THALASSEMIA

Supervised by: Dr Felicia

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CASE STUDY

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• 7 years 9 months, boy
• Immunisation up to age
• Antenatally uneventful
• Not known medical illness, not known allergy
• No history of hospitalisation
• Height 117 cm (at 5th -10th centile), Weight 19 kg (< 5th centile)
• Admitted from 17 -20/3/2023

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• Main concern: pallor and jaundice looking since December 2022 (for about
4 months)

• Presented with:
1. high grade fever
• up to 380c on 11/3/2023-14/3/2023
• no chills or rigors
• temporarily settled in between for two days
• however reoccur back on 17/3/2023,requiring paracetamol 6 hourly
at home
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2. Pallor and jaundice for about 4 months
• Mother noted pallor and jaundice more prominent after child
developed fever

3. Abdominal distention for 1-week prior admission

4. Loss of weight for 1 week since having fever

• claimed by mother weight loss of approximately 0.4-0.5kg

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• Otherwise, still active, appetite remains good, no tea colored urine, no
hematura,no headache, no dizziness, no dyspnoea, no palpitations no
URTI symptoms, no sick contact, no recent travelling or river
swimming, no rodent

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• On further history, prior marriage, father has screened for
thalassemia, claim he himself was diagnosed with beta
thalassemia? Trait (no documentation, or any formal report traced
from SGH), never required blood transfusion previously.

• Paternal aunty has beta thalassemia? trait as well.

• No other family members in both paternal and maternal family has

history of blood transfusion previously.

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Diet history
• 1 meal/day
• Taking rice ~4 spoons to 1 plate
• Also taking friend chicken (2 wings), eggs, fish
• Does not like vegetables (leafy vegetables, fruit)
• Taking 1 glass pediasure 2x/day

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• Developmental up to age
• Currently Standard 2, mother stated no issues at school.
• Family history

Has family member of

thalassemia over paternal side

B- thalassemia trait (?) NKMI

(Not treatment dependent

NKMI

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• Brought to Private clinic on 17/3/2023, then referred to Hospital Sibu
for further investigation and management

• At ETD, PR 131 /min, RR 21/ min, T: 36.1 C, SpO2: 100%, HGT 5.1
mmol/L
• Documented pale, P/A : splenomegaly
• Hb: 6.8 WBC 11.4 PLT 417 ALC 4.5 ANC 6.0
• MCV 64.3 MCH 20.8 RBC 3.27
• Mentzer index: 19.7
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Physical examination
• Alert, pale looking, not tachypneic, RR 24/min, good pulse volume,
CRT <2 seconds, warm peripheries
• Chipmunk facies – frontal bossing, prominent zygomatic bones
• Broad ribs
• Lungs: clear, good air entry
• CVS: soft systolic murmur, apex beat at 6th intercostal space,
• Abdomen: soft not distended, spleen 7 cm, bilateral cervical lymph
nodes palpable prominent over left side largest 3x3cm,bilateral shotty
cervical lymph nodes palpable, no body rashes seen

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Progression in ward
• Hemodynamically child was stable throughout the ward stay
• Transfused 20ml/kg packed cell (380mls over 4 hours) on 17/3/2023.
Uneventful
• Has few episodes of temperature spike in ward, given syrup
paracetamol.
• Developed some mild dry cough on 20/3/2023, no rhinorhea.
• Apettite and activity remains good.

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13
Investigations
17/3/23 18/3/23 (post packedcell transfusion)

Hb (g/dL) 5.8 8.6

TWC (x 103/uL) 10.3 7.0

Plt ( x 103 /uL ) 304 291

Lymphocytes 5.4 2.3

Neutrophils 3.8 3.6

HCT 19.4

MCV 62 72.3

MCH 18.5 22.5

MCHC 29.9

RBC 3.14

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Na (mmol/L) 132

K (mmol/L) 3.4

Cl (mmol/L) 100

Urea (mmol/L) 1.9

Creatinine (mmol/L) 43

Calcium 2.29

Mg 1.02

P04 2.39

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Total Bilirubin (umol/L) 12.9

Direct Bilirubin (umol/L) 44

AST (U/L) 44

ALT(U/L) 20

Total protein (g/L) 81

Albumin (g/L) 44

Globulin (g/L) 37

ALP (U/L) 147

UA 306

Retic Count 3.9

Iron Studies Iron 17.31/UIBC 18.8/TIBC 36.1

Ferritin 528.70

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•Hep B/Hep C/HIV/VDRL (17/3/2023):Non-Reactive
•PBF(17/3/2023): Suggestive of Thalassemia Intermediate

•RBC : Severe anaemia, hypochromic microcytic red blood cells, marked anisopoikilocytosis with many target
cells, tear drop cells, tear drop cells, few fragmented red blood cell and irregular contracted red blood cells. Few
nucleated red blood cells seen. White cell count within normal range with adequate absolute neutrophil count.
Lymphocytosis. Presence of few myelocytes and reactive lymphocytes. No blast cell seen. Adequate platelet

•Hb Analysis(17/3/2023):Pending
•Hb Analysis (Father and younger sister taken in ward on 20/3/2023):Pending
•Hb Analysis (Mother 2/12/2014) :Increase Hb A2/E with normal Hb F level. Findings are compatible with HbE
trait
•RBC phenotyping(17/3/2023) prior transfusion: Pending

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Upon discharge
• Active, cheerful, pink tolerating orally well, fever settled, no GI losses. Last fever spike 38.9 0c 10.00pm
19/3/2023,no cough
•Clinically ,comfortable, lungs clear, heart S1S2 no murmur, abdomen soft not distended
•Liver 4cm,spleen 4 cm soft

Discharge with Syrup Folic Acid 1mg OD

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Plan:
1. TCA Peads Oncology Visiting Clinic under Dr Betty on 14/4/2023 10am with repeated FBC/DC taken on
13/4/2023
2. To take FBC/DC and GSH on 13/4/2023 in ward 26 (to see Dr. Darshini to trace the HB analysis with RBC
phenotyping)
3. To trace the RBC Phenotyping and Hb Analysis (taken 17/3/2023) on 13/4/2023.

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Differential diagnosis
Leptospirosis
• Points for: jaundice, fever
• Points against: no rodent exposure, no history of river swimming
Malaria
• Points for: fever
• Points against: no history of jungle trekking
Iron deficiency anaemia
• Points for: pale looking
• Points against: fever, presence of splenomegaly
Viral fever
• Points for: fever
• Points against: no sick contact, pallor, jaundice

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Theory

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• Thalassemia is an inherited blood disorder characterized by decreased
haemoglobin production.

• There are two main types:

• Alpha thalassemia
• Beta thalassemia

• There are many forms of thalassemia:

• Thalassemia major
• Thalassemia intermedia
• Thalassemia minor (or thalassemia trait)
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• Hemoglobin is a tetramer consisting of 2 pairs of globin chains (α &
β).
• Abnormalities in these proteins are referred to as hemoglobinopathies.
• Two hemoglobin (Hb) gene clusters involved in Hb production are
located at chromosomes 16 and 11.

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• On chromosome 11, there are 5 genes within the beta (β) gene cluster:
• epsilon (ε)
• gamma 1 (γ1 )
• gamma 2 (γ2 )
• delta (δ)
• beta (β)
• On chromosome 16, there are 3 genes within the alpha (α) gene cluster:
• zeta (ζ)
• alpha 1 (α1 )
• alpha 2 (α2 ).

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• Thalassemia is inherited
through autosomal recessive

• Beta thalassemia
• point mutations on
chromosome 11

• Alpha thalassemia
• gene deletions on chromosome
16

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 Pathophysiology: β-Thalassemia Syndromes
Inadequate β-globin
gene production leads
to decreased levels of
normal hemoglobin
(HbA)
Unbalanced α- and β-
globin chain production
leads to ineffective
erythropoiesis
Nelson Textbook of Paediatrics 21 ed
st
Anemia and increased erythroid
production
Excess α-globin chains
are very unstable,
precipitate in RBC Marked increase in erythropoiesis,
precursors, damage the with early erythroid precursor
RBC membrane, and death in the bone marrow
shorten RBC survival
Ineffective erythropoiesis and the
compensatory massive marrow
expansion and hepatospleenomegaly
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β-Thalassemia Genotype Clinical features FBC parameters

Minor (ββº/ ββ+) • Asymptomatic • Hb (>10g/dL)

• No organomegaly • Low MCV and MCH
• Decreased HbA >90%
• Increased HbA2 (4-9%)
• Increased HbF (2.5-5%)

Intermedia (β+β+) • Moderate anaemia • Hb (8-10g/dL)

• Thalassaemia facies • Low MCH and MCV
• Hepatosplenomegaly • HbA (5-90%)
• HbA2 (4-9%)
• HbF (>10%)

Major (βºβº/ βºβ+) • Severe anaemia • Hb (<7g/dL)

• Hepatosplenogealy • Low MCH and MCV
• Jaundice • HbA (usually absent)
• Thalassemia faces • HbA2 (normal or high)
• Growth failure/mental retardation • HbF (>90%)

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 Pathophysiology: α-Thalassemia Syndromes
Silent Carrier
(-α/αα)

α-Thalassaemia
trait
(-α/-α, αα/--)
Deletion mutation of α- A reduction in α-globin
globin gene production
Hb H Disease
(--/-a)

Hydrops Fetalis/
Hb Bart
(--/--)
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Nelson Textbook of Paediatrics 21 ed
st 28
α-Thalassemia Genotype Clinical features FBC parameters

Silent carrier (-α/αα) • Asymptomatic • Hematological parameter

• Clinically normal usually normal

Trait (-α/-α, αα/--) • Clinically normal / mild anaemia • Haematological parameters may
have mild anaemia with reduced
MCV & MCH

Hb H Disease (--/-α) • Anaemia • Hb range 7-11 g/dL

• Mild splenomegaly • MCV 51-73 fl
• Occasionally, scleral icterus or
cholelithiasis

Hydrops Fetalis/Hb (--/--) • Fetus relies on HbF (ααγγ) to get oxygen from mother’s blood
Bart • No production of α-globin chain but normal γ-globin production
• Excess γ-globin bind to each other and form Hb Barts (γ4)
• Hb Barts have high oxygen affinity, prevent oxygen release to tissue
• Tissue hypoxia and hydrops fetalis

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Clinical Features of β-Thalassaemia major
• Presentation at 3-6 months-old or younger than 2 years-old
• Thalassaemic facies / Chipmunk facies :
• Frontal bossing
• Prominent maxilla
• Depressed nose bridge
• Hepatosplenomegaly
• Failure to thrive/growth failure
• Stunting

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CPG Management of Transfusion Dependent Thalassaemia, 2009.
• Pallor
• Jaundice
• Severe anaemia (Hb 3-7
g/dl)
• Need for repeated blood
transfusion

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 Clinical Features of β-Thalassaemia Intermedia

• Presentation at later age

• Milder anaemia
• Extensive thalassaemic facies
• Hepatosplenomegaly

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CPG Management of Transfusion Dependent Thalassaemia, 2009.
Baseline investigations for ALL new patients
• Full blood count ( in typical cases, the Hb is usually below than 7g/dl)
• Peripheral blood film
• Mandatory: Hemoglobin analysis by electrophoresis or HPLC (High-performance liquid
chromatography)
• Typical findings for Beta thalassemia major:
HbA decreased or absent, HbF increased, HbA2 variable
Others:
• Red cell phenotyping (required) before first transfusion.
• DNA analysis
• β- gene analysis & α-gene analysis
• Infective screening: HIV, Hepatitis B & C, VDRL (prior transfusion)
• All nuclear family members must be investigated by Hb nalysis for genetic counselling
• 1st & 2nd degree relatives is encouraged to be screened & counselled ( for cascade screening)
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Genetic counselling

• The process of providing information to at-risk couple and

families about a genetic condition, in particular information about
• the diagnosis
• recurrence risk
• burden of disorder and
• the various reproductive option, together with helping the
families coming to terms with the issues in a non-directive
manner.

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CPG Management of Transfusion Dependent Thalassaemia, 2009.
Cascade screening

Definition: A genetic-screening strategy that targets relatives of

carriers/affected individuals of genetic disorders through the testing of
their phenotypes or genotypes.

Role:
1. Preventing thalassaemia births is based on identifying individuals at
risk, providing adequate information on risk and possibilities to reduce
that risk.
2. Screening family members of an index case (thalassaemia major or
carriers)
CPG Management of Transfusion Dependent Thalassaemia, 2009.
35
CPG Management of Transfusion Dependent Thalassaemia, 2009. 36
Management of Thalassemia
- Blood transfusion therapy
- Iron chelation therapy
- Splenectomy
- Hematopoietic stem cell transplantation
- Monitoring of Patients

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 Blood Transfusion Therapy
• Aim: To suppress extramedullary haemopoiesis while minimizing complications of
transfusion & maintain normal well being.

When to start?

THALASSEMIA MAJOR:
 Once dx confirmed THALASSEMIA
• Bone changes
OR INTERMEDIA:
•  Hb <8g/dl (maxillary /
After completing  Hb <7g/dl on 2
 Evidence of impaired mandibular
blood investigations occasions > 2 weeks
apart growth attributed to prominence)
to confirm the
 Absence of other anaemia after • Enlarging liver and
diagnosis. excluding other causes
factors e.g. infection spleen
 Poor growth (CPG) e.g. dietary, • Para spinal masses
constitutional

CPG Management of Thalassaemia, Nov 38 2009

Paediatric Protocols For Malaysian Hospitals384th Ed
 β-Thalassemia Major
• Transfusion targets
(all thal major/severe E- β-Thalassaemia should be transfused so as to: )
• Maintain pre transfusion Hb level ~ 9-10 g/dl.
• Keep mean post-transfusion Hb at 13.5-15.5 g/dl. (Taken at least 1 hr after)
• Keep mean Hb 12-12.5 g/dl.

• The above targets allow for normal physical activity & growth, abolishes
chronic hypoxaemia & reduces compensatory marrow hyperplasia which
causes irreversible facial bone changes & para spinal masses.

Paediatric Protocols For Malaysian Hospitals394th Ed

• Transfusion interval:
 Usually 4 weekly interval
(usual rate of Hb decline is 1g/dl/week)
 Interval varies depending on
patients (3-6 weekly)
• Transfusion volume:
 15-20 mls/kg packed red cells
(PRBC)
 Round-up to nearest unit of cross-
matched blood provided
 If calculated vol >1 unit – 1 unit
 If calculated vol <2 unit – 2 units
 This minimizes exposure to
immunological units of blood &
avoid wastage to donated blood.
• Notes:
 Presence of cardiac failure or Hb
<5g/dl,
 Use low volume PRBC (~5-10
ml/kg)
 Slow infusion rate over >4 hours
 IV Frusemide 1mg/kg (max 20 mg)
Recommended to receive
leucodepleted PRBC
 Minimizes non-haemolytic febrile
reactions & alloimmunization by
removing white cells in PRBC.
40
Paediatric Protocols For Malaysian Hospitals40
4 th Ed
 β-Thalassemia Intermedia
• A clinical diagnosis where pt presents with less severe anaemia at >2
years of age (Hb <8 g/dl)
• Severity varies
• All mandatory pre-infusion investigations as similar with thal major is
required
• Assessment & decision to start regular transfusion by specialist.

α-Thalassemia (HbH disease)

• Transfuse only
 If Hb persistently < 7g/dl
 Symptomatic chronic anaemia
Paediatric Protocols For Malaysian Hospitals41
4 th Ed
 Monitoring During Complications of Blood
Blood Transfusion Transfusion
• Review prior to each transfusion, to • Chronic iron overload
determine pre-transfusion Hb level & (Haemochromatosis)
planned transfusion is appropriate.
• Cardiac failure
• Liver cirrhosis
• Transfusion at proper clinical area
with proper supervisions. • Diabetes
• Infertility
• STOP IMMEDIATELY if suspected • Growth failure
acute transfusion reaction &
resuscitation measure taken &
appropriate investigations to determine
causes.
CPG Management of Thalassaemia, Nov 2009
Illustrated Textbook of Paediatrics,42
5 th Ed
 Iron Chelation Therapy

• To prevent iron overload in transfusion dependent thal.

• Start iron chelation therapy in
• Patient > 10 units of blood
• Serum ferritin > 1000 µg/L on more than 2 occasion 2 weeks apart
• Reliable tools to measure iron overload
 Serum ferritin level (< 1000 µg/L)
• 3 approved iron chelators;
 Desferrioxamine (DFO)
 Deferiprone (DFP)
 Deferasirox (DFX)
CPG Management of Thalassaemia, Nov 2009
Paediatric Protocols For Malaysian Hospitals43
4 th Ed
 Desferrioxamine (Desferal®)
• Age > 3 years old
Initiate when • Serum ferritin reaches 1000 µg/L
• Usually after 10-20 blood transfusion

• Average daily dose: 20-40 mg/kg/day

Dosage & Route • Via subcutaneous continuous infusion using portable pump over 8-10 hours daily,
5-7 nights a week

• Aim to maintain serum ferritin < 1000 µg/L

• Given together with Vit C (Augments iron excretion with Desferal)
• Severely iron overload requires longer or continuous SC or IV infusion of Desferal (via central line if
necessary)
• Local skin reaction due to inadequate diluted Desferal / infection
 Yersinia infection: fever, abdominal pain, diarrhoea
 Tx: Cotrimoxazole, Aminoglycoside / 3 rd gen cephalosporin
Complications • Desferal toxicity ( >50mg/kg/day with low ferritin in children)
• Ocular (↓ vision, visual field defect, night blindness; Reversible)
• Auditory (High tone deafness; Not usually reversible)
• Skeletal (Pseudo rickets, metaphyseal changes, vertebral growth retardation)
44
Paediatric Protocols For Malaysian Hospitals 4 th Ed
 Deferiprone / L1 (Ferriprox® / Kelfer®)
• When optimal dose of Desferal is ineffective/inadequate or contraindicated
Use when
• Patient > 6 years; risk of cardiac iron toxicity

• Via oral route

Dosage & Route • Dosage: 75 – 100 mg/kg/day in 3 divided doses
• Can combine with Desferal using low dose of 50 mg/kg/day

• GI disturbances
• Arthritis
Complications • Idiopathic agranulocytosis (rare)
 Weekly FBC monitoring is recommended
 Stop if neutropenic (< 1,500/mm3)

CPG Management of Thalassaemia, November

45 2009
Paediatric Protocols For Malaysian Hospitals 4th Ed
 Deferasirox (Exjade®)
• Transfusional iron overload in patient 2 years or older
Use when
• For patient that are intolerable/inadequate to DFO.

• Via oral route

Dosage & Route
• Dosage: 20-30 mg/kg/day in liquid dispersible tablet, once daily

• Transient skin rash

• GI disturbance
Adverse Effect
• ↑ creatinine
 Require monthly monitoring renal function

46
Paediatric Protocols For Malaysian Hospitals 4th Ed
 Complications of Chronic Iron Overload
Endocrine Growth retardation
Impaired glucose tolerance
Pubertal delay
Hypothyroidism
Hypoparathyroidism
Diabetes Mellitus
Cardiac Arrhythmias
Pericarditis
Cardiac failure
Hepatic Liver cirrhosis
(with Hep B/C infection)

47
Paediatric Protocols For Malaysian Hospitals 4 th Ed
 Splenectomy
• Indication:
 Evidence of hypersplenism
 Splenomegaly
 Persistent leucopaenia or thrombocytopenia
 Defined by blood consumption volume of RBC >1.5X normal or >200-220
mls/kg/year in patient > 5 years of age to maintain Hb levels.
• NB!
 Pneumococcal & HIB vaccinations 4-6 weeks prior to splenectomy
 Meningococcal vaccine required in endemic areas
 Penicillin prophylaxis for life after splenectomy
 Low dose aspirin (75 mg/day) if thrombocytosis > 800,000/mm3 after
splenectomy
48
Paediatric Protocols For Malaysian Hospitals 4 th Ed
 Complications of Splenectomy
1. Sepsis
• Major long-term risk.
• Streptococcus pneumoniae (50-90%) infection in post-splenectomy patient.
• Others organism: Haemophilus, Neisseria & other capsulated gram-negative organism;
Protozoan like babeosis, malaria
• Note if there are febrile episode in 1st 2 years post-splenectomy

• Overwhelming Post-Splenectomy Infection (OPSI)

 Sudden onset of fever & chills, vomiting & headache
 Can progress rapidly to hypotensive shock & DIVC
 RF: < 4 years old, 1st 2 years post-splenectomy
 Tx: Empirical broad spectrum parenteral antibiotics
 3rd gen cephalosporins
 Aminoglycosides
CPG Management of Transfusion Dependent Thalassaemia, Nov 2009
49
2. Thromboembolic Risk
• Common in intermedia compared to thalassaemia major.
• Short-term anti-coagulant may be indicated during period of ↑ risk e.g.,
immobilisation & post-surgery.

3. Thrombocytosis
• Known complication
• May consider use of low dose aspirin or dipyridamole if platelet count > 800 x
109/L

4. Pulmonary hypertension
• Occurs due to thromboembolic involvement in pulmonary microvasculature.

CPG Management of Transfusion Dependent Thalassaemia, Nov 2009

50
 Haemopoietic Stem Cell Transplantation
(HSCT)
• It is a bone marrow transplantation from human leucocyte antigen (HLA) identical
family donors which is as established curative treatment option for thalassaemic
patient.

• Classification of patients into Pesaro Risk Group & Outcome:

Risk factors: Classification of patient:

- Inadequate iron chelation therapy Class 1: None
- Presence of liver fibrosis Class 2: 1-2 risks
- Hepatomegaly (> 2cm) Class 3: All risk factors

CPG Management of Transfusion Thalassaemia, Nov 2009

Paediatric Protocols For Malaysian Hospitals514th Ed
 Pesaro Risk Groups & Outcome following BMT
Class RF Event Free Survival % Mortality % Rejection %
1 0 91 7 2
2 1-2 83 13 3
3 3 21 21 28
Adults - 34 34 -

• Best results if performed at earliest age in Class 1 patients.

• In newly diagnosed transfusion dependent thalassaemics, family should be
informed this option & referred early to Paediatrician for counselling & HLA
typing of patient & unaffected siblings to identify potential donor.

Paediatric Protocols For Malaysian Hospitals 4th Ed

52
CPG Management of Thalassaemia, Nov 2009 53

Each admission for blood transfusion
Monitoring of Patients
Clinical assessment: Height, weight, liver & spleen size
Any adverse effect of chelation therapy
Pre-transfusion Hb, platelet count, WBC* (Deferiprone)
Volume of pure RBC transfused based on haematocrit of PRBC given

Every 3-6 months Serum ferritin level

Serum T4/TSH
Random blood sugar
Infection screen – Hepatitis B & C, HIV, VDRL (6 monthly)

Yearly Annual volume of pure RBC transfused per kg body weight (use median body weight)
Evaluate growth & development
Endocrine assessment (Modified GTT, T4/TSH, Ca, PO4; If CA low, check PTH & Vit D)
Bone: osteoporosis & skeletal abnormalities

10 years onwards (Yearly) Pubertal & sexual development

 Tanner stage of breast & genitalia
 FSH, LH, estradiol or testosterone level

Variable interval (especially 10 years Cardiac assessment

onwards) • Annual echocardiography, ECG / Holter for arrhythmia, Cardiac T2* MRI
Liver assessment
• Liver iron assessment, Liver T2* MRI, biopsy (prior to BMT)

54
Paediatric Protocols For Malaysian Hospitals 4th Ed
 • Diet & Supplements • Support Group

• Avoid iron rich food such as red • Thalassaemia Societies that

meat & iron fortified cereals or • Provide support & education for
milk. families
• Drinking tea is advised as it may • Organises thalassaemia related
help ↓ intestinal iron absorption. activies & awareness campaign.

• Diary products are recommended • E.g.: Thalassaemia Association

- ↑ Ca of Malaysia
• Vit E (antioxidant), Ca & zinc
supplement recommended
• Low dose Vit C augments iron
excretion for those with Desferal
only
55
Paediatric Protocols For Malaysian Hospitals 4 th Ed
COMPLICATIONS OF THALASSEMIA
• Endocrine Complications
• Cardiac Complications
• Infections

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Endocrine Complications
Hypogonadism

Hypoparathyroidism Hypoadrenalism

Endocrine Short stature

Complications
Hypothyroidism & stunted
growth

Glycemic
Osteoporosis
abnormalities

Management of Transfusion Dependent Thalassaemia, CPG (2009) 57

Cardiac Complications
• Due to iron overload is a major cause of mortality (71%) and
morbidity in patients with transfusion dependent thalassemia.
• Repeated blood transfusion in thalassemic patient cause iron overload.
The iron will be deposited in the myocardium and induce peroxidation
injury and apoptosis causing dysfunction of myocardial contractility
and enlargement of the heart chamber.
• Onset of cardiac iron overload can be as early as 10 years old although
the risk is usually higher in the late teens and 20s.

Management of Transfusion Dependent Thalassaemia, CPG

58 (2009)
Infections

HEPATITIS B HEPATITIS C

INFECTIONS

BACTERIAL INFECTIONS IN
HIV TRANSFUSION DEPENDENT
THALASSAEMIA

Management of Transfusion Dependent Thalassaemia, CPG

59 (2009)
 Thank you
References:
Management of Transfusion Dependent Thalassaemia, CPG (2009)
Paediatric Protocols For Malaysian Hospitals 4 th Ed
Nelson Textbook of Paediatrics 21st ed

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