ACUTE

Leukemia

What Is Leukemia?
Cancer of the white blood cells
Acute or Chronic
Affects ability to produce normal blood cells
Bone marrow makes abnormally large number of
immature white blood cells called blasts

History
Means white blood in Greek
Discovered by Dr. Alfred Velpeau in France, 1827
Named by pathologist Rudolf Virchow in Germany, 1845

Main Types
Acute Lymphocytic Leukemia (ALL)
Acute Mylogenous Leukemia (AML)
Chronic Lymphocytic Leukemia (CLL)
Chronic Mylogenous Leukemia (CML)

Classification of Leukaemia
Acute
Chronic
Myeloid
Lymphoid

4/18/16

Demographics of Leukemia
Patients (2001 Data)
CLL=Chronic
Lymphocytic
ALL=Acute
Lymphocytic

ALL
11%

others
17%

CML=Chronic
Mylogenous
AML=Acute
Mylogenous

CML
15%

CLL
26%

AML
31%

Sources from Leukemia, Lyphoma,

Myeloma Facts 2001

Total Reported Cases = 31,500

Symptoms
When there are excessive white blood cells -->
Infections
When there are few red blood cells: Paleness -->
Anemia
When there are few platelets --> Excessive bleeding

Tests For Diagnosis

Finger prick
Blood sample
Blood dye
Bone marrow sample
Spinal Tap/Lumbar Puncture

Pictures Of Blood
Platelet
White Cell

Platelet
Red Cell

Normal human blood

Sources from Arginine.umdnj.edu

White Cell

Red Cell

Blasts

Blood with leukemia

Sources from beyond2000.com

Effects On the Body

Attacks the immune system
Infections
Anemia
Weakness
No more regular white blood cells, red blood
cells, and platelets
Blasts clog blood stream and bone marrow

Development of Leukemia in the

Bloodstream

Stage 1- Normal

Stage 2- Symptoms

Stage 3- Diagnosis

Legend
White Cell
Red Cell
Platelet
Blast
Germ

Stage 5a- Anemia

Stage 4- Worsening

Stage 5b- Infection

Sources from Leukemia, by D. Newton and D. Siegel

Causes
High level radiation/toxin exposure
Viruses
Genes
Chemicals
Mostly unknown

Treatment
Chemotherapy
Immunotherapy
Radiation
Bone marrow transplant

ACUTE LEUKAEMIA

 Rapidly progressive
Proliferation of primitive blast cells
Acute myeloblastic (myeloid) leukaemia
Acute non-lymphoblastic leukaemia

Acute lymphoblastic leukaemia

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15

CLINICAL PRESENTATION
Symptoms of acute leukaemia are largely the
result
of
interference
with
normal
haematopoiesis.
Generally it is not possible on clinical
presentation to differentiate lymphoid from
myeloid leukaemia.

Causes of Acute Leukemias

Idiopathic (most)
underlying hematologic disorders
chemicals, drugs
ionizing radiation
viruses (Human T Lymphotropic Virus I)
hereditary/genetic conditions
Preceding bone marrow disorders
Chemotherapy especially alkylating agents, epipodophyllotoxins
and anthracyclines

CLINICAL SIGNS
pallor
lymphadenopathy
hepatosplenomegaly
sternal tenderness
purpura / petechiae
retinal haemorrhages
mouth ulcers
gum hypertrophy (monocytic type)

LABORATORY FINDINGS
Hb is invariably low (30-80 g/L)
WBC is usually high (especially lymphoblastics
and monocytics). Can be normal or low.
Plts usually dangerously low
Generally it is not possible to differentiate
myeloblasts from lymphoblasts by morphology
alone.

MANAGEMENT
Cytotoxic chemotherapy, radiotherapy and bone
marrow transplantation. The goal is to eradicate the
leukaemic cell mass while giving supportive care. In
children with ALL postremission therapy includes
central nervous system (CNS) prophylaxis.
PROGNOSIS
Young patients do better than old. Patients presenting
with low white counts do better. Must achieve
complete remission (no signs of leukaemia and return
of normal haematology parameters) to prolong
survival.

Acute Lymphoblastic Leukaemia

WHO classification:

Precursor B cell ALL

Precursor T cell ALL
Burkitts mature B lymphoblastic leukaemia/lymphoma
Bi-phenotypic leukaemia

FAB
L1, L2, L3

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21

Epidemiology of ALL

Peak incidence in
children aged 4
years
Rising incidence in
old age

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22

Prognostic factors in ALL

Sex: female > male
Ethnicity: caucasian > non-caucasian
Age: <10 and >1 year old
WBC < 50 x 109/l
CNS involvement is bad
Initial response to treatment (day 14 BM)
Morphological and genetic sub-types
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Clinical features of ALL

Bone pain children
CNS involvement
Lymphadenopathy

Continue
Involvement of other tissue such as spleen, liver, lymph
node, and meninges are common
Involvment of CNS may give rise to headach,
vomiting and irritable behaviour.

Principles of Treatment
combination chemotherapy

first goal is complete remission

further Rx to prevent relapse
supportive medical care

transfusions, antibiotics, nutrition,

metabolic /electrolyte abnormalities
psychosocial support

patient and family

Therapeutic Concepts in ALL

Induce a complete remission and restore
normal hematopoiesis avoiding excessive
toxicity
Reduce inapparent leukemia with shortterm, high-dosage cytocidal therapy early
in remission when the child is well and
drug sensitivity is greatest
Prevent CNS leukemia
Use
prolonged
combination
chemotherapy to eradicate residual
disease when there is no evidence of
leukemia

Basic Therapy in Childhood ALL

Induction Treatment
wk
Consolidation treatment (intensification)
10 wk
Continuation treatment (maintenance)
3y

4-8
22-

Reinduction therapy (delayed intensification) 2-7

wk
CNS-directed therapy (intrathecal injection of
methotrexate and cranial radiation)
3 wk