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    Acute Lymphoblastic Leukaemia

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    Princewill Seiyefa
    Acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML) are cancers of the blood and bone marrow characterized by uncontrolled proliferation of lymphoblasts or myeloblasts. ALL is more common in children while AML occurs mostly in adults. Treatment involves supportive care and intensive chemotherapy with the goal of achieving remission and preventing relapse through consolidation and maintenance therapies. Prognosis depends on specific genetic abnormalities, response to initial treatment, and patient age.

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    Acute Lymphoblastic Leukaemia

    Uploaded by

    Princewill Seiyefa
    28 views20 pages
    Acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML) are cancers of the blood and bone marrow characterized by uncontrolled proliferation of lymphoblasts or myeloblasts. ALL is more common in children while AML occurs mostly in adults. Treatment involves supportive care and intensive chemotherapy with the goal of achieving remission and preventing relapse through consolidation and maintenance therapies. Prognosis depends on specific genetic abnormalities, response to initial treatment, and patient age.

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    Acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML) are cancers of the blood and bone marrow characterized by uncontrolled proliferation of lymphoblasts or myeloblasts. ALL is more common in children while AML occurs mostly in adults. Treatment involves supportive care and intensive chemotherapy with the goal of achieving remission and preventing relapse through consolidation and maintenance therapies. Prognosis depends on specific genetic abnormalities, response to initial treatment, and patient age.

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    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    28 views20 pages

    Acute Lymphoblastic Leukaemia

    Uploaded by

    Princewill Seiyefa
    Acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML) are cancers of the blood and bone marrow characterized by uncontrolled proliferation of lymphoblasts or myeloblasts. ALL is more common in children while AML occurs mostly in adults. Treatment involves supportive care and intensive chemotherapy with the goal of achieving remission and preventing relapse through consolidation and maintenance therapies. Prognosis depends on specific genetic abnormalities, response to initial treatment, and patient age.

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    © All Rights Reserved
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    Download as pptx, pdf, or txt
    of 20

    Acute Lymphoblastic Leukaemia

    Prof. C.A. Nwauche


    Definition
    • Neoplastic-Acute Immunoproliferative
    disorder
    • Clonal expansion
    • Uncontrolled Proliferation and accumulation
    • Lymphobasts
    • Bone marrow and Peripheral blood
    Incidence
    • Common in children
    • Bi-peaked frequency-Early childhood (3-7 yrs)
    - Adults(>40 yrs)
    • Two Types
    B-ALL (85% with equal sex ratio)
    T-ALL (15% with male dominanace)
    Aetiology
    • Uncertain-Multi -factoral-Genetic (SNPs)
    - Environmental
    • Inherited-Downs Syndrome, Fanconi’s anaemia,
    • Chromosomal –Translocations, deletions,
    mutations, inversions, etc
    • Infections- Viral, Malaria, Bacteria
    • Environmental Chemicals, Drugs and toxins
    • Radiation
    Pathogenesis
    • Neoplastic clonal expansion
    • Accumulation of leukaemic blasts in the BM
    • “Crowding out” of normal haemoepoitic cells
    • Bone marrow failure-less normal cells
    • Loss of function- Red Cells: Anaemia
    - WBC: Recurrent infections
    - Platelets:Bleeding dyscrasias
    • Organ infiltration-Spleen, lymph nodes, Liver
    Classification
    • FAB classification-L1, L2 and L3.
    • WHO(Modified):
    • Based on specific genetic defects including
     Translocations t(9;22) or t(12;21);
     Rearrangement of the MLL gene,
     Alterations of the chromosome
    number(hyper or hypodiploidy)
    • 9 subtypes-8 B-ALL and 1 T-ALL
    Clinical Features
    • Acute illness-Sepsis, Heart failure, multiple blood
    transfusions, coma
    • Bone marrow failure:
     Anaemia( Weakness, pallor, dyspnoea)
     Leucopenia(febrile Illness, recurrent infections-mouth, throat,
    respiratory, skin, etc
     Thrombocytopenic bleeding disorders-Bleeding gums,
    Purpuras, spontaneous bruises, menorrhagia
    • Organ Infiltration-Splenomegaly, Hepatomegaly,
    Lymphadenopathy, bone pains, testicular swelling, meningeal
    syndrome, mediastinal compression
    Diagnosis
    • FBC-Anaemia, > N< WBC, Thrombocytopenia
    • Blood film- Leukaemic blasts
    • BMA - Hypercellular > 20% Leukaemic blasts
    • Morhphology: scanty cytoplasm with no granules
    • Cytochemistry: PAS Coarse block positivity
    • Immunophenotyping: B-ALL(CD19,22,79a,10,TdT)
    T-ALL(CD3,7,2,TdT)
    • Cytogenetic analysis-t(9;22), t(12;21), TEL-AML,)
    • Germ-line analysis: Abberant Immunoglobulin or T-cell
    receptor gene rearrangement
    Diagnosis II
    • Radiological: X-ray/Ultrasonography may
    reveal Mediastinal mass-Thymus or
    mediastinal nodes) and Lytic bone lesions
    • Lumbar puncture
    • Lymph node biopsy
    • Biochemistry: Uric acid, serum Lactate
    dehydrogenase, hypercalceamia
    • LFT and Renal FT
    Prognostic Index
    Good Bad
    • Race Non-Negroid Negroid
    • Age Child Adult(Infant<1 yr)
    • Time to remission Induction < 4 Wks > 4Wks
    • WBC Low High(> 50x10 9/L)
    • Sex Girls Boys
    • Cytogentics N or Hyperdip; TEL regt. PH+, MLL regt., Hypodip
    • Time to clear blasts from blood < 1Wk > 1 Wk
    • CNS disease at presentation Absent Present
    • Minimal residual disease NEG at 1-3Mths POS at 3-6 Mths
    Treatment
    • Supportive Treatment
    • Psychosocial support
    • Nursing care(Reverse barrier nursing)
    • Nutrition and Antiemetic support
    • Blood and blood products
    • Prophylaxis and treatment of infection
    • Tumour Lysis syndrome-Raised U/A, K+, Ph, Ca
    • Central Venous catheter insertion from skin tunnel to SVC-
    Drugs, blood products, Laboratory samples, IV feeding,
    etc
    Treatment II
    • Definitive
    • Baseline investigations-FBC, LFT, RFT, Radiology, Viral profile, Tissue typing
    • Combination Chemotherapy
    • Induction-Vincristine, Prednisolone, Asparaginase,
    Daunorubicin, Dexamethasone or (COAP-Locally)
    • Consolidation-Same drugs, Cytosine Arabinoside, Etoposide,
    Thioguanine,Mercaptopurine
    • POSSIBLE Stem Cell Transplantation
    • Cranial Prophylaxis- IT Methotrexate, High dose Methotrexate
    • Maintenance-Daily MPP, weekly Methotrexate; V+P
    • Late intensification(As Consolidation-Every 3 Months)
    • Prolonged maintenance :2( yrs (Girls) or 3 yrs (Boys)
    Acute Myeloid Leukaemia
    • Typical Myeloid Immunophenotype:
    • CD13+
    • CD33+
    • CD117+
    • TdT-
    Classification of AML
    (WHO, 2008)Modified
    • AML with recurrent genetic abnormalities.
    • AMLK with Myelodysplasia-related changes.
    • Therapy-related myeloid neoplasms(t-AML).
    • Myeloid Sarcoma
    Incidence
    • More common in adults.

    • Minor fraction of leukaemias in children(10-15.

    • Cytogenetic abnormalities are common and


    influence prognosis and treatment.
    Clinical Features
    • Features of Bone marrow failure:
    • Infections-frequent.
    • Anaemia
    • Thrombocytopenia.
    • Promyelocytic AML-bleeding tendency with
    DIC.
    • Tissue infiltration by tumour cells-Gum
    hypertrophy, skin infiltrations, CNS disease.
    Investigations
    • Specialized tests include:
    • Cytochemistry-Myeloperoxidase, Sudan black,
    Non-specific esterase.
    • Immunological markers-CD13, CD33,CD117;
    Glycophorin; Platelet antigens(e.g. CD 41);
    Myeloperoxidase.
    • Chromosomal and genetic analysis.
    Prognostic factors in AML I
    Good Bad
    • Cytogentics: t(15;17) Deletions of Chrom. 5 or 7
    t(8;21) abnormal (3q)
    inv(16) t(6;11)
    NPM mutation t(10;11)
    CEBPA mutation t(9;22)
    complex rearrangements
    FLT3 internal tandem repeats
    Prognostic factors in AML II
    • Bone marrow response <5% blasts after 1st course >20% blasts after 1st course
    to remission induction

    • Age >60 years


    Treatment
    • General supportive treatment- Bone marrow failure features.
    • Specific Therapy:
    • Aim-Induce complete remission
    Consolidation with intensive chemotherapy
    Stem cell transplantation-poor prognosis/relapse patients
    • Maintenance treatment-no value except promyelocytic AML.
    • CNS treatment-not usually given.
    • New drugs-FLT3 inhibitors.
    • ATRA-Promyelocytic AML
    • Haemorrhagic complications-DIC

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