim of complete remission.
- CNS prophylaxis: intrathecal methotrexate, cytarabine and hydrocortisone are given during induction and consolidation as per protocol, and cranial irradiation is now mainly reserved for selected high-risk cases.
- Ph-positive ALL: imatinib, dasatinib or ponatinib added to chemotherapy or reduced-intensity regimens; allogeneic transplant in first remission is considered for eligible patients.
- Intensive regimens: hyper-CVAD alternates cyclophosphamide, vincristine, doxorubicin and dexamethasone with methotrexate and cytarabine, and is suited to fit younger adults.
- Residual disease: measurable residual disease by flow cytometry or PCR after induction and consolidation guides whether further therapy or transplant is needed.
A risk-adapted pathway from diagnosis to consolidation
Treatment has to begin promptly, because hyperleucocytosis, cytopenias and tumour lysis can cause early death before induction is complete. The steps below follow the order in which a clinician makes decisions, and each one feeds the next.
- Confirm lineage and genetics. Flow cytometry fixes the lineage, and cytogenetics or BCR-ABL1 testing identifies Ph-positive disease, which changes the regimen.
- Assign risk. Age, white cell count at presentation, cytogenetic abnormalities and early response together place the patient in a risk group.
- Induce remission. Vincristine, a corticosteroid, an anthracycline and asparaginase form the backbone, with intensity chosen by risk and fitness.
- Protect the CNS. Intrathecal methotrexate, cytarabine and hydrocortisone are given according to protocol, not only when neurological symptoms appear.
- Add targeted therapy. A tyrosine kinase inhibitor is combined with the backbone for Ph-positive disease, and doses are adjusted for tolerability.
- Consolidate and monitor. Consolidation follows remission, and measurable residual disease results guide transplant or the choice of maintenance.
Where the exam tries to catch you
The questions reward the sequence of decisions, not isolated facts about single drugs.
- Trap: B-lineage and T-lineage disease are treated identically because both are lymphoid. Correct: lineage is fixed by flow cytometry and shapes the plan, and a T-ALL patient with a mediastinal mass needs urgent airway assessment before induction.
- Trap: Cranial irradiation is the default CNS prophylaxis. Correct: intrathecal chemotherapy has largely replaced it, with irradiation kept for selected high-risk or CNS-positive cases.
- Trap: Ph-positive ALL is managed as standard ALL with a longer course. Correct: adding a tyrosine kinase inhibitor is what changes the outcome, so the answer should name the drug class.
Treatment abandonment because of cost is a recognised problem in Indian leukaemia care, so a counselling and support plan belongs in the clinical answer.
Frequently asked questions
Which immunophenotype markers separate B-lineage from T-lineage acute lymphoblastic leukaemia?
Flow cytometry identifies B-lineage acute lymphoblastic leukaemia with CD19 and CD10, with CD20 expressed in some cases. Cytoplasmic CD3 identifies T-lineage acute lymphoblastic leukaemia, so lineage is confirmed before the regimen is chosen.
What is the treatment for Philadelphia chromosome positive acute lymphoblastic leukaemia?
Philadelphia chromosome positive acute lymphoblastic leukaemia is treated with a tyrosine kinase inhibitor such as imatinib, dasatinib or ponatinib added to chemotherapy or reduced-intensity regimens. Allogeneic transplant in first remission is considered for eligible patients.
Why is cranial irradiation avoided in adult acute lymphoblastic leukaemia?
Intrathecal methotrexate, cytarabine and hydrocortisone protect the central nervous system without the long-term cognitive burden of cranial irradiation. Irradiation is therefore kept for selected high-risk or CNS-positive adult cases.
What is hyper-CVAD and when is it used in adult acute lymphoblastic leukaemia?
Hyper-CVAD is an intensive alternating regimen of cyclophosphamide, vincristine, doxorubicin and dexamethasone with methotrexate and cytarabine. It suits fit younger adults, while older or frail patients usually receive reduced-intensity protocols.
What is measurable residual disease in acute lymphoblastic leukaemia?
Measurable residual disease is the small number of leukaemic cells that remain after treatment, detected by flow cytometry or molecular PCR when morphology looks normal. Its level after induction and consolidation guides decisions on transplant and further therapy.