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Hematologic System, Anemias &

Oncologic Disorders in Children

Agus Fitrianto

Department of child health Medical faculty Jenderal Soedirman University/

Margono Soekarjo General Hospital Purwokerto Indonesia

7/09/2017
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HEMATOLOGY

• Study of blood and blood forming tissues

• Key components of hematologic system are:
• Blood
• Blood forming tissues
• Bone marrow
• Spleen
• Lymph system

07/09/2017
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WHAT DOES BLOOD DO?

• Transportation
• Oxygen
• Nutrients
• Hormones
• Waste Products
• Regulation
• Fluid, electrolyte
• Acid-Base balance
• Protection
• Coagulation
• Fight Infections

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COMPONENTS OF BLOOD
• Plasma
• 55%
• Blood Cells
• 45%
• Three types
• Erythrocytes/RBCs
• Leukocytes/WBCs
• Thrombocytes/Platelets

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ERYTHROCYTES/RED BLOOD
CELLS
• Composed of hemoglobin
• Erythropoiesis
• = RBC production
• Stimulated by hypoxia
• Controlled by erythropoietin
• Hormone synthesized in kidney

• Hemolysis
• = destruction of RBCs
• Releases bilirubin into blood stream
• Normal lifespan of RBC = 120 days

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LEUKOCYTES/WHITE BLOOD CELLS

• 5 types
• Basophils
• Eosinophils
• Neutrophils
• Monocytes
• Lymphocytes

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 TYPES AND FUNCTIONS OF
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LEUKOCYTES
TYPE CELL FUNCTION
Granulocytes
Neutrophil Phagocytosis, early phase of
inflammation
Eosinophil Phagocytosis, parasitic
infections
Basophil
Inflammatory response, allergic
response
Agranulocytes
Lymphocyte Cellular, humoral immune
Monocyte response
Phagocytosis; cellular immune
response
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THROMBOCYTES/PLATELE
TS
• Must be present for clotting to occur
• Involved in hemostasis

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NORMAL CLOTTING MECHANISMS

• Hemostasis
• Goal: Minimizing blood loss when injured
1. Vascular Response
• vasoconstriction
2. Platelet response
• Activated during injury
• Form clumps (agglutination)
3. Plasma Clotting Factors
• Factors I – XIII
• Intrinsic pathway
• Extrinsic pathway

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ANTICOAGULATION
• Elements that interfere with blood clotting
• Countermechanism to blood clotting—keeps blood
liquid and able to flow

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STRUCTURES OF THE HEMATOLOGIC

SYSTEM

• Bone Marrow
• Liver
• Lymph System

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BONE MARROW

• Bone Marrow
• Soft substance in core of bones
• Blood cell production (Hematopoiesis):The
production of all types of blood cells generated
by a remarkable self-regulated system that is
responsive to the demands put upon it.
• RBCs
• WBCs
• Platelets

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LIVER
Receives 24% of the cardiac
output (1500 ml of blood each
minute)
• Liver has many functions
• Hematologic functions:
• Liver synthesis plasma proteins
including clotting factors and
albumin
• Liver clears damaged and non-
functioning RBCs/erythrocytes
from circulation

19/04/2011
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SPLEEN

• Located in upper L quadrant

of abdomen
• Functions
• Hematopoietic function
• Produces fetal RBCs
• Filter function
• Filter and reuse certain cells
• Immune function
• Lymphocytes, monocytes
• Storage function
• 30% platelets stored in
spleen

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EFFECTS OF AGING ON THE

HEMATOLOGIC SYSTEM
• CBC Studies
•  Hemoglobin (Hb or Hgb)
•  response to infection (WBC)
• Platelets=no change
• Clotting Studies
•  PTT

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ASSESSMENT OF THE
HEMATOLOGIC SYSTEM
• Subjective Data
• Important Health Information
• Past health history
• Medications
• Surgery or other treatments

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ASSESSMENT OF
THE HEMATOLOGIC SYSTEM (CONT.)

• Objective Data
• Physical Examination
• Skin
• Eyes
• Mouth
• Lymph Nodes
• Heart and Chest
• Abdomen
• Nervous System
• Musculoskeletal System

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DIAGNOSTIC STUDIES OF THE
HEMATOLOGIC SYSTEM: COMPLETE
BLOOD COUNT (CBC)

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DIAGNOSTIC STUDIES OF THE HEMATOLOGIC
SYSTEM: COMPLETE BLOOD COUNT (CBC)
CONT’D

• Platelet count
• Normal 150,000- 400,000
• Thrombocytopenia- platelet count
• Spontaneous hemorrhage likely when count is below
20,000

• Pancytopenia
• Decrease in number of RBCs, WBCs, and platelets

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DIAGNOSTIC STUDIES
OF THE HEMATOLOGIC
SYSTEM
• Radiologic Studies
• CT/MRI of lymph tissues
• Biopsies
• Bone Marrow examination
• Lymph node biopsies

19/04/2011
 ANEMIA
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• Anemia is a reduction in the number of RBCs,

the quantity of hemoglobin, or the volume of
RBCs
• Because the main function of RBCs is
oxygenation, anemia results in varying
degrees of hypoxia

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ANEMIA
• Prevalent conditions
• Blood loss
• Decreased production of erythrocytes
• Increased destruction of erythrocytes

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 ANEMIA (CONT’D)
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• Clinical Manifestations:
1. Pallor.
2. Fatigue, weakness.
3. Dyspnea.
4. Palpitations, tachycardia.
5. Headache, dizziness, and restlessness.
6. Slowing of thought.
7. Paresthesia.

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ANEMIA CAUSED BY
DECREASED ERYTHROCYTE
PRODUCTION
• Iron Deficiency Anemia
• Thalassemia
• Megablastic Anemia

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IRON-DEFICIENCY ANEMIA
Etiology
1. Inadequate dietary intake
• Found in 30% of the
world’s population
2. Malabsorption
• Absorbed in duodenum
• GI surgery
3. Blood loss
• 2 mls blood contain 1mg iron
• GI, GU losses
4. Hemolysis

19/04/2011
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IRON-DEFICIENCY ANEMIA
• Clinical Manifestations
• Most common: pallor
• Second most common: inflammation of the
tongue (glossistis)
• Cheilitis=inflammation/fissures of lips
• Sensitivity to cold
• Weakness and fatigue
• Diagnostic Studies
• CBC
• Iron studies Diagnostics:
• Iron levels: Total iron-binding capacity (TIBC),
Serum Ferritin.
• Endoscopy/Colonscopy
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IRON-DEFICIENCY ANEMIA
• Collaborative Care
• Treatment of underlying disease/problem
• Replacing iron
• Diet
• Drug Therapy
• Iron replacement
• Oral iron
• Elemental Fe 3 mg/kgWB 2-3 months
• Absorbed best in acidic environemtn (vit C
100 mg/day)
• GI effects
• Parenteral iron
• IM or IV
• Less desirable than PO
19/04/2011
 MEGALOBLASTIC ANEMIAS
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• Characterized by large RBCs

which are fragile and easily
destroyed
• Common forms of
megaloblastic anemia
1. Cobalamin deficiency
2. Folic acid deficiency

This picture shows large,

dense, oversized, red blood
cells (RBCs) that are seen in
megaloblastic anemia.

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COBALAMIN (VITAMIN B12) DEFICIENCY

• Cobalamin Deficiency--formerly known as
pernicious anemia
• Vitamin B12 (cobalamin) is an important
water-soluble vitamin.
• Intrinsic factor (IF) is required for cobalamin
absorption
• Causes of cobalamin deficiency
• Gastric mucosa not secreting IF
• GI surgery loss of IF-secreting gastric mucosal cells
• Long-term use of H2-histamine receptor blockers
cause atrophy or loss of gastric mucosa.
• Nutritional deficiency
• Hereditary defects of cobalamine utilization
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COBALAMIN (VITAMIN B12) DEFICIENCY

• Clinical manifestations
• General symptoms of anemia
• Sore tongue
• Anorexia
• Weakness
• Parathesias of the feet and hands
• Altered thought processes
• Confusion  dementia

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COBALAMIN DEFICIENCY
DIAGNOSTIC STUDIES
• RBCs appear large
• Abnormal shapes
• Structure contributes to erythrocyte destruction
• Schilling Test: a medical investigation used for
patients with vitamin B12 deficiency. The purpose of
the test is to determine if the patient has
pernicious anemia.

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COBALAMIN
DEFICIENCY
• Collaborative Care
• Parenteral administration of cobalamin
• ↑ Dietary cobalamin does not correct the anemia
• Still important to emphasize adequate dietary intake
• Intranasal form of cyanocobalamin (Nascobal) is
available
• High dose oral cobalamin and SL cobalamin can use
be used

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FOLIC ACID DEFICIENCY

• Folic Acid Deficiency also causes megablastic
anemia (RBCs that are large and fewer in number)
• Folic Acid required for RBC formation and
maturation
• Causes
• Poor dietary intake
• Malabsorption syndromes
• Drugs that inhibit absorption
• Alcohol abuse
• Hemodialysis

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FOLIC ACID DEFICIENCY

• Clinical manifestations are similar to those of
cobalamin deficiency
• Insidious onset: progress slowly
• Absence of neurologic problems
• Treated by folate replacement therapy (1 mg/day)
• Encourage patient to eat foods with large amounts
of folic acid
• Leafy green vegetables
• Liver
• Mushrooms
• Oatmeal (‫)ااالشوفانااالمجروش‬
• Peanut butter
• Red beans

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 THALASSEMIA
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• Etiology
• Autosomal recessive genetic disorder of inadequate
production of normal hemoglobin
• Found in Mediterranean ethnic groups
• Clinical Manifestations
• Asymptomatic  major retardation  life
threatening
• Splenomegaly, hepatomegaly

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THALASSEMIA
COLLABORATIVE CARE
• No specific drug or diet are effective in treating
thalassemia
• Thalassemia minor
• Body adapts to ↓ Hgb
• Thalassemia major
• Blood transfusions with IV deferoxamine (used to
remove excess iron from the body)

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ANEMIA OF CHRONIC
DISEASE
• Underproduction of RBCs, shortening of RBC
survival
• 2nd most common cause of anemia (after
iron deficiency anemia
• Generally develops after 1-2 months of
sustained disease
• Causes
• Impaired renal function
• Chronic, inflammatory, infectious or malignant
disease
• Chronic liver disease
• Folic acid deficiencies
• Splenomegaly
• Hepatitis 19/04/2011
 APLASTIC ANEMIA
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• Characterized by Pancytopenia
• ↓ of all blood cell types
• RBCs
• White blood cells (WBCs)
• Platelets
• Hypocellular bone marrow
• Etiology
• Congenital
• Chromosomal alterations
• Acquired
• Results from exposure to ionizing radiation,
chemical agents, viral and bacterial infections

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APLASTIC ANEMIA
• Etiology
• Low incidence
• Affecting 4 of every 1 million persons
• Manageable with erythropoietin or blood
transfusion
• Can be a critical condition
• Hemorrhage
• Sepsis

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APLASTIC ANEMIA
• Clinical Manifestations
• Gradual development
• Symptoms caused by suppression of any or all
bone marrow elements
• General manifestations of anemia
• Fatigue
• Dyspnea
• Pale skin
• Frequent or prolonged infections
• Unexplained or easy bruising
• Nosebleed and bleeding gums
• Prolonged bleeding from cuts
• Dizziness
• headache 19/04/2011
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APLASTIC ANEMIA
• Diagnosis
• Blood tests
• CBC
• Bone marrow biopsy

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APLASTIC ANEMIA
• Treatment
• Identifying cause
• Blood transfusions
• Antibiotics
• Immunosuppressants (neoral, sandimmune)
• Corticosteroids (Medrol, solu-medrol)
• Bone marrow stimulants
• Filgrastim (Neupogen)
• Epoetin alfa (Epogen, Procrit)
• Bone marrow transplantation

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ANEMIA CAUSED BY BLOOD

LOSS
• Acute Blood Loss
• Chronic Blood Loss

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ACUTE BLOOD LOSS

• Result of sudden hemorrhage
• Trauma, surgery, vascular disruption
• Collaborative Care
1.Replacing blood volume
2.Identifying source of hemorrhage
3.Stopping blood loss

19/04/2011
 CHRONIC BLOOD LOSS
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• Sources/Symptoms
• Similar to iron deficiency anemia
• GI bleeding, hemorrhoids, menstrual blood loss
• Diagnostic Studies
• Identifying source
• Stopping bleeding
• Collaborative Care
• Supplemental iron administration

19/04/2011
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ANEMIA CAUSED BY INCREASED

ERYTHROCYTE DESTRUCTION

• Hemolytic Anemia
• Sickle Cell disease (peds)
• Acquired Hemolytic Anemia
• Hemochromatosis
• Polycythemia

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HEMOLYTIC ANEMIA
• Destruction or hemolysis of RBCs at a rate that
exceeds production
• Third major cause of anemia
• Intrinsic hemolytic anemia
• Abnormal hemoglobin
• Enzyme deficiencies
• RBC membrane abnormalities
• Extrinsic hemolytic anemia
• Normal RBCs
• Damaged by external factors
• Liver
• Spleen
• Toxins
• Mechanical injury (heart valves)
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SEQUENCE OF EVENTS IN HEMOLYSIS 48

Fig. 30-1
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ACQUIRED HEMOLYTIC
• Causes
ANEMIA
• Medications
• Infections
• Manifestations
• S/S of anemia
• Complications
• Accumulation of hemoglobin molecules can
obstruct renal tubules  Tubular necrosis
• Treatment
• Eliminating the causative agent

19/04/2011
LEUKEMIAS IN CHILDREN

AGUS FITRIANTO

Department of child health Medical faculty Jenderal Soedirman University/

Margono Soekarjo General Hospital Purwokerto Indonesia
 KEY POINTS :
• Acute leukemia constitute 30-35% of all childhood
malignancy, ALL is the commonest.
• The ages and total WBC count at diagnosis remain the
most important prognostic indicators
• Diagnosis must be confirmed by BONE MARROW
(morphologic), immunophenotypic & genetic (if possible)
• The four main components of therapy of ALL include
remission induction, CNS prophylaxis, consolidation and
maintenance therapy
• Clinically it is usually difficult to differentiate ALL from
AML
• AML still remains a disease that is difficult to treat
DISTRIBUTION OF CHILDHOOD
CANCER
 THREE TYPE OF LEUKEMIA
ARE SEEN IN CHILDREN
• Acute Lymphoblastic Leukemia (ALL- 75%- 83% of all
leukemia)
• Acute Myeloid Leukemia (AML- about 17% - 20% of
leukemia)
• Chronic Myeloid Leukemia (CML – 5% of all leukemias)
chronic Lymphocytic leukemia is not seen in children.
 ACUTE LYMPHOBLASTIC
LEUKEMIA
ALL
Clinical Feature :
• Anemia (fatigue, irritability, pallor)
• Thrombocytopenia (petechiae, ecchymosis, purpura, bleeding in 48%)
• Neutropenia (fever in 60%) or extramedullary diseases in the form of
lymphadenopaty (50%)
• Hepatosplenomegali (68%) bone and joint pain (leukemic infiltrate of
joint, 28%).
Mediastinal Lymphnodes-ALL

Organomegaly

ALL:Cervical Lymphadenopathy
 DIFFERENTIAL DIAGNOSIS
Non-Malignant conditions
• Juvenile rheumatoid arthritis
• Infectious mononucleosis
• Idiopathic thrombocytopenic purpura
• Pertusis / parapertusis
• Aplastic anemia
• Acute infectious lymphocytosis

Malignant conditions (with bone marrow involvement)

• Neuroblastoma
• Retinoblastoma
• Rhabdomyosarcoma

Unusual presentation
• Hypereosinophilic syndrome
Pizzo and Poplack.Ped.Onc.,2006
 DIAGNOSIS

ALL-L1

Bone marrow aspirate

French-American-British Co-operative group (FAB)
proposed criteria for classifying ALL into 3 subtypes L1,
L2, and L3 :

 ALL-L1 is the most frequent subtype in childhood ALL-L2

ALL
 ALL-L2 morphology is more common in adults
 ALL-L3 morphology is usually associated with B-cell
leukemia with t(8; 14) requiring a specific
therapeutic approach

ALL-L3
 HENCE SURFACE ANTIGEN
MERKERS WERE USED TO
CHARACTERIZE ALL IN TERMS OF
CELL OF ORIGIN AND STAGE OF
DIFFERENTIATION :

PRE-B ALL
PRE-B ALL AND TRANSITIONAL B cell leukemia
PRE-B ALL
B-CELL ALL
T-CELL ALL

T cell leukemia
PROGNOSTIC FACTORS
• WBC count at diagnosis
• Age at diagnosis
• Rapidity of leukemic cytoreduction during the
early period of treatment.
• Cytogenetics [t(8; 14), t(9; 22), t(4; 11), t(1;
19), unfavourable; t(12; 21) favourable]
• Ploidy (DNA index > 1.16, favourable)
• Mediastinal mass (unfavourable)
• CNS disease at presentation (unfavourable)
 HIGH RISK
• Age : < 1 year and > 10 year
• WBC > 50.000/mm3
• Mediastinal mass : +
• Meningeal leukemia : +
• After one week treatment in induction :
lymphoblast>1.000/mm3
 WHEN TO SUSPECT

classical clinical situations is likely to help in early diagnosis :

• Recurrent fever with bone pains
• Pallor and fatigue with or without neck nodes
• Hepatosplenomegaly with petechiae
• Pancytopenia
• Leucocytosis
 TREATMENT
• Spesific Therapy :
 The risk category : standard risk , high risk
 These include remission induction, CNS prophylaxis, consolidation
and maintenance therapy

• Induction : Vincristine, L-asparaginase with or without Daunorubicin.

This is the most critical period of treatment as the patient has very low
counts and is susceptible to complications.
A bone marrow is done at the end of induction to establish remission
status (CR=less than 5% blasts in marrow)
 TREATMENT (CON’T)
• CNS Prophylaxis in the form of intrathecal methotrexate (some
also use cytarabine) starts during induction after achieving CR,
radiation to be brain is also given to children > 2 years

• Consolidation is an intensification of treatment and many

protocols use same drugs as in induction and call it re-
induction treatment
Workshop Bone Marrow Diagnosis
bambangsdmt@gmail.com
Aula Lab RSDK, 25 Nov 2010
Workshop Bone Marrow Diagnosis
bambangsdmt@gmail.com
Aula Lab RSDK, 25 Nov 2010
TREATMENT OF RELAPS ALL

• Side of relapse: medullar , testes, CNS

• Chemotherapy
• Role of stem cell transplantation
• Minimal residual disease
• Recent developments and future plans
 MONITORING OF PATIENT
DURING MAINTENANCE
• ANC (usually 1000 to 1500)
• It is important to always monitor for clinical signs of
relapse:
 persistent unexplained fever
 hepatosplenomegaly
 lymphadenopathY
Testicular enlargement
new CNS deficits
• peripheral blood values
 WHEN TO REFER

• Immediately after suspecting acute leukemia either

clinically or by laboratory parameters

• Early referral by GP can avoid many disease related

potentially life threatening conditions like severe infection,
bleeding and metabolic problems
ESSENTIAL LABORATORY WORK-UP

• Hb, total and differential WBC count

• Bone marrow aspirate
• Chest X-ray (mediastinal mass)
• Uric acid and electrolytes : Na, K, Ca, PO4
• LDH/KFT/LFT
• Diagnostic spinal tap
Acute Myelogenous Leukemia
AML
INTRODUCTION AND
INCIDENCE
• Acute Myelogenous Leukemia (AML) accounts for 15-20% of
all childhood leukemia.
• Ratio AML : ALL = 1 : 4.

• Congenital leukemia’s have higher frequency of AML

• Age incidence is similar between 0 – 10 years

• AML is equally distributed among the sexes

• Treatment related mortality and death in aplasia remain

significant and survival rates are between 35% and 40% at
different centre and with different subtypes of AML
Etiologic Factors
• Acquired
• Genetic predisposing factors :
Down syndrome, Fanconi anemia, Bloom syndrome,
Kostmann syndrome, Diamond Blackfan anemia,
paroxysmal nocturnal haemoglobinuria, Li-Fraumeni
syndrome, neurofibromatosis etc. Well established inciting
agents include exposure to benzene, alkylating agents
(AML M1, M2) nitrosoureas, epipodophyllotoxins (M4, M5)
and ionizing radiation.

• A link between infectious agents and AML has not been

established
 CLINICAL PRESENTATION

• These children may present either with very few symptoms

or with severe sepsis and or bleeding.

• The clinical feature usually reflect marrow failure and

involvement of extramedulllary organ.

• Characteristic presentations of AML are gingival

hyperplasia (M4/M5);DIC (M3),soft tissue chloromas,
leukemia cutis (blue berry muffin)

• CNS involvement is very rare.

 DIAGNOSIS

• A high index suspicion is needed in cases with fever,

bruise, pallor and or bone pains.

• History and physical examination followed by a complete

hemogram and peripherals smear examination should help
confirm suspicion.

AML-M5 - Gum Hypertrophy

 FAB CLASSIFICATION AND
CHILDHOOD AML
FAB Class Histochemistry* Cell surface marker Associated
cytogenetic findings

AML M0 MP– CD33+, CD13+, CD14+, HLA DR-

NSE–
AML M1 MP+ CD33+, CD13+, CD11+, HLA DR+ +8, -5, -7
AML M2 MP+ CD33+, CD13+, CD11+ t(8;21)
AML M3 MP+ CD33+, CD13+, CD11+ t(15;17)
AML M4 MP+ CD33+, CD13+, CD11+, HLA DR+ inv 16
NSE+
AML M5 NSE+ CD33+, CD13+, CD11+, HLA DR+ t(1;11)
t(9;11)
AML M6 Pas+ Glycophorine+
MP+ Spectrin+, HLA DR+
AML M7 PPO+ Clycoprotein inv 3 or
IIb/IIIa (CD 41) t(3;3), t(1;23)
or IIIa (CD61)+

Abbreviations :
*MP, Myeloperoxidase; NSE, Non-Specific Esterase; PPO, Platelet Peroxidase
 Diagnosis

ACUTE MYELOID LEUKEMIA

AML-M0

ACUTE MYELOID LEUKEMIA

AML-M1

ACUTE MYELOID LEUKEMIA

AML-M2
AML-M6 :
Erythroleukemia

AML-M5b : AML-M4 : Myelomonocytic ACUTE MYELOID LEUKEMIA

AML-M3
 IMMUNOPHENOTYPING

• Normal haematopoetic cell undergo maturation they

also undergo chjanges in expression of cell surface
markers.

• Monoclonal antibodies have been developed that react

with lineage specific and stage specific myeloid antigen.

• Most AML cases express CD13; CD33,

CD15,CD14,CD11b,or CD36.

• Most of the FAB subtypes have their own characteristic

CD markers.
 CYTOGENETICS
• Clonal chromosomal abnormalities are detected in
cases of AML.

• AML M3 t(15;17)(q22;q21)

• The 11q23 translocation involving the MLLgene

occurs in ceratin secondary AMLs as well as other
AML subtypes signifying poor prognosis.

• Philadelphia chromosome translocation t(9;22)

(q34;q11)accounts for <1%.
 TREATMENT
• Supportive care: antibiotic; transfusion; nutrition and metabolic
complication

• Specific therapy:
Antracyclin: Daunorubicin;doxorubicin
Survival with chemotherapy alone is 35-40%.
In most studies 5 year actuarial leukemia free survival
averages about 60%.
• Bone marrow transplant (allogenic)
• The post transplant relapse rate in these studies is less than
20%.
 PROGNOSIS

• High WBC count

• Secondary AML/MDS
• Monosomy 7-or 7q
Poor risk factors
 PRACTICAL POINTS FOR THE
GP
• High index of suspicion will aid early diagnosis
• Early referral may minimize life threatening
complications
• Treatment should be in an experienced set up
• Bone marrow to be done at treating centre
• Disseminate information on treatment options and
survival
 PROBLEMS IN TREATMENT

• Children come in more advanced stage

• Malnourished children tolerate
chemotherapy poorly
• Cost of drugs
• Organization of care
• Treatment leukemia in poor countries is
much more difficult

Workshop Bone Marrow Diagnosis

bambangsdmt@gmail.com
Aula Lab RSDK, 25 Nov 2010
 TOXIC EFFECTS OF
CHEMOTHERAPY

ANTHRACYCLIN Cardiomyopathy & heart failure

ASPARGINASE Hypertensitivity reaction

Coagulopathies
CYTARABINE Acute cerebelar syndrome

METHOTREXATE Nephrotoxic & hepatotoxic (high dose)

CYCLOPHOSPHAMIDE Cystitis hemorrhagica

VINCRISTIN Peripheral sensory & motor neuropathy

Workshop Bone Marrow Diagnosis
Aula Lab RSDK, 25 Nov 2010
bambangsdmt@gmail.com
Thank you