Iron deficiency anemia-

pathophysiology and
lab diagnosis
Introduction
• Anemia is functionally defined as an insufficient RBC mass to
adequately deliver oxygen to peripheral tissues.
• Anemia is considered to be present if the hemoglobin (Hb)
concentration or the hematocrit (Hct) is below the lower limit of
the 95% reference interval for the individuals age, sex, and
geographic location.
• Anemia may be absolute, when red blood cell mass is decreased,
or relative, when associated with a higher plasma volume.
• Causes of absolute anemia
• 1. impaired red cell production
• 2. increased erythrocyte destruction or loss in excess of the
ability of the marrow to replace these losses.
• Iron deficiency is the most common anaemia.
• 83-90% of all anemia constitute IDA
• Every day about 30 mg iron is used to make new hemoglobin.
• Daily iron loss is around 1 mg.
• In women menstruation and childbirth increase iron losses to
about 1.5 mg/day.
 • The total content of iron in the body - about 4.2g.

From them:
- 75-80% belongs to the hemoglobin

- 20 - 25% reserve

- 5-10% part of the myoglobin

-1% is part of the enzyme for the tissue respiration

DIETARY IRON
• There are 2 types of iron in the diet; heme iron and non-heme
iron.
• Heme iron is present in Hb containing animal food like meat,
liver & spleen.
• Non-heme iron is obtained from cereals, vegetables & beans.
Iron cycle
• Most body iron is present in hemoglobin in
circulating red cells
• The macrophages of the reticuloendotelial
system store iron released from
hemoglobin as ferritin and hemosiderin.
• In the plasma, total iron averages 110µg/dL
• Majority bound to the transferrin (capacity
to bind 330 µg of iron per deciliter)
• So only one third of transferrin is saturated.
IRON METABOLISM
• Iron concentration (Fe)
N: 50-150 g/dl
• Total Iron Binding Capacity
N: 250-450 g/dl
• Transferrin saturation
• Transferrin receptor concentration
• Ferritin concentration
N: 50-300 g/dl
Overview of Iron Homeostasis
IRON ABSORPTION
• Site- Proximal small intestine i.e. duodenum (first part-
maximum absorption) and jejunum.
• 10% of dietary iron is absorbed
• it is determined by intraluminal factor i.e. pH and redox
potential.
• Therapeutic ferrous iron is well absorbed on empty stomach.
• Haem iron is not affected by ingestion of other food items.
• Heme iron → Acid and gastric juices release it from apoprotein
→ Oxidised → hemin → directly absorb through mucosal cell
intact.
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%.
• Food containing phytic acid i.e. Bran
• Cow’s milk due to its high calcium & casein contents.
Promoters of Iron Absorption
• Foods containing ascorbic acid like citrus fruits, broccoli &
other dark green vegetables
• Foods containing muscle protein
• Food fermentation aids iron absorption by reducing the
phytate content of diet
Iron absorption at molecular
level
• Iron is converted from Fe3+ to
Fe2+ by ferrireductase
(DCYTB).
• Fe2+ transported across
mucosal surface of enterocyte
by DMT1, stored as ferritin.
• Ferritin releases Fe2+ which is
transported across basolateral
surface of enterocyte with
help of ferroportin .
• Fe2+ converted back to Fe3+ by
Hephaestin .
• Fe3+ binds to transferrin in
plasma.
Regulation of Iron Absorption
• Regulated at two stages
• Mucosal uptake
• At stage of transfer to blood
• 1. HIF-2 ά- a mediator of cellular adaptation to hypoxia,
regulates DMT1 transcription and thus regulates mucosal
uptake of iron because mucosal uptake depend on DMT 1.
• 2. Iron transfer to the plasma depends on the requirements of
the erythron for iron and the level of iron stores.
• This regulation is mediated directly by hepcidin.
Cellular iron uptake & release
• The reticuloendothelial macrophages play a major role in
recycling iron resulting from the degradation of haemoglobin
from senescent erythrocytes.
• They engulf red blood cells and release the iron within using
haem oxygenase.
• The protein transporting iron to plasma is ferroportin.
Ferroportin and Hepcidin
• Hepcidin- its synthesis is controlled at molecular level.
• Interaction of diferric transferrin, bone morphogenetic
proteins (BMPs), interleukin (IL)-6 and other inflammatory
cytokines with cell surface receptors TfR1, TfR2, hemojuvelin
(HJV) and IL-6 receptor lead to upregulation of the hepcidin
gene.
• Mechanism of action- it binds to both TfR1 and TfR2,
decreasing the affinity of each for transferrin.
• Stabilization and endocytosis of TfR2 stimulates hepcidin
production
• Diferric transferrin displaces the protein HFE from TfR1,
leaving it free to interact with TfR2, thus stimulating hepcidin
production in response to plasma iron levels.
 • Increased erythropoiesis causes decreased hepcidin.
Hepcidine function
• Blocks ferroportin
• Prevents absorption of iron from enterocytes.
• Prevents iron exportation from macrophages.
• Increased in inflammation.
• Leads to reduced serum iron, microcytic anemia, and
incomplete response to iron therapy.
• Ferroportin
• Transporter protein of iron in enterocytes and
macrophages.
• Blocked by hepcidin .
Newborn Iron Stores
• Endowed with 75 mg/kg of iron at birth
• Dependent on hemoglobin concentration at birth (majority of
iron in circulating RBCs)
• Depleted by 3 months in low birth weight infants without
supplementation
• Depleted by age 5-6 months in term infants
• Delayed cord clamping (by 2 minutes) leads to higher ferritin
and iron stores at 6 months of age
Iron storage
• Iron stored in two forms
• Soluble ferritin
• Insoluble hemosiderin- denatured form of ferritin in which the
protein shells have partly degraded, allowing the iron cores to
aggregate.
• Hemosiderin deposits are seen on Prussian-blue positivity after
staining of tissue sections with potassium ferrocyanide in acid.
Regulation of Iron Metabolism
• Iron metabolism is regulated post transcriptionally by iron
regulatory proteins- IRP 1 and IRP 2.
• The conformation of IRP1 required for binding to mRNA iron-
responsive elements (IREs).
• IRP2 are directly affected by the amount of iron within a cell.
• When the labile iron pool is deficient of iron, IRP1 has
an available binding site for IRE.
• When the labile iron pool is saturated with iron, the iron binds to
IRP1 to produce a 4Fe-4S cluster which blocks the IRE binding site
and prevents IRP1 binding to the IRE.
• In the presence of iron, IRP2 is degraded.
• Regulation of iron proteins by IRP on basis of location of IRE on
mRNA
• at 3’UTR- Stabiles translocation of TfR & DMT 1
• 5’UTR- inhibit translation of mRNA
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.
• One molecule of transferrin binds two molecules of iron.
• Both transferrin saturation & transferrin receptors are
important in assessing iron status
 • Transferrin, when incompletely saturated with iron, exists in
four forms:
1. Apotranferrin
2. Monoferrric transferrin A
3. Monoferrric transferrin B
4. Diferric Transferrin
• There distribution may be determined by urea-polyacrylamide
electrophoresis.
• The plasma iron pool (transferrin-bound iron)
is about 3 mg.
 Other iron transporter proteins
1. Haptoglobin- Serum glycoprotein
• It binds with Hemoglobin άẞ dimer released into the bloodstream by
hemolysis.
• Hemoglobin–haptoglobin complex is removed from plasma by
macrophages having receptor CD 163.
2. Hemopexin- Plasma glycoprotein that binds heme and transports the
haem to cells by a process that involves receptor-mediated endocytosis
3. Ferritin-
• present in low conc in plasma.
• Mostly appears as glycosylated and has low content of iron.
• It is also released into the circulation as a result of tissue damage.
4. Non-transferrin-bound iron-
• Iron that is not bound to transferrin.
• Have low molecular mass and can be bound by specific iron
chelators.
• Chemical form is not known but rapidly removed from circulation
by liver.
• This removal involve zinc transporter ZIP14.
AT RISK GROUPS
1. Infants
2. Under 5 children
3. Children of school age
4. Women of child bearing age
5. Geriatric age group
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
• Growing infants and children
• Menstruating women
• Multiparity
• Parturition
Decreased intake
• Decreased iron in the diet
• Vegetarian diet
• Low socioeconomic status
• Lack of balanced diet or poor intake
• Alcoholism
• Decreased absorbtion
• Gastric surgery
• Achlorhydria
• Duodenal pathology
• Chronic renal failure patients
• Coeliac Sprue
• Pica
Increased iron loss
• Menorrhagia • Meckel
• Gastrointestinal hemorrhage diverticula
• P.Ulcer
• Oesophagitis
• Colitis or
• Varices imperforated
• Hiatal hernia bowel disease
• Malignancy
• Hemorrhoids
• NSAID use
• Parasites
• Angiodysplasia
• Diverticulosis
Increased iron loss
• Bleeding disorder
• Pulmonary lesions with bleeding
• Hemoglobinuria – hemosiderinuria (chronic intravascular
hemolysis)
• Hemodialysis
• Hematuria (chronic)
• Frequent donation
• 250 mg iron /unit-blood
Pathogenesis of iron deficiency
anemia
• There are three pathogenic factors
• Impaired Hb synthesis d/t reduced iron supply
• Generalized defect in cellular proliferation
• Survival of erythroid precursor and erythrocytes is reduced
When transferrin saturation ‹15%, marrow supply of iron reduced
and is inadequate to meet basal requirement for Hb production.
• erythrocyte protoporphyrin raised
• each RBC contain less Hb so microcytic and hypochromic
Clinical features of iron deficiency
anemia
• Fatigue and Other Nonspecific Symptoms
• irritability, palpitations, dizziness, breathlessness, headache, and
fatigue
• Neuromuscular System
• impair muscular performance, abnormalities in muscle
metabolism , behavioral disturbances,
• Neurologic development in infants and scholastic performance in
older children may be impaired.
• Sometimes neuralgia pains, vasomotor disturbances, or
numbness and tingling.
Epithelial tissues
Site findings
Nails Flattening
Koilonychia
Tongue Soreness
Mild papillary atrophy
Absence of filiform papillae
Mouth Angular stomatitis
Hypopharynx Dysphagia
Esophageal webs
Stomach Achlorhydria
Gastritis
Plummer-Vinson syndrome
• The most common
anatomic lesion is a
“web” of mucosa at
the juncture between
the hypopharynx and
the esophagus
• Immunity and Infection
• Defective lymphocyte-mediated immunity and impaired bacterial killing
by phagocytes.
• Pica
• “craving to eat earth”
• Pagophagia is, defined as the purposeful eating of at least one tray
of ice daily for 2 months,
• Food pica- compulsively eating one food, often something that is
brittle and makes a crunching sound when chewed.
• Genitourinary System- Disturbances in menstruation,
• Skeletal System
• diploic spaces may be widened, and the outer tables thinned
Developmental Stages of Iron
Deficiency Anemia (WHO)
• Pre-latent –
• reduction in iron stores without reduced serum iron levels
• Hb, MCV, Transferrin saturation- Normal, Iron absorption -increase,
Serum ferritin and marrow iron reduced
• no clinical manifestation
• Latent-
• iron stores are exhausted, but the blood hemoglobin level remains
normal
• index of the blood within the standard
• clinical picture is caused by the sideropenic syndrome
• Iron Deficiency Anemia
• blood hemoglobin concentration falls below the lower limit of normal
• the clinical manifestations in the form of sideropenic syndrome and
general anemic symptoms
Stages in the Development of Iron
Deficiency

Stage 1 (Prelatent) Stage 2 (Latent) Stage 3 (Anemia)

Bone marrow iron Reduced Absent Absent

Serum ferritin Reduced <12 μg/L <12 μg/L

Transferrin saturation Normal <16% <16%

Free erythrocyte protoporphyrin, zinc Normal increased increased

protoporphyrin
Serum transferrin receptor Normal increased increased

Reticulocyte hemoglobin content Normal reduced reduced

Hemoglobin Normal Normal Reduced

Mean corpuscular volume Normal Normal Reduced

Symptoms Fatigue, malaise Pallor, pica, in some

patients
Laboratory diagnosis
• Complete blood count
• Bone marrow
• Serum parameter
• ferrokinetic Studies
BLOOD AND
BONE MARROW FINDINGS
• BLOOD: peripheral smear findings
• microcytosis, hypochromia, anisocytosis , poikilocytosis
AUTOMATED ANALYSER
FINDINGS
 IRON DEFICIENCY ANEMIA
• MCV - Reduced ( N : 80-100 fl)
• MCH - Reduced ( N : 27-32 pg)
• MCHC– Normal to reduced (N: 30-34 mg/dl)
• Iron- Reduced (N: 4 gm )
• TIBC- Increased (N: 47-70 µmol/l)
• Transferin Saturation- Reduced (N :16-50%)
• Ferritin- Reduced (N:15–300 µg/l)
• RDW: High ( N : 11.5- 14 %)
• Reticulocytes: Normal/Low (N: 0.5- 2.5%)
• Platelates: Normal/Low/High
• WBC: Normal/Low
• Smear: Hypochromia,anisocytosis,
microcytosis, poikilocytosis
Bone marrow findings
• BONE MARROW
• Early stage - Normoblastic hyperplasia
• Normoblasts - smaller than normal
• deficient in hemoglobin
• Irregular shaped with frayed margins
• polychromatic and pyknotic cytoplasm of erythroblasts is vacuolated
and irregular in outline (micronormoblastic erythropoiesis)
• absence of stainable iron
• WBCs- Giant neutrophil bands or metamyelocytes
• Storage iron is absent
Marrow film- Iron deficiency
anemia
Marrow film- prussian blue
stain
Lab tests of iron deficiency of
increased severity
NORMAL Fe deficiency Fe deficiency Fe deficiency
Without anemia With mild anemia With severe
(prelatent) (latent) anemia (IDA)

Serum Iron 60-150 60-150 <60 <40

Iron Binding 300-360 300-390 350-400 >410

Capacity

Saturation 25-55 30 <15 <10

Hemoglobin Normal Normal 9-12 6-7

Serum Ferritin 40-200 <20 <10 0-10

 Methods for assessing iron status
Measurements Reference range Diagnostic Value Confounding factors

1. Hemoglobin Male: 13–17 g/dl • Defining anemia and Other causes of anemia
concentration Female: 12–15 g/dl assessing its besides iron deficiency
severity.
• Response to a
therapeutic
trial of iron confirms
iron deficiency
anaemia (IDA).
2. Red cell indices Low values indicate iron May be reduced in
Mean cell volume 83–101 fl deficient erythropoiesis. disorders of
Mean cell haemoglobin synthesis,
haemoglobin (MCH) 27–32 pg other than iron deficiency
(thalassaemia, sideroblastic
anaemias, anaemia of
chronic disease)

3. Tissue iron supply Reduced in acute and

Serum iron 10–30 µmol/l Low values in iron chronic disease; labile,
deficiency, high use of fasting morning
values in iron overload sample reduces variability
MEASUREMENT REFERENCE RANGE DIAGNOSTIC USE CONFOUNDING FACTORS
(ADULTS)
Total iron binding 47–70 µmol/l High values -tissue iron Rarely used on its own.
capacity (TIBC) deficiency Reliable reference ranges
Low value- iron overload not available

Transferrin 16–50% Low- iron deficiency Reduced in acute and

saturation (TS) anemia chronic
(iron/TIBC × 100) disease

Iron supply to the bone Reduced red cell ferritin or • sTfR concentration is
marrow increased ZPP, sTfR and % related to extent of
Serum transferrin 2.8–8.5 mg/l hypochromic red cells erythroid activity as
receptor (sTfR) indicate impaired iron well as iron supply to
Red cell zinc <80 µmol/mol Hb supply to the bone cells.
protoporphyrin marrow. • ZPP may be increased
(ZPP) • Identifying early iron by other causes of
deficiency and, with a impaired iron
measure of iron incorporation
stores. into haem
• Distinguishing (sideroblastic
this from anemia of anaemias, lead
chronic disease. poisoning,
inflammation)
MEASUREMENT REFERENCE RANGE DIAGNOSTIC USE CONFOUNDING
(ADULTS) FACTORS
Iron stores Male 15–300 µg/l Correlated with body iron • Increased: as acute-
Serum ferritin Female 15–200 µg/l stores from deficiency to phase protein
overload • By release of tissue
ferritin after organ
damage.
• Decreased:
vitamin C deficiency

Bone marrow Grade • Graded as absent, Adequate sample

present or increased required
• Used to d/b ACD and
IDA.
Serum Iron
• Reference interval is 50–160 µg/dL
• Determination of iron status requires-
• Estimate of the amount of haemoglobin iron (usually by measuring the
haemoglobin concentration (Hb) in the blood).
• Level of storage iron (measuring serum ferritin concentration).
• Assay of serum iron- It is modification of method recommended by the
International Council for Standardization in Haematology (ICSH) and is
based on the development of a coloured complex when ferrous iron
released by serum protein denaturation in the presence of reducing
agent is treated with a chromogen solution.
• Alternate methods-
• 1. Microtitre plate method
• 2. Automated Methods for Serum Iron- non-precipitation method ,
available from Randox Ltd .
• INTERPRETATION
• Level reduced in - Iron deficiency anemia
• Anemia of chronic diseases
• Infections
Serum ferritin
• Normal value- 15–300 µg/L (Men>women)
• Water-soluble complex of iron hydroxide with the protein
apoferritin.
• It is located in cells of the liver, spleen, bone marrow .
• Ferritin assay- Immunoradiometric assay ( 1st method)
• MOA- Excess radiolabelled antibody react with ferritin and antibody
not bound to ferritin was removed with an immunoadsorbent.
• Interpretation –
• Ferritin is the basic protein which deposits iron.
• Serum ferritin concentration reflects iron reserve of individual.
• Reduced in iron deficiency anemia.
• It is acute phase reactant so raised in some hepatocellular diseases,
malignancies, and inflammatory diseases, so may give
disproportionately high estimate of storage iron .
• Age between 6 months- 15 yrs reference value is low.
Transferrin
• Transferrin has a very high affinity for iron at neutral pH and iron
release takes place through a specific membrane receptor

LIMITATION
• The concentration of transferrin is subjected to the daily variations
• Acute inflammation contributes to lowering the transferrin level
CLINICAL SIGNIFICANCE
• Basic clinical index for the differentiation between the iron-
deficiency ([TF]↑) and hemolytic anemia ([TF]↓)
• More precise index than total iron binding capacity
• After the liberation of iron from the complex, TF ion of Fe3+ must
be restored into Fe2+
Serum (Total) Iron-Binding Capacity
(TIBC)
• Iron in plasma binds to transferrin and TIBC is the measure of this
protein.
• The additional iron-binding capacity of transferrin is known as the
unsaturated iron-binding capacity (UIBC).
• TIBC = UIBC + serum iron concentration .
• TIBC(µmol/l) = Transferrin conc (gm/l) × 25
• Estimation of TIBC- By adding an excess of iron to a solution and
measuring the iron retained in solution after the addition of a suitable
reagent such as ‘light’ magnesium carbonate or an ion-exchange resin
that removes excess iron.
• Principle
Excess iron as ferric chloride is added to serum. Any iron that does
not bind to transferrin is removed with excess magnesium carbonate.
The iron concentration of the iron-saturated serum is then measured.
• Raised in iron deficiency anemia
UIBC DETERMINATION
• The UIBC may be determined by methods that detect
iron remaining and able to bind to chromogen, after
adding a standard and excess amount of iron to the
serum.
• The UIBC is the difference between the amount
added and the amount binding to the chromogen.
• METHODS-
• Chromogen solution
• Microtitre tray
• UIBC is being evaluated as a screening test for iron overload in genetic
haemochromatosis.
Serum Transferrin (Beta-globulin)
• Main function - transport of absorbed iron in the depot (liver,
spleen), into the medullary erythroid predecessors and into
the reticulocytes.
• Basic place of synthesis - liver.
• Reference interval for adults is 200–300 µg/dL (2.0–3.0 g/l )
• 1 mg of transferrin binds 1.4 µg of iron.
• ESTIMATION OF SERUM TRANSFERRIN-
• by an immunological assay-Rate immunonephelometric
methods
• INTERPRETATION
• An increase in the content of transferrin with lowering in the
level of iron of serum is characteristic for the iron-deficiency
state.
• A decrease in the level of transferrin can be with the damage
of the liver (different genesis) and with the loss of protein (for
example, in nephrotic syndrome).
• The level of transferrin is increased in the last term of
pregnancy.
Transferrin saturation
• The transferrin saturation is the ratio of the serum iron
concentration and the TIBC expressed as a percentage
• Normally, this is 20%–55%.
• A transferrin saturation of <16% is usually considered to
indicate an inadequate iron supply for erythropoiesis.
• Used for detection of genetic haemochromatosis.
• Normal diurnal variation serum iron is as much as 30% with
highest values in the morning and lowest values late in the
day.
• fasting morning blood specimens are preferred for the
diagnosis of iron deficiency.
• Transferrin Index
It is serum iron concentration ( µmol/l) divided by the
transferrin concentration (determined immunologically and
expressed as µmol/l)
SERUM TRANSFERRIN
RECEPTOR
• There are two types of
transferrin receptors
TfR1 and TfR2 .
• TfR1 is essential for
tissue iron delivery
• Transferrin binds to
TfR1, the complex is
internalized and iron is
released when the pH of
the internal vesicles is
reduced to about 5.5 .
Estimation of transferrin receptors
(TfR)
• Transferrin receptors have been purified from placenta
and from serum.
• Three enzymes immunoassay kits
• Fully automated, diagnostic, immunoassay systems .
• Four different units (nmol/l, µg/ml, mg/l and ku/l)
• INTERPRETATION
• sTfR concentrations are high in neonates and decline
until adult concentrations are reached at 17 years.
• Increased during pregnancy
sTfR CONCENTRATION CONDITION

Increased Increased erythroid proliferation:

Autoimmune haemolytic anaemia
Hereditary spherocytosis
ẞ Thalassaemia intermedia or major
ẞ Thalassaemia/HbE
Haemoglobin H disease
Sickle cell anaemia
Polycythaemia vera
Decreased tissue iron stores:
Iron deficiency anaemia
Normal to increased Idiopathic myelofibrosis
Myelodysplastic syndrome
Chronic lymphocytic leukaemia
Normal Haemochromatosis
Acute and chronic myeloid leukaemia
Most lymphoid malignancies
Solid tumours
Anaemia of chronic disease
Decreased Chronic renal failure
Aplastic anaemia
After bone marrow transplantation
 Erythrocyte Porphyrins
• Protoporphyrin IX is the immediate precursor to haem.
• The enzyme ferrochelatase is able to insert ferrous iron to produce haem or zinc
cation to form zinc protoporphyrin (ZPP).
• When iron supply to ferrochelatase is limiting, ZPP increases.
• When ferrochelatase is limiting, free protoporphyrin accumulates.
• Normal reference value is adults is less than 70 µmol/mol haem.
• ANALYSIS- Two dedicated analysers are available: the Proto Fluor Z
from Helena Laboratories, Beaumont, Texas (www.helena.com) and the ZPP 206D
from Aviv Biomedical Inc
• The measurement of EP levels as an indicator of iron deficiency has particular
advantages in pediatric hematology.
• Mean ZPP values Female > Male
• Level of porphyrins in Iron def anemia according to WHO
• Children younger than age 5 years- >61 µmol/mol haem
• all other subjects, levels should be >70 µmol/mol haem.
• Erythrocyte porphyrins became elevated before the development of anemia
• One of the earliest indicators of iron defiiency
Serum Transferrin Receptor–to–
Serum Ferritin Ratio (TfR/F)
• New approach to estimate total body iron stores.
• Have limited value in identifying anemia of chronic disease
(ACD)
• Better utilized in identifying iron defiiency anemia coexisting
with ACD
 Differential diagnosis of
Microcytic anaemia
Iron deficiency Anemia of Sideroblastic
Thalassaemia
anemia chronic disease anemia

MCV Reduced Low normal or Low Low in inherited

normal but normal in
acquired

Serum iron Reduced Reduced Normal Raised

Serum TIBC Raised Reduced Normal Normal

Serum Ferritin Reduced Normal or raised Normal Raised

Iron in BM Absent Present Present Present

Iron Deficiency in Infancy
and Childhood
• INFANTS- There are rapid changes in iron status in the first
year of life as fetal Hb is replaced by adult hemoglobin.
• The serum ferritin concentration is a less useful because of
rapid decline in concentration in the first 6 months and the
low concentrations generally found in children older than 6
months of age.
• Children- reason for detecting iron deficiency is to identify
those who will respond to iron therapy.
• Best predictor of response was the initial Hb,
• Serum ferritin, transferrin saturation and
erythrocyte protoporphyrin (EP) had lower efficiencies.
• ZPP provides a useful indicator of iron deficient erythropoiesis
 Iron Balance in Pregnancy
Iron Fate Mean Amount (mg) Range (mg)
Lost to fetus 270 200–370

Lost in placenta, cord 90 30–170

Lost with bleeding at 150 90–310

delivery
Normal body iron loss 170 150–200

Added to expanded 450 200–600

red blood cell mass
Total 1,130 670–1,650

Returned to stores 450 200–600

when
Net loss (over 9 mo) 680 470–1,050
Iron deficiency in Pregnancy
• In early pregnancy serum ferritin concentrations usually provide a
reliable indication of iron deficiency
• Haemodilution in the 2nd and 3rd trimesters of pregnancy reduces
the concentrations of all measures of iron status.
• determination of values as ratios (ZPP µmol/
mol haem, transferrin saturation and sTfR/ferritin) should be more
reliable.
• In healthy women who were not anaemic and who were
supplemented with iron, serum iron, transferrin saturation and
serum ferritin fell from the 1st to the 3rd trimester and increased
after delivery; TIBC increased during pregnancy and fell after
delivery.
• sTfR concentrations increased (approximately two-fold) during
pregnancy and this probably reflects increased erythropoiesis.
CONCLUSION
• Body iron status can usually be assessed by considering the
Hb, red cell indices and serum ferritin concentration, along
with evidence of inflammation, infection and liver disease.
•