Synopsis
Recognise and classify adult acute lymphoblastic leukaemia, stabilise infection and tumour lysis, deliver lineage- and genotype-directed multi-phase therapy and use measurable residual disease to guide immunotherapy and transplantation.
- Suspect ALL with unexplained cytopenias, circulating blasts, bone pain, lymphadenopathy, hepatosplenomegaly, testicular symptoms or a mediastinal mass; total WBC may be low, normal or high.
- First-line confirmation is expert FBC and film followed urgently by marrow aspirate and trephine, multiparameter flow, cytogenetics or FISH and a comprehensive molecular panel.
- Determine B- versus T-lineage and urgently test BCR::ABL1 because Philadelphia-positive ALL requires a tyrosine kinase inhibitor integrated into the systemic protocol.
- Preserve diagnostic material before non-essential corticosteroids: even brief steroid exposure can reduce blasts, obscure immunophenotype and complicate risk stratification.
- Adult treatment is multi-phase: prephase when used, induction, consolidation or intensification, CNS-directed intrathecal therapy and prolonged maintenance, with exact drugs and timing set by UKALL or centre protocol.
- Measurable residual disease after induction and consolidation is the principal response measure and guides blinatumomab, allogeneic transplant and relapse-risk decisions.
- NICE now supports blinatumomab with chemotherapy at the start of consolidation for eligible adults with Philadelphia-negative, CD19-positive B-cell precursor ALL that is MRD negative.
- Blinatumomab is also commissioned for defined MRD-positive remission and relapsed or refractory B-ALL populations; monitor cytokine-release and neurological toxicity in a trained service.
- Relapsed B-ALL is re-phenotyped before commissioned antibody, TKI, cellular or transplant treatment is selected.
Key red flags
Fever, hypotension, confusion or hypoxia with neutropenia needs immediate broad-spectrum antibiotics; do not wait for leukaemia confirmation or a positive culture.
Orthopnoea, stridor, facial swelling, venous distension or inability to lie flat with an anterior mediastinal mass suggests airway or superior vena cava compromise and makes sedation hazardous.
Hyperkalaemia, hyperphosphataemia, hypocalcaemia, rising urate or creatinine before treatment suggests spontaneous tumour lysis and requires cardiac monitoring and metabolic intervention.
Headache, cranial neuropathy, vomiting, focal deficit, testicular enlargement or pain can represent sanctuary-site involvement and changes staging and treatment.
Cough, orthopnoea, facial swelling, stridor or inability to lie flat signals compressive anterior mediastinal disease and procedural risk.
Investigation priorities
Identify cytopenias, blast burden and an urgent acute-leukaemia pattern.
Management branches
Blasts, unexplained cytopenia, mediastinal mass or lymphoblastic tissue disease is found.
- Obtain blood and marrow flow, genetic and MRD-marker material before non-essential steroid exposure when physiology permits.
- Treat sepsis and lysis, assess airway and SVC compromise and use anaesthetic expertise before sedation or supine procedures.
- Classify B or T lineage, BCR::ABL1 and current risk genetics through the specialist MDT.