Iron Deficiency Anemia

Maj.Dr. Philip Pelema Gevao

Iron Deficiency Anemia
 One of the most common medical problems
 Most common cause of anemia
 Iron deficiency anemia is the last step ;
– Iron depletion: absent or decreased iron stores
– Iron deficiency: depletion of stores + low serum
iron and ferritin
– Iron deficiency anemia: Anemia developing in an
iron deficient patient
Total amount of body iron:3-5 g
Iron Metabolism
 Iron is located at the center of Hem molecules
of Hb (amount:1.5-2 gr)
and it is also;
 Part of the myoglobin
 Takes place in the tissue enzymes
 Storage forms are (1gr in men,0.5gr in women):
– Ferritin
– Hemosiderin
– Location: Bone Marrow, Liver, Spleen
 Transport iron is about 7 mg and bound to
transferrin.
 Iron Metabolism

 Transferrin picks up iron from ;

1. The GI cells to deliver it to Hb forming cells
2. Storage parts as a step of iron recycling
process
 Absorbtion + recycling provides the
constant iron supply of 20 mg/day (up to 35 mg)
necessary for Hb synthesis
Daily Iron Demands

Male 1 mg

Adolesc. 2-3 mg
Women in repr.age 2-3 mg
Pregnant 3-4 mg
Iron Metabolism
 Iron absorbtion is restricted to the
needs of the body
 1mg of iron is lost each day
– Sweating
– Epidermal shedding
– Menstruation and pregnancy/lactation are
other major causes of iron loss and
incresed demand in women
Iron Metabolism
 Normal diet contains about 15 mg of iron/day
 1/10 of ingested iron is absorbed
 Gastric acid releases iron from food
 Iron is absorbed in the reduced form
 Ascorbate increases absorbtion (by reducing)
 Phytates,tannates,antacids decrease
absorbtion by making complexes with iron
Iron Metabolism

 Main sites of absorbtion are;

– Duodenum
– Upper jejunum
 Malabsorbtive states or
gastrojejunostomy prevent absorbtion.
Iron Metabolism

Transport of iron
– Transferrin is the main iron carrier in
plasma
– It is produced in liver cells with increased
synthesis in iron deficiency
– Transferrin binds 1-2 ferric iron molecules
– Transferrin-iron complex is endocytosed
by Hb producing cells after linking to
receptors.
Iron Metabolism
 Total iron binding capacity and iron
– Transferrin is measured by quantifying
the iron binding sites available
– This is also called “Total iron binding
capacity”
– TIBC is 1/3 saturated under normal
conditions
 DIETARY IRON

There are 2 types of iron in the diet;

haem iron and non-haem iron
Haem iron is present in Hb containing
animal food like meat, liver & spleen
Non-haem iron is obtained from cereals,
vegetables & beans
Milk is a poor source of iron, hence
breast-fed babies need iron supplements
 IRON ABSORPTION

Haem iron is not affected by ingestion of

other food items.
It has constant absorption rate of 20-30
which is little affected by the iron balance
of the subject.
The haem molecule is absorbed intact and
the iron is released in the mucosal cells.
 IRON ABSORPTION (2)

The absorption of non-haem iron varies

greatly from 2% to 100% because it is
strongly influenced by:

The iron status of the body

The solubility of iron salts
Integrity of gut mucosa
Presence of absorption inhibitors or
facilitators
INHIBITORS OF IRON ABSORPTION

Food with polyphenol compounds

Cereals like sorghum & oats
Vegetables such as spinach and
spices
Beverages like tea, coffee, cocoa and
wine.
A single cup of tea taken with meal
reduces iron absorption by up to 11%.
 OTHER INHIBITORS

Food containing phytic acid i.e.

Bran, cereals like wheat, rice, maize
& barely. Legumes like soya beans,
black beans & peas.

Cow’s milk due to its high calcium

& casein contents.
 INHIBITION-HOW?

The dietary phenols & phytic acids

compounds bind with iron decreasing
free iron in the gut & forming
complexes that are not absorbed.
Cereal milling to remove bran reduces
its phytic acid content by 50%.
 Promoters of Iron
Absorption
 Foods containing ascorbic acid like citrus
fruits, broccoli & other dark green vegetables
because ascorbic acid reduces iron from ferric
to ferrous forms, which increases its
absorption.
 Foods containing muscle protein enhance iron
absorption due to the effect of cysteine
containing peptides released from partially
digested meat, which reduces ferric to ferrous
salts and form soluble iron complexes.
IRON ABSORPTION (3)

Some fruits inhibit the absorption of

iron although they are rich in ascorbic
acid because of their high phenol
content e.g strawberry banana and
melon.
Food fermentation aids iron absorption
by reducing the phytate content of diet
 IRON TRANSPORT

Transferrin is the major protein

responsible for transporting iron in the
body.
Transferrin receptors, located in almost
all cells of the body, can bind two
molecules of transferrin.
Both transferrin concentration &
transferrin receptors are important in
assessing iron status.
ROLE OF IRON IN THE BODY

Iron have several vital functions

Carrier of oxygen from lung to tissues
Transport of electrons within cells
Co-factor of essential enzymatic
reactions:
Neurotransmission
Synthesis of steroid hormones
Synthesis of bile salts
Detoxification processes in the liver
Causes of iron deficiency
 Chronic blood loss
 Increased demand
 Malabsorbtion of iron
 Inadequate iron intake
 Intravascular hemolysis and
hemoglobinuria-hemosiderinuria
 Combinations
Increased demands

 Pregnancy

 Lactation

 Rapid growth
Decreased intake
 Decreased iron in the diet
– Vegetarianism
 Decreased absorbtion
– Gastric surgery
– Achlorhydria
– Sprue
– Pica
Increased iron loss
 Menorrhagia
 GIS hemorrhagia
•Angiodysplasia
•P.Ulcer •Diverticulosis
•Oesophagitis •Meckel diverticula
•Varices •Colitis or imf. Bovel
•Hiatal hernia disease
•Malignancy •Hemorrhoids
•NSAID use
•Parasites
Increased iron loss
 Bleeding disorder
 Pulmonary lesions with bleeding
 Hemoglobinuria – hemosiderinuria
(chronic intravascular hemolysis)
 Hemodialysis
 Hematuria (chronic)
 Frequent donation
– 250 mg iron /unit-blood
Clinical features
 General symptoms of anemia
 Fatigue may be disproportional to the degree of
anemia due to deficiency of tissue enzymes
which also need iron
 Chlorosis

 Glossitis

 Angular stomatitis

 Paterson-Kelly (Plummer Vinson) syndrome

(oesephageal web leading to disphagia)

Clinical features

 Gastric atroph
 Nail changes
– Brittle/fragility
– Koilonchia/spooning
 Hair loss
 Splenomegaly
 Clinical features
 Pica:Appetite for bizzare food/substances
– Geophagy (earth,clay)
– Pagophagia(ice)
– Amylophagia(starch)
 Developmental problems
 Splenomegaly
 Tayanc-Prasad syndrome
(growth retardation, hypogonadism, hepatosplenomegaly, zinc and
iron deficiency, geophagia)
 Immun-deficiency
Lab. Features
 Hb,Htc,RBC:Low
 MCV,MCH,MCHC:Low
 RDW: High
 Retics: Normal/Low
 Plt:Normal/Low/High
 WBC:Normal/Low
 Smear: Hypochromia,anisocytosis,microcytosis,
poikilocytosis
 Lab.Features
 Serum Iron:  (N: 60 – 180 μg/dL)
 TIBC:  (250 - 430 μg/dL)
 Serum Ferritin 

(N:Female;10-150 μg/L, Male;29-248 μg/L)

Males and post menopausal women<10 μg/L
Premenopausal women <5 μg/L
Iron def+Chr.Disease< 60 μg/L
 Lab.Features

 Transferrin saturation (Fe/TIBC):  (<15%)

<5%:definitely indicates iron deficiency
 Serum Transferrin Receptor: 
 Free Erythrocyte Protoporphyrin  (17 – 27 μg/dL)
 Bone marrow :
– Erythroid hyperplasia,
– Absence of hemosiderin
Differential diagnosis

 Microcytic anemias
– Iron deficiency anemia
– Thalassemia ,HbC,HbE etc
– Sideroblastic anemia
– Lead poisoning
– Anemia of chronic diseases (sometimes)
Important !!!!!!!

 The diagnostic procedure is not

complete until the underlying
pathology is disclosed.
Treatment
 Replace iron and treat underlying disease.
 Oral route is preferred for replacement.
 Response can be followed by retic. increase in
1-2 weeks (5-7 days)
 Hb response to treatment
– half normal by a month
– returns to normal by 2-4 months
 Replacement therapy is prolonged by 6-12
months to replenish stores of iron.
 Ongoing bleeding may cause indefinite therapy.
Treatment

Oral iron therapy:

dose (mg) elemental
iron(mg)
Fe fumarate 200 65
Fe gluconate 300 35
Fe sulphate 200 65
Treatment
Oral iron therapy:
Total daily dose:150-200 mg elemental iron
Give in 3-4 divided doses,
Each one hour before meals.
Do not prefer enteric coated forms.
In case of GIS intolerance;
 Change the route of administration or
 Change the preparation or
 Reduce dose
Treatment
Non responding patient:
 possible causes

– Misdiagnosis
– Patient does not take the medicine
– Continuing blood loss
– Malabsorbtion
 Change the drug
 Change the route of administration

– Underlying disease /comorbidity

– Combined deficiency
Treatment
 Parenteral iron therapy:
Routine use is not justified,
Response is not faster than oral replacement.
Indications
– Malabsorbtion
– Intolerance to oral replacement
 Colitis/enteritis
– Needs in excess of amount that can be given
orally
– Patient uncooperative/poor compliance
– Autologous blood donation setting
– Hemodialysis
Treatment
Parenteral iron therapy:
Total iron dose: (15-patient Hb) x bw x 3
– Iron Dextran: 50 mg/ml (iv/im)
 Max daily dose is 100 mg im
– Ferric gluconate:
 A test dose of 25 mg elemental iron (2 mL) must be
given in 50 mL saline over 60 minutes

– Ferric-hydroxy-sucrose (100 mg/5mL)

– 2.5 ml first day
– 5ml third day
– 2x5 ml/week
Treatment
Parenteral replacement therapy may cause
– allergic reactions,
– local pain or induration,
– serum sickness like disease,
– lymphadenomegaly,
– arthralgia,
– myalgia etc.
preventive iron supplementation
 Pregnants ( at 20-24 weeks Hb< 11
g/dL, Ferritin ).
 Lactation.
 Frequent blood donation.
 Autologous blood donation settings.
 Gastrectomised patients.
 High dose asprin treatment.
THALASSEMIA

BY DR PP GEVAO

43
 Thalassemia

• At the end of this lecture, you will be introduced

to the thalassemias.  You will learn about the
pathophysiology, clinical signs and symptoms,
laboratory test results, and treatments for both
the alpha and beta forms of thalassemia. 
Subclasses of each major form of thalassemia
will be discussed.

44
 Thalassemia
• Diverse group of disorders which manifest
as anemia of varying degrees.
• Result of defective production of globin
portion of hemoglobin molecule.
• Distribution is worldwide.
• May be either homozygous defect or
heterozygous defect.
• Defect results from abnormal rate of
synthesis in one of the globin chains. 
• It is an autosomal recessive syndrome 
 Thalassemia
• Results in overall decrease in amount of
hemoglobin produced and may induce
hemolysis.
• Two major types of thalassemia:
– Alpha (α) - Caused by defect in rate of synthesis
of alpha chains.
– Beta (β) - Caused by defect in rate of synthesis in
beta chains.
• May contribute protection against malaria.
 Genetics of Thalassemia

• Adult hemoglobin composed two alpha

and two beta chains.
• Alpha thalassemia usually caused by
gene deletion;  Beta thalassemia usually
caused by mutation.
• Results in microcytic, hypochromic
anemias of varying severity.
 Beta
Thalassemia
 Classical Syndromes of Beta Thalassemia
• Silent carrier state – the mildest form of beta
thalassemia.
• Beta thalassemia minor - heterozygous disorder
resulting in mild hypochromic, microcytic
hemolytic anemia.
• Beta thalassemia intermedia - Severity lies
between the minor and major.
• Beta thalassemia major - homozygous disorder
resulting in severe transfusion-dependent
hemolytic anemia.
 Silent Carrier State for β Thalassemia

• Are various heterogenous beta

mutations that produce only small
decrease in production of beta chains.
• Patients have nearly normal beta/alpha
chain ratio and no hematologic
abnormalities.
• Have normal levels of Hb A2.
50
 Beta Thalassemia Minor
• Caused by heterogenous mutations that affect
beta globin synthesis. 
• Usually presents as mild, asymptomatic
hemolytic anemia unless patient in under stress
such as pregnancy, infection, or folic acid
deficiency.
• Have one normal beta gene and one mutated
beta gene.
• Hemoglobin level in 10-13 g/dL range with
normal or slightly elevated RBC count. 
 Beta Thalassemia Minor
• Anemia usually hypochromic and
microcytic with slight aniso and poik,
including target cells and elliptocytes;  May
see basophilic stippling.
• Rarely see hepatomegaly or splenomegaly.
• Have high Hb A2 levels (3.5-8.0%) and
normal to slightly elevated Hb F levels.
• Are different variations of this form
depending upon which gene has mutated.
• Normally require no treatment. 
 Beta Thalassemia Intermedia
• Patients able to maintain minimum hemoglobin (7
g/dL or greater) without transfusions. 
• Expression of disorder falls between thalassemia
minor and thalassemia major.  May be either
heterozygous for mutations causing mild decrease
in beta chain production, or may be homozygous
causing a more serious reduction in beta chain
production.
• See increase in both Hb A2 production and Hb F
production.
• Peripheral blood smear picture similar to
thalassemia minor.
 Beta Thalassemia Intermedia
• Have varying symptoms of anemia, jaundice,
splenomegaly and hepatomegaly.
• Have significant increase in bilirubin levels. 
• Anemia usually becomes worse with infections,
pregnancy, or folic acid deficiencies.
• May become transfusion dependent as adults.
• Tend to develop iron overloads as result of
increased gastrointestinal absorption.
• Usually survive into adulthood.
 Beta Thalassemia Major
• Characterized by severe microcytic, hypochromic
anemia. 
• Detected early in childhood:
– Infants fail to thrive. 
– Have pallor, variable degree of jaundice, abdominal
enlargement, and hepatosplenomegaly.
• Hemoglobin level between 4 and 8 gm/dL.
• Severe anemia causes marked bone changes due to
expansion of marrow space for increased
erythropoiesis.
• See characteristic changes in skull, long bones, and
hand bones. 
 Beta Thalassemia Major
• Have protrusion upper teeth and Mongoloid
facial features. 
• Physical growth and development delayed.
• Peripheral blood shows markedly hypochromic,
microcytic erythrocytes with extreme
poikilocytosis, such as target cells, teardrop cells
and elliptocytes.  See marked basophilic stippling
and numerous NRBCs. 
• MCV in range of 50 to 60 fL.
• Low retic count seen (2-8%).
• Most of hemoglobin present is Hb F with slight
increase in Hb A2.
 Beta Thalassemia Major
• Regular transfusions usually begin around one
year of age and continue throughout life. 
• Excessive number of transfusions results in
tranfusional hemosiderosis; Without iron
chelation, patient develops cardiac disease.
• Danger in continuous tranfusion therapy:
– Development of iron overload.
– Development of alloimmunization (developing
antibodies to transfused RBCs).
– Risk of transfusion-transmitted diseases.
• Bone marrow transplants may be future
treatment, along with genetic engineering and
new drug therapies.
 Comparison of Beta Thalassemias
GENOTYPE HGB A HGB A2 HGB F

NORMAL Normal Normal Normal

SILENT Normal Normal Normal

CARRIER
MINOR Dec Normal to Normal to
Inc Inc
INTERMEDIA Dec Normal to Usually Inc
Inc
MAJOR Dec Usually Inc Usually Inc
Other Thalassemias Caused by Defects in
the Beta-Cluster Genes

• 1. Delta Beta Thalassemia

• 2. Hemoglobin Lepore
• 3. Hereditary Persistence of Fetal
Hemoglobin (HPFH)
 Delta Beta Thalassemia
• Group of disorders due either to a gene
deletion that removes or inactivates only
delta and beta genes so that only alpha
and gamma chains produced.
• Similar to beta thalassemia minor.
• Growth and development nearly normal. 
Splenomegaly modest.  Peripheral blood
picture resembles beta thalassemia.
 Hemoglobin Lepore

• Rare class of delta beta thalassemia.

• Caused by gene crossovers between
delta locus on one chromosome and
beta locus on second chromosome.
 Hereditary Persistence of Fetal Hemoglobin
(HPFH)
• Rare condition characterized by  continued
synthesis of Hemoglobin F in adult life. 
• Do not have usual clinical symptoms of
thalassemia.
• Little significance except when combined with
other forms of thalassemia or
hemoglobinopathies.
• If combined with sickle cell anemia, produces
milder form of disease due to presence of Hb
F.
 Beta Thalassemia with Hbg S
• Inherit gene for Hb S from one parent and gene
for Hb A with beta thalassemia from second
parent.
• Great variety in clinical severity.   Usually
depend upon severity of thalassemia inherited. 
Production of Hb A ranges from none produced
to varying amounts.  If no Hb A produced, see
true sickle cell symptoms.  If some Hb A
produced, have lessening of sickle cell anemia
symptoms.
 Beta Thalassemia with Hgb C

• Shows great variability in clinical

and hematologic symptoms.
• Symptoms directly related to
which type thalassemia inherited.
• Usually asymptomatic anemia
 Beta Thalassemia with Hgb E
• Is unusual because results in more severe
disorder than homozygous E disease.
• Very severe anemia developing in
childhood. 
• Transfusion therapy required.
Alpha Thalassemia
 Alpha Thalassemia
• Has wide range clinical expressions.
• Is difficult to classify alpha thalassemias due to
wide variety of possible genetic combinations.
• Absence of alpha chains will result in increase
of gamma chains during fetal life and excess
beta chains later in life;  Causes molecules like
Bart's Hemoglobin (γ4) or Hemoglobin H (β4),
which are stable molecules but physiologically
useless.
 Alpha Thalassemia
• Predominant cause of alpha thalassemias is
large number of gene deletions in the alpha-
globin gene.
• Are four clinical syndromes present in alpha
thalassemia:
– Silent Carrier State
– Alpha Thalassemia Trait  (Alpha Thalassemia Minor)
– Hemoglobin H Disease
– Bart's Hydrops Fetalis Syndrome
 Silent Carrier State
• Deletion of one alpha gene, leaving three
functional alpha genes.
• Alpha/Beta chain ratio nearly normal.
• No hematologic abnormalities present.
• No reliable way to diagnose silent carriers
by hematologic methods;  Must be done by
genetic mapping.
• May see borderline low MCV  (78-80fL).
 Alpha Thalassemia Trait
(Alpha Thalassemia Minor)
• Also called Alpha Thalassemia Minor.
• Caused by two missing alpha genes.  May be
homozygous (-a/-a) or heterozygous (--/aa).
• Exhibits mild microcytic, hypochromic anemia.
• MCV between 70-75 fL.
• May be confused with iron deficiency anemia.
• Although some Bart's hemoglobin (γ4) present
at birth, no Bart's hemoglobin present in
adults.
 Hemoglobin H Disease
• Second most severe form alpha thalassemia.
• Usually caused by presence of only one gene
producing alpha chains (--/-a). 
• Results in accumulation of excess unpaired
gamma or beta chains. Born with 10-40% Bart's
hemoglobin (γ4).   Gradually replaced with
Hemoglobin H (β4). In adult, have about 30-50%
Hb H.

γ4 β4
 Hemoglobin H Disease
• Live normal life; however, infections,
pregnancy, exposure to oxidative drugs may
trigger hemolytic crisis.
• RBCs are microcytic, hypochromic with marked
poikilocytosis.  Numerous target cells.
• Hb H vulnerable to oxidation.  Gradually
precipitate in vivo to form Heinz-like bodies of
denatured hemoglobin.  Cells been described
has having "golf ball" appearance, especially
when stained with brilliant cresyl blue.
 Bart’s Hydrops Fetalis Syndrome
• Most severe form.  Incompatible with life.  Have no
functioning alpha chain genes (--/--).
• Baby born with hydrops fetalis, which is edema and ascites
caused by accumulation serous fluid in fetal tissues as result
of severe anemia.  Also see hepatosplenomegaly and
cardiomegaly.
• Predominant hemoglobin is Hemoglobin Bart, along with
Hemoglobin Portland and traces of Hemoglobin H.
• Hemoglobin Bart's has high oxygen affinity so cannot carry
oxygen to tissues.  Fetus dies in utero or shortly after birth. At
birth, see severe hypochromic, microcytic anemia with
numerous NRBCs.
• Pregnancies dangerous to mother.  Increased risk of toxemia
and severe postpartum hemorrhage.
 Comparison of Alpha Thalassemias

Genotype Hb A Hb Bart Hb H

Normal 97-98% 0 0

Silent Carrier 96-98% 0-2% 0

Alpha Thalassemia 85-95% 5-10% 0

Trait
Hemoglobin H Dec 25-40% 2-40%
Disease
Hydrops Fetalis 0 80% (with 20% 0-20%
Hgb Portland)
 Alpha Thalassemia with Hgb S
• Alpha thalassemia can occur in
combination with hemoglobin S.  Is fairly
common combination in populations of
African descent.
• Patient usually asymptomatic.  Have less
Hb S present than those with sickle cell
trait.  Have increased presence of Hb F.
Laboratory Diagnosis
of Thalassemia
 Laboratory Diagnosis of Thalassemia
• Need to start with patient's individual
history and family history.  Ethnic
background important.
• Perform physical examination:
– Pallor indicating anemia.
– Jaundice indicating hemolysis.
– Splenomegaly due to pooling of abnormal cells.
– Skeletal deformity, especially in beta
thalassemia major.
 CBC with Differential
• Decrease in hemoglobin, hematocrit, mean
corpuscular volume (MCV), and mean
corpuscular hemoglobin (MCH).  See normal to
slightly decreased Mean Corpuscular
Hemoglobin Concentration (MCHC).  Will see
microcytic, hypochromic pattern.
• Have normal or elevated RBC count with a
normal red cell volume distribution (RDW).
• Decrease in MCV very noticeable when
compared to decrease in Hb and Hct.
 CBC with Differential
• Elevated RBC count with markedly
decreased MCV differentiates thalassemia
from iron deficiency anemia.
• On differential, see microcytic, hypochromic
RBCs (except in carrier states).  See mild to
moderate poikilocytosis.  In more severe
cases, see marked number of target cells
and elliptocytes.  Will see polychromasia,
basophilic stippling, and NRBCs.
 Reticulocyte Count

• Usually elevated.  Degree of

elevation depends upon severity of
thalassemia.
 Osmotic Fragility

• Have decreased osmotic fragility.

• Is not very useful fact for
diagnosing thalassemia.  Is an
inexpensive way of screening for
carrier states.
 Brilliant Cresyl Blue Stain
• Incubation with brilliant cresyl blue stain
causes Hemoglobin H to precipitate. 
Results in characteristic appearance of
multiple discrete inclusions -golf ball
appearance of RBCs.   Inclusions smaller
than Heinz bodies and are evenly
distributed throughout cell.
 Acid Elution Stain

• Based on Kleihauer-Betke procedure.  Acid

pH will dissolve Hemoglobin A from red
cells.  Hemoglobin F is resistant to
denaturation and remains in cell.  Stain slide
with eosin.  Normal adult cells appear as
"ghost" cells while cells with Hb F stain
varying shades of pink.
• Useful way to differentiate between
pancellular HPFH and heterocellular HPFH.
 Hemoglobin Electrophoresis
• Important role in diagnosing and differentiating
various forms of thalassemias.
• Can differentiate among Hb A, Hb A2, and Hb F,
as well as detect presence of abnormal
hemoglobins such as Hemoglobin Lepore,
hemoglobin Bart's, or Hemoglobin Constant
Spring.
• Also aids in detecting combinations of
thalassemia and hemoglobinopathies.
 Hemoglobin Quantitation
• Elevation of Hb A2 excellent way to
detect heterozygote carrier of beta
thalassemia.  Variations in gene
expression in thalassemias results in
different amounts of Hb A2 being
produced.
• Can also quantitate levels of Hb F.
 Routine Chemistry Tests
• Indirect bilirubin elevated in
thalassemia major and intermedia.
• Assessment of iron status, total iron
binding capacity, and ferritin level
important in differentiating
thalassemia from iron deficiency
anemia.
86
 Other Special Procedures

• Globin Chain Testing - determines

ratio of globin chains being
produced.
• DNA Analysis - Determine specific
defect at molecular DNA level.

87
 Differential Diagnosis of Microcytic,
Hypochromic Anemias

RDW Serum TIBC Serum FEP

Iron Ferritin
Iron Deficiency Inc Dec Inc Dec Inc
Alpha Thal Norm Norm Norm Norm Norm
Beta Thal Norm Norm Norm Norm Norm

Hgb E Disease Norm Norm Norm Norm Norm

Anemia of Norm Dec Dec Inc Inc
Chronic Disease
Sideroblastic Inc Inc Norm Inc Dec
Anemia
Lead Poisoning Norm Norm Norm Norm Inc
88