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Hemolytic Anemia's I

 Dr Abdifatah Ahmed
 Supervisor: Prof Silva
 October 2022
 Outline
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 Hereditary spherocytosis  Thalassemia syndromes

⚫ Introduction ⚫ Introduction

⚫ Etiology ⚫ Etiology

⚫ Pathogenesis ⚫ Pathogenesis

⚫ Clinical manifestations ⚫ Clinical manifestations

⚫ Diagnosis ⚫ Diagnosis

⚫ Management ⚫ Management
 Outline
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 G6PD
⚫ Introduction

⚫ Etiology

⚫ Pathogenesis

⚫ Clinical manifestations
⚫ Diagnosis

⚫ Management
 Definitions

 Hemolysis:
⚫ Is the destruction or removal of red blood cells from the
circulation before their normal life span of 120 days.
 Hemolytic anemia's:
⚫ Anemia's which result from an increase in RBC
destruction in the body with increased erythropoiesis in
Bone Marrow
 Physiolog
y
 Bone Marrow produces RBCs
 Life span of RBCs is 120 days
 RBC count in blood is about 5 million/ul
 Old and damaged RBCs are destroyed in the reticulo-
endothelial system especially spleen
 1 % of circulating RBCs are destroyed daily and replaced
by new RBCs
 Pathophysiology of Hemolytic
Anemia
 In Hemolytic Anemia, life span of RBCs is shortened
 RBCs destruction is increased
 Hemoglobin and RBC count in blood is reduced
 Cellular hypoxia stimulates erythropoietin production
 Bone marrow becomes hyperplastic and increases its
output of erythrocytes
Cont.

Classification of Hemolytic
anemia
 Classification

 Hemolytic anemia's are classified in a variety of ways:

1. Location of hemolysis
⚫ Intra-vascular (vascular space)
⚫ Extra-vascular (reticuloendothelial system)
 Classification

2. Source of defect causing hemolysis:

⚫ Intra corpuscular defect (intrinsic)
⚫ Extra corpuscular defect (extrinsic)

3. Mode of onset:
⚫ Hereditary

⚫ Acquired
Intrinsic hemolytic anemia
 Intrinsic Defects
1. Hereditary
⚫ Membrane defect
⚫ Haemoglobin defect
⚫ Enzyme defect
2. Acquired
⚫ Paroxysmal nocturnal haemoglobinuria .
Extrinsic haemolytic anaemia
 Extrinsic haemolytic anaemias
Extrinsic hemolytic anemia

1. Hereditary 2. Acquired
⚫ LCAT deficiency. ⚫ Immune mediated H.A
⚫ Abetalipoproteinemia. ⚫ Non-immune mediated
HA:
 Acquired haemolytic
Extrinsic Extrinsic hemolytic
anaemias
…….
1. Immune mediated H.A
2. Non-immune mediated HA
⚫ Autoimmune H.A.
⚫ Mechanical
⚫ Alloimmune H.A.
⚫ Infectious agent
⚫ Drug induced.
⚫ Hypersplenism

⚫ Thermal
15
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 Classification

Lab features of all hemolytic

anemia
 Evidence of haemolysis

 The lab findings are divided into 2 groups

⚫ Features of increased red cell breakdown.

⚫ Features of increased red cell production.
 Features of increased red cell
destruction

 Serum bilirubin: high

 Serum LDH: high

 Urine urobilinogen: high

 Serum haptoglobins: absent

 Features of increased red cell
production
 P.B: Reticulocytosis and Circulating nucleated red cells

 B.M: Erythroid hyperplasia.

 Hemolytic Anemia: Diagnostic Clues
Based
on Red Blood Cell (RBC) Shape
 Sickle cells:
⚫ Sickle cell disease
 Target cells:
⚫ Hemoglobinopathies (HbC, HbS, thalassemia), liver
disease
 Schistocytes/burr cells/helmet cells/RBC fragments:
⚫ Microangiopathic hemolytic anemia (DIC, HUS, TTP)
 Hemolytic Anemia: Diagnostic Clues
Based
on Red Blood Cell (RBC) Shape
 Spherocytes:
⚫ Hereditary spherocytosis, autoimmune hemolytic anemia

 Cigar-shaped cells:
⚫ Hereditary elliptocytosis
 Hemolytic Anemia: Diagnostic Clues
Based
on Red Blood Cell (RBC) Shape
 “Bite” cells:
⚫ G6PD deficiency

 Poikilocytosis, microcytosis, fragmented erythrocytes,

elliptocytes:
⚫ Hereditary pyropoikilocytosis
 Cont.

Hereditary Spherocytosis
 Hereditary spherocytosis

 HS is a common cause of inherited hemolytic anemia, with

a prevalence of approximately 1 in 2,000-5,000 persons.

 Described in patients of all ethnic groups, it is the most

common inherited abnormality of the erythrocyte associated
with inherited hemolytic anemia in persons of Northern
European origin.
 Hereditary spherocytosis

 Symptomatology ranges from asymptomatic patients with

well compensated anemia to severely affected patients with
hemolytic anemia requiring regular blood transfusions.
 Etiology

 The pathophysiology underlying HS is twofold:

⚫ An intrinsic defect of the erythrocyte membrane and

⚫ An intact spleen that selectively retains, damages, and
removes mutant HS erythrocytes.
 Etiology

 Abnormalities of ankyrin or spectrin are the most common

molecular defects .

 Defects in these membrane proteins result in uncoupling of

the “vertical” interactions of the lipid bilayer with the
underlying membrane skeleton, with subsequent release of
membrane microvesicles.
 Etiology

 The loss of membrane surface area without a proportional

loss of cell volume causes decreased erythrocyte
deformability.

 This impairs cell passage from the splenic cords to the

splenic sinuses, leading to the trapping and premature
destruction of HS erythrocytes by the spleen
Cont.
 Clinical manifestations

 Hereditary spherocytosis is usually transmitted

(approximately 75%) as an autosomal dominant trait.
 However, as many as 25% of patients have no previous
family history, representing recessive inheritance or de novo
mutations.
 Clinical manifestations

 In the neonatal period, HS is a significant cause of

hemolysis and can manifest as anemia and/or
hyperbilirubinemia severe enough to require phototherapy,
transfusion, or exchange transfusions.

 The need for transfusions in infancy is not indicative of

more severe disease later in life
 Clinical manifestations

 Gallstones can form as early as 4-5 yr and are present in

most adult HS patients.

 HS patients are susceptible to aplastic crises primarily as a

result of parvovirus B19 infection, hypoplastic crises
associated with other infections, and megaloblastic crises
caused by folate deficiency.
 Clinical manifestations

 During these crises, high RBC turnover in the setting of

erythroid marrow failure can result in profound anemia
(hematocrit <10%), high-output heart failure, cardiovascular
collapse, and death.

 Leukocyte and platelet counts may also fall.

 Disease severity

 Mild cases (20–30% of all HS) are asymptomatic into

adulthood and have well-compensated mild anemia, where
reticulocyte production and erythrocyte destruction are
essentially balanced.
 Moderate or “typical” HS (60–70%) have partially
compensated hemolytic anemia with reticulocytosis,
frequently with symptoms of fatigue, pallor, and intermittent
jaundice.
 Disease severity

 Splenomegaly is common after infancy and is present in

almost all HS patients by young adulthood.

 Severe HS (3–5%) have life-threatening anemia and are

transfusion dependent.
 Complications of HS

 Rare complications associated with HS include splenic

sequestration crisis, gout, cardiomyopathy, priapism, leg
ulcers, and neurologic or muscular abnormalities, including
spinocerebellar degeneration.
 Initial testing

 CBC and RBC indices – The mean corpuscular hemoglobin

concentration (MCHC) is often the most useful parameter
for assessing spherocytosis; an MCHC ≥36 g/dL is
consistent with spherocytes.
 A low mean corpuscular volume (MCV) is also helpful in
some cases, especially in neonates, but variable degrees of
reticulocytosis make the MCV less useful in older children
and adults.
 Initial testing

 Blood smear review – All individuals with suspected HS

should have a blood smear reviewed by an experienced
individual. RBC parameters to be assessed include the
presence and abundance of spherocytes, other abnormal
RBC shapes, and the degree of polychromatophilia, which
reflects reticulocytosis.
 Initial testing

 Hemolysis testing – Testing for hemolysis is also

appropriate in all patients. This includes lactate
dehydrogenase (LDH), indirect bilirubin, haptoglobin, and
reticulocyte count.
 Initial testing

 Coombs testing – If hemolysis is present, Coombs testing

(also called direct antiglobulin testing [DAT]) is usually
done to eliminate the possibility of immune-mediated
hemolysis, which may be due to hemolytic disease of the
fetus and newborn (HDFN) in neonates or autoimmune
hemolytic anemia (AIHA) in older children and adults. 
 Confirmatory tests

 EMA binding:
⚫ Binding of fluorescence labeled eosin-5-maleimide
(EMA) to band 3 and other membrane proteins is
decreased in HS erythrocytes.
⚫ This flow cytometry–based test is easy to perform and has
good diagnostic sensitivity and specificity.
 Confirmatory tests

 Osmotic fragility 
⚫ In this test, fresh RBCs are incubated in hypotonic
buffered salt solutions of various osmolarities, and the
fraction of hemoglobin released (due to hemolysis) is
measured. The test takes advantage of the increased
sensitivity of spherocytes to hemolysis, which is due to
their reduced surface area to volume (SA/V) ratio. The
OFT has relatively low sensitivity and specificity.
 Confirmatory tests

 Other assays, such as the cryohemolysis test, the acidified

glycerol lysis test, and osmotic gradient ektacytometry, have
been used for diagnosis of HS, but these tests are not
available in many laboratories.

 Genetic diagnosis is available, and the cost continues to

decrease.
 Confirmatory tests

 The precise role of molecular testing in HS is evolving.

 Some experts suggest molecular testing before splenectomy
to verify the diagnosis of HS.
 Diagnosis

 The diagnosis of HS is made in an individual who presents

with Coombs-negative hemolysis, an increased MCHC, a
positive family history for HS, and/or spherocytes on the
peripheral blood smear, by finding a positive result from
one or more confirmatory tests such as, EMA binding, or
osmotic fragility. 
 Differential diagnosis

 The differential diagnosis for spherocytosis on peripheral

blood smear includes isoimmune and autoimmune
hemolysis.

 Isoimmune hemolytic disease of the newborn, particularly

when a result of ABO incompatibility, closely mimics the
appearance of HS.
 Differential diagnosis

 Rare causes of spherocytosis include thermal injury,

hemolytic transfusion reaction, clostridial sepsis, severe
hypophosphatemia, Wilson disease, congenital
dyserythropoietic anemia type II, hereditary stomatocytosis,
and snake, bee, or wasp envenomation,
Cont.

Management of HS
 General Supportive Care

 Infants born to a parent with known HS should be

monitored carefully because hyperbilirubinemia may peak
several days after birth.
 Parents should be advised of the risk of neonatal anemia,
jaundice, and the potential need for transfusion,
phototherapy, and exchange transfusion to treat anemia or
hyperbilirubinemia.
 General Supportive Care

 A subset of infants will be transfusion dependent until

development of adequate erythropoiesis to compensate for
the ongoing hemolysis, usually between 6 and 12 mo of age.

 Transfusion dependence after this time is rare and is most

likely caused by recessive HS.
 General Supportive Care

 Once the baseline level of disease severity is reached, an

annual visit to the hematologist usually is sufficient follow-up.

 Growth should be monitored, and exercise tolerance and

spleen size should be documented.

 Vaccinations should be up to date.

 General Supportive Care

 Screening for gallbladder disease should begin at about 4 yr

of age, repeated every 3-5 yr, or as indicated clinically.

 Documentation of parvovirus B19 susceptibility or

immunity should be obtained in new patients.
 Similarly, HIV and hepatitis serology should be documented
in patients who have received transfusions.
 General Supportive Care

 Folic acid supplementation is recommended in patients with

moderate and severe HS because of the demands of brisk
erythropoiesis.
 Parents should receive anticipatory guidance regarding the
risk of aplastic crisis secondary to parvovirus infection and
hypoplastic crises with other infections. Parents and patients
should be informed of an increased risk for gallstone
development.
 Splenectomy and/or cholecystectomy 

 For those with relatively severe hemolysis, splenectomy is

effective at improving anemia. Ideally, this is delayed until
the individual is older than six years to reduce the likelihood
of sepsis due to absent splenic function.
 Simultaneous cholecystectomy can be performed if
gallstones are also present.
Cont.

Thalassemia Syndromes
 Introduction

 Thalassemia refers to a group of genetic disorders of globin-

chain production in which there is an imbalance between the
α-globin and β-globin chain production.
 β-Thalassemia syndromes result from a decrease in β-globin
chains, which results in a relative excess of α-globin chains.
 β0-thalassemia refers to the absence of production of the β-
globin..
 Introduction

 When patients are homozygous for the β0-thalassemia gene,

they cannot make any normal β-globin chains (HbA).
 β+-thalassemia indicates a mutation that makes decreased
amounts of normal β-globin (HbA).
 β0-thalassemia syndromes are generally more severe than
β+-thalassemia syndromes, but there is significant
variability between the genotype and phenotype.
 Introduction

 β-thalassemia major, or transfusion-dependent thalassemia,

refers to severe β-thalassemia that requires early transfusion
therapy.
 β-thalassemia intermedia (or non–transfusion dependent) is
a clinical diagnosis of a patient with a less severe clinical
phenotype that usually does not require regular transfusion
therapy in childhood.
 Introduction

 Many of these patients have at least 1 β+-thalassemia

mutation.
 β-thalassemia syndromes usually require a β-thalassemia
mutation in both β-globin genes.
 Carriers with a single β-globin mutation are generally
asymptomatic, except for microcytosis and mild anemia.
 Introduction

 In α-thalassemia, there is an absence or reduction in α-

globin production usually due to deletions of α-globin
genes.

 Normal individuals have 4 α-globin genes; the more genes

affected, the more severe the disease.
 Introduction

 α0-thalassemia indicates no α-chains produced from that

chromosome (− −/).

 α+-thalassemia produces a decreased amount of α-globin

chain from that chromosome (-alpha/).
 Introduction

 The primary pathology in the thalassemia syndromes stems

from the quantity of globin produced, whereas the primary
pathology in sickle cell disease is related to the quality of β-
globin produced.
 Epidemiology

 There are >200 different mutations resulting in absent or

decreased globin production.
 Although most are rare, the 20 most common abnormal
alleles constitute 80% of the known thalassemias
worldwide; 3% of the world’s population carries alleles for
β-thalassemia, and in Southeast Asia 5–10% of the
population carry alleles for α-thalassemia.
 Pathophysiology

 Two related features contribute to the sequelae of β-

thalassemia syndromes:
⚫ inadequate β-globin gene production leading to decreased
levels of normal hemoglobin (HbA) and
⚫ unbalanced α- and β-globin chain production leading to
ineffective erythropoiesis.
 Pathophysiology

 This results in a marked increase in erythropoiesis, with

early erythroid precursor death in the bone marrow.

 Clinically, this is characterized by a lack of maturation of

erythrocytes and an inappropriately low reticulocyte count.
 Pathophysiology

 This ineffective erythropoiesis and the compensatory

massive marrow expansion with erythroid hyperactivity
characterize β-thalassemia.

 Due to the low or absent production of β-globin, the α-

chains combine with γ-chains, resulting in HbF (α2γ2) being
the dominant hemoglobin.
 Pathophysiology

 In the α-thalassemia syndromes, there is a reduction in α-

globin production.
 Normally, there are 4 α-globin genes (2 from each parent)
that control α-globin production.
 α-thalassemia syndromes vary from complete absence
(hydrops fetalis) to only slightly reduced (α-thalassemia
silent carrier) α-globin production.
 Pathophysiology

 In the α-thalassemia syndromes, an excess of β- and γ-

globin chains are produced.
 These excess chains form Bart hemoglobin (γ4) in fetal life
and HbH (β4) after birth. These abnormal tetramers are
nonfunctional hemoglobins with very high oxygen affinity.
 They do not transport oxygen and result in extravascular
hemolysis.
 Pathophysiology

HOMOZYGOUS β-THALASSEMIA
(THALASSEMIA MAJOR, COOLEY
ANEMIA)
 Clinical Manifestations

 If not treated, children with homozygous β0-thalassemia

usually become symptomatic from progressive anemia, with
profound weakness and cardiac decompensation during the
2nd 6 mo of life.
 Depending on the mutation and degree of HbF production,
regular transfusions are necessary beginning in the 2nd mo
to 2nd yr of life, but rarely later.
 Clinical Manifestations

 The decision to transfuse is multifactorial but is not

determined solely by the degree of anemia.

 The presence of signs of ineffective erythropoiesis, such as

growth failure, bone deformities secondary to marrow
expansion, and hepatosplenomegaly, are important variables
in determining transfusion initiation.
 Clinical Manifestations

 The classic presentation of children with severe disease

includes thalassemic facies (maxilla hyperplasia, flat nasal
bridge, frontal bossing), pathologic bone fractures, marked
hepatosplenomegaly, and cachexia and is primarily seen in
countries without access to chronic transfusion therapy.
 Clinical Manifestations

 In nontransfused patients with severe ineffective

erythropoiesis, marked splenomegaly can develop with
hypersplenism and abdominal symptoms.
 Clinical Manifestations

 Chronic transfusion therapy dramatically improves the

quality of life and reduces the complications of severe
thalassemia.

 Transfusion-induced hemosiderosis becomes the major

clinical complication of transfusion dependent thalassemia.
 Laboratory testing

 CBC and hemolysis testing — The following findings are

consistent with thalassemia:
⚫ Microcytic anemia – Microcytic, hypochromic anemia is
typical in all thalassemia syndromes except asymptomatic
carriers.
⚫ High RBC count; mildly increased reticulocyte count
 Laboratory testing

⚫ Hemolysis Thalassemia causes non-immune hemolysis,

with high LDH, high indirect bilirubin, low haptoglobin,
and negative Coombs testing.
⚫ Normal WBC and platelet count 
 Confirmation

 Hemoglobin analysis and genetic testing — Hemoglobin

analysis and/or genetic testing is required to confirm the
diagnosis of thalassemia. 
 Management and Treatment of
Thalassemia
 Transfusion Therapy
 The goal being to maintain a pretransfusion Hb level of 9.5-
10.5 g/dL.
 Transfusions should generally be given at intervals of 3-4
wk.
 Management and Treatment of
Thalassemia
 Chelation Therapy
 DeferoxamineIt, requires subcutaneous or IV administration
 Deferoxamine is initially started at 25 mg/kg and can be
increased to 60 mg/kg in heavily iron-overloaded patients.
 Treatment cont…

 Hydroxyurea: used in β-thalassemia intermedia patients

 Splenectomy may be required in thalassemia patients who
develop hypersplenism.
 Complication

 Cardiac Disease
⚫ Cardiac disease is the major cause of death in
thalassemia. Serial echocardiograms should be monitored
to evaluate cardiac function and
 Endocrine function
⚫ progressively declines with age secondary to
hemosiderosis and nutritional deficiencies. starts early,
about 5 yr of age.
 Complication

 Psychosocial Support
⚫ Early social service consultation to address financial and
social issues is mandator
Cont.

G6PD
 Introduction

 This X-linked deficiency affects >400 million people

worldwide, representing an overall 4.9% global prevalence.

 Synthesis of RBC G6PD is determined by a gene on the X

chromosome.
 Introduction

 The deficiency is caused by inheritance of any of a large

number of abnormal alleles of the gene responsible for the
synthesis of the G6PD protein.

 About 140 mutations have been described in the gene

responsible for the synthesis of the G6PD protien.
Glucose-6-phosphate
dehydrogenase
 Etiology

 G6PD catalyzes the conversion of glucose 6-phosphate to 6-

phosphogluconic acid.
 This reaction produces NADPH, which maintains GSH
(glutathione in its reduced, functional state;.
 GSH provides protection against oxidant threats from
certain drugs and infections that would otherwise cause
precipitation of hemoglobin (Heinz bodies) or damage the
RBC membrane.
 Etiology

 G6PD variants
 Approximately 13% of male Americans of African descent
have a mutant enzyme (G6PD A−) that results in a deficiency
of RBC G6PD activity (5–15% of normal).
 Italians, Greeks, and other Mediterranean, Middle Eastern,
African, and Asian ethnic groups also have a high incidence,
ranging from 5– 40%, of a variant designated G6PD B−
(G6PD Mediterranean ).
 Agents Precipitating Hemolysis in Glucose-6-
Phosphate Dehydrogenase Deficiency

 Antibacterials  Antimalarials
 Sulfonamides  Primaquine
 Ciprofloxacin  Pamaquine
 Moxifloxacin  Chloroquine
 Norfloxacin
 Ofloxacin
 Quinacrine
 Dapsone
 Trimethoprim-
sulfamethoxazole
 Nalidixic acid
 Chloramphenicol
 Nitrofurantoin
Agents Precipitating Hemolysis in Glucose-6-
Phosphate Dehydrogenase Deficiency

 Anthelminthics  Chemicals
 β-Naphthol  Phenylhydrazine
 Stibophen  Benzene
 Niridazole  Naphthalene (mothballs)
 Others  2,4,6-Trinitrotoluene
 Acetanilide  Illness
 Vitamin K analogs  Diabetic acidosis
 Methylene blue  Hepatitis
 Toluidine blue  Sepsis
 Probenecid
 Dimercaprol
 Acetylsalicylic acid
 Clinical manifestations

 Most individuals with G6PD deficiency are asymptomatic,

with no clinical manifestations of illness unless triggered by
infection, drugs, or ingestion of fava beans.
 Typically, hemolysis ensues in about 24-48 hr after a patient
has ingested a substance with oxidant properties.
 In severe cases, hemoglobinuria , jaundice , and anemia.
 Clinical manifestations

 The degree of hemolysis varies with the inciting agent,

amount ingested, and severity of the enzyme deficiency.
 In some individuals, ingestion of fava beans also produces
an acute, severe hemolytic syndrome, known as favism.
 Favism is thought to be more frequently associated with the
G6PD B− variant.
 Clinical manifestations

 In G6PD A–, spontaneous hemolysis and hyperbilirubinemia

have been observed in preterm infants.
 In newborns with the G6PD B− and G6PD Canton varieties,
hyperbilirubinemia and even kernicterus may occur.
 When a pregnant woman ingests oxidant drugs, they may be
transmitted to her G6PD-deficient fetus, and hemolytic
anemia and jaundice may be apparent at birth.
 Laboratory findings

 The onset of acute hemolysis usually results in a precipitous

fall in hemoglobin and hematocrit.
 The blood film may contain red cells with what appears to
be a bite taken from their periphery (“bite cells”) and
polychromasia (evidence of bluish, larger RBCs),
representing Heinz bodies.
Cont.
 Diagnosis

 The diagnosis depends on direct or indirect demonstration

of reduced G6PD activity in RBCs.
 By direct measurement, enzyme activity in affected persons
is ≤10% of normal, and the reduction of enzyme activity is
more extreme in Americans of European descent and in
Asians than in Americans of African descent.
 Diagnosis

 The diagnosis can be suspected when G6PD activity is within

the low-normal range in the presence of a high reticulocyte
count.
 G6PD variants also can be detected by electrophoretic and
molecular analysis.
 G6PD deficiency should be considered in any neonatal
patients with hyperbilirubinemia and borderline-low G6PD
activity.
 Prevention and treatment

 The cornerstone of management of G6PD deficiency is the

avoidance of oxidative stress to red blood cells (RBCs).
 This is usually straightforward once the diagnosis is known.
 However, there may be instances in which an oxidant drug
is absolutely required, or cases in which oxidative stress
comes from an infection or other acute medical condition
that cannot be avoided.
 Prevention and treatment

 In these settings, management depends on the severity of

hemolysis and anemia and the patient's age and
comorbidities.
 Prevention and treatment

 Treatment of neonatal jaundice and chronic

hemolysis — 
 The management of neonatal jaundice due to G6PD
deficiency does not differ from that recommended for
neonatal jaundice arising from other causes.
 Prevention and treatment

 For those rare individuals with chronic hemolysis, routine

supplementation with folic acid is reasonable.
⚫ In such cases, a dose of 1 mg daily is adequate.

 For G6PD-deficient individuals who do not have chronic

hemolysis, there is no need for supplemental folic acid.
 Prevention and treatment

 Treatment of acute hemolytic episodes  

⚫ Whenever hemolysis occurs in an individual with G6PD
deficiency, any inciting agent(s) should be removed as
soon as possible.
⚫ Other interventions may include aggressive hydration for
acute intravascular hemolysis or transfusion for severe
anemia.
 Prevention and treatment

 Avoidance of unsafe drugs and chemicals —

⚫  The principle intervention for reducing hemolysis in

individuals with G6PD deficiency is avoiding exposure to
drugs and chemicals known to trigger hemolysis.
⚫ There is not universal agreement on which drugs are safe;
different sources provide lists that may differ slightly.
 Prevention and treatment

 Dietary restrictions —
⚫  It has also been known since antiquity that ingestion of
fava beans can cause acute hemolytic anemia in some
individuals.
 Prevention and treatment

 Blood donation  
⚫ As a general rule, donated blood is not screened for
G6PD deficiency, and individuals with G6PD deficiency
can donate blood as long as they are otherwise able to
donate and do not have anemia
Cont.

The End
Thank you
 References

 Nelson Text Book of Pediatrics 21st edition

 Up-to-date 2022