It is defined patholo gically as blast cells leukemia or
malignancy of immature hemopoeitic cells.
Bone marrow shows more than 30% blast cells.
They are classified into two types; acute myeloblastic
leukemia (AML) an d acute lymphoblastic leukemia
The different types of blast cells are recognized by:
2. Cytochemical stain.
3. Immunological markers (MC antibodies).
5. Molecular biology techniques.
6. Rarely electron microscopy.
** In c hildhood le uke mia (age less than 15 years), ALLconstitute s 80% of them; while in adulthood leukemia
(age more than 15 years), AML constitute s 80% of them.
Causes of acute leukemia:Mostly unknown; but a number of environmental
agents have been implicated as induc ers of certain
types of leukemia, e.g.:
1. Ionizing radiation: Atomic bomb explosion in
2. Chemical carcinogens: Benzene in shoes factory
and alkylating agents used to treat other
3. Genetic disorders: Down syndrome and Fanconi's
4. Acquired disorders: Myelodysplastic syndrome,
aplastic anemia, chemotherapy and radiotherapy.
5. Chromosomal and oncogen abnormalities.
F.A.B. (French. American. British) classification :It is an international classification of acute leukemias
according to morphology and cytochemistry.
ALL is classified into:
L1: small blast cells.
L2: intermediate size blast cells.
L3: Large size blasts with cytoplasmic vaculations
AML is classified into:
M0 : undifferentiated myeloblasts (need cell ma rker).
M1: Differentiated myeloblasts without maturation.
M2: Differentiated myeloblasts with maturation.
M3: Hypergranular promyelocytic.
M3 -variant: Micro - or hypo -granular bi -lobed
M4: Myelo -monocytic with both granulocytic and
M5: M5a (Monoblastic) and M5b (Promonocytic
M6: Erythroblastic (erythroblasts more than 50% while
blasts either more or less than 30%).
M7: Me gakaryoblastic (need cell marker).
** There is another less popular but more preciseclassification called M.I.C. (morphology. Immunology.
Clinical features:1. Features of bone marrow failure due to infiltration
by leukemia cells (blasts):
Bleeding tendency (thrombocytopenia or DIC
as in M3).
3. Bone & joint pain (more in ALL).4. Hepatosplenomegally (more in ALL).
5. Lymphadenopathy (more in ALL, M4 and M5).
6. Mediastinal masses (as in T cell -ALL).
7. Extra -medullary disease: skin lesions and gum
swelling (as in M4 and M5).
8. Chloroma (granulocytic sarc oma: a localized tumor
of blast cells).
9. Hyperleukocytic syndrome: In 5% of AML patients,
the WBC count exceeds 100 ×10 9/L and this leads
to leukostasis and endothelial damage (It affects
respiratory and central nervous systems).
Diagnosis1. History and phys ical examination.
2. Peripheral blood film: Mostly anemia &
thrombocytopenia, in 50% leukocytosis and less
frequently leucopenia or normal WBC count. Blast
cells may be seen.
** Aleukemic leukemia: No blasts are seen in
3. Bone marrow: Hyperce llular marrow due to diffuse
blast cells infiltration with suppression of normal
4. Biochemical changes: Hyper uricemia (increased
serum uric acid from increased cell turnover),
hypercalcemia, hyperphosphatemia, hypo - or
hyperkalemia and hyponatremia (due to
antidiuretic hormone release).
TreatmentCombinations of chemotherapy.
Chronic lymphocytic leukemia (CLL)It is a malignant proliferation of mature lymphocytes.
CLL can be distinguished from ALL by:
Cell morphology and degree of maturation: In ALL
cells are blasts which are immunologically
CLL affects mainly adults (older than 30 years);
whereas ALL affects mainly children and young
Clinical features1. Asymptomatic in 30% diagnosed during routine
blood examinatio ns.
2. Symmetrical painless lymphadenopathy: Cervical,
axillary and inguinal.
4. non specific systemic features, e.g. fever, sweating
or weight loss.
5. Infection, e.g. severe chest infection (pneumonia).
6. Splenomegally in about 50% of cases and
hepatomegall y is less frequent.
Investigations1. Peripheral blood film: persistent lymphocytosis 5 -
10 ×10 9/L, prolymphocytes less than 10% and
smear cells (smudge cells) correlating with degree
2. Anemia & thrombocytopenia: Both are important in
prognos is and staging.
3. Bone marrow: At least 40% lymphocytic infiltration,
also see pattern of infiltration whether diffuse, focal
4. Others: Hyperuricemia, auto -immune hemolytic
anemia and hypogammaglobulinemia.
Chronic myeloid leukemia (CML) It i s a clonal disease resulted from an acquired
genetic change in hemopoeitic stem cells.
This change alters stem cells proliferation and
generates population of differentiated cells
that gradually replace normal hemopoeitic
tissue and lead to greatly expande d total
At time of diagnosis; majority of patients have
Splenomegally, leukocytosis and Philadelphia
chromosome which is a translocation
chromosome (9:22) found in 92% of patients.
Median age of onset is 40 -50 years.
The incidence is slightly higher in males than
CML characterizes by three phases; chronic,
accelerated and blastic phases. The ir criteria
1. Chronic phase: blast cells are less than 12% in
blood & bone marrow.
2. Accelerated phase:
Increasing spleen size.
Increasing leuko cytes count despite
Short leukocytes doubling time.
Blast cells more than 5% , but still less than
30% in bone marrow.
Anemia (Hb less than 10g/dl).
Thrombocytosis (platelets more than 1000
Specific new cytogenetic abnormalities.
Increa sed marrow fibrosis.
3. Blastic phase: blast cells more than 30% in blood
or bone marrow. Mostly progress to AML (70%) and
less frequently to ALL.