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Iron deficiency anemia (IDA)

It is the most common cause of anemia in India
Physiology of Iron Metabolism
  1. Hb is 0.34% iron by weight.
  2. Acid medium favors formation of soluble macromolecular complexes of iron with vitamin C, sugar, amino acid
  3. or bile in the duodenum.
  4. Only 10% of the ingested iron is absorbed.
  5. Normal serum iron level is 50 to 150 μg/dl.
Factors which influences iron absorption FAQ
Factor Factor which increase iron absorption Factor which decrease absorption.
A. Dietary factor
  1. Increase Haema iron
  2. Increase animal food
  3. Ferrous salt
  1. Decrease Haem iron
  2. Decrease Animal food
  3. Ferric salt
B. Luminal factor
  1. Acidic pH
  2. Food like
    1. Vit C                  
    2. Sugar
    3. Amino acid      
    4. ​Citric acid
  1. Alkaline pH (Pancreatic secretion)
  2. Decrease iron absorption by
    1. Phytates    
    2. Tannic acid in tea
    3. Carbonate  
    4. Oxalate    
    5. Phosphate
    6. High phosphorous diet (Bread, mild, bran)
C. Systemic factor
  1. Iron Def state
  2. Increased erythropoiesis
  3. Pregnancy                  
  4. Hypoxia
  1. Iron overload state
  2. Decrease erythropoiesis
  3. Inflammatory conditions.
Important Points: Iron absorption NOT increased in all types of anemia (it depends on iron store & in some anaemia iron stores are not depleted. e.g Aplastic anaemia, Fanconi Anaemia)
Extra Edge:

Normally 1 mg of elemental iron is lost from shedding of senescent cells of GIT and genitourinary tract, and from desquamation of skin.

  1. Iron requirement in males                   1 mg per day
  2. Iron requirement in females                2 mg per day
  3. Iron requirement in pregnancy            3 mg per day


Causes of Iron Deficiency
  1. Increased demand for iron and/or hematopoiesis
    1. Rapid growth in infancy or adolescence      
    2. Pregnancy  
    3. ​Erythropoietin therapy
  2. Increased iron loss
    1. Acute & Chronic blood loss                          
    2. Menses        
    3. ​Hookworm infestation
  3. Decreased iron intake or absorption
    1. Inadequate diet                                              
    2. ​Malabsorption (sprue, Crohn's disease, post-gastrectomy)                                 
Clinical Features– All features of anaemia and any of the following.
  1. Patients may have angular stomatitis, atrophic glossitis,
  2. Koilonychia, brittle hair, pica,
  3. Plummer – Vinson syndrome (postcricoid web)
  1. Microcytic, hypochromic RBC
  2. Serum ferritin level is low (first to reflect iron deficiency).
  3. Total iron binding capacity rises.
  4. Chromium labeled red cells may be used to measure blood loss into the gut.
  5. Transferrin saturation is reduced.
Important Points: of IDA: 
  1. Most sensitive and specific test for diagnosis of iron deficiency is Serum ferritin levels.
  2. Bone marrow iron is decreased earlier than serum iron                                                                         
Table- Diagnosis of Microcytic Anemia (Ref. Hari. 18th ed., Pg-848, 103.4)
Tests Iron Deficiency Inflammation Thalassemia Sideroblastic Anemia Normal
P/S Micro/hypo Normal micro/hypo Micro/hypo with targeting Variable NCNC
Serum Iron <30 <50 Normal to high Normal to high 50 – 150 mg%
TIBC >360 <300 Normal Normal 250 – 360mg%
Percent saturation <10 10–20 30–80 30–80 30 – 50%
Ferritin (ng/ml) <15 30–200 50–300 50–300 50 – 200(ng/ml)
Hb pattern Normal Normal Abnormal Normal Normal
Extra Edge:
  1. In IDA, MCH, MCV, MCHC (may be <50%) all are decreased.
  2. In IDA, Serum iron & ferritin are reduced and TIBC is increased
Red cell distribution width (RDW)
  1. RDW is essentially an indication of the degree of anisocytosis (Abnormal variation in size of RBCS).
  2. Reference value: 11.5 – 14.5 coefficient of variation (CV) of red cell size.
Clinical implications
  1. The RDW can be helpful in distinguishing uncomplicated heterozygous thalassemia from iron deficiency anemia.
    1. Thalassemia   Low MCV, Normal RDW
    2. Iron deficiency anemia   Low MCV, High RDW 
  2. The RDW can be helpful in distinguishing anemia of chronic disease from early iron deficiency anemia.
    1. Anemia of chronic disease   Low normal MCV, Normal RDW
    2. Early iron deficiency anemia   Low normal MCV, elevated RDW
Red cell distribution width
  Increased                                                         Normal
  1. Iron deficiency                                                 1. (Anemias with homogenous red cell size)
  2. Vitamin B12 or folate deficiency                         2. Chromic disease
  3. Acute blood loss                                               3. Acute blood loss
  4. Aplastic anemia                                                4. Aplastic anemia
  5. Immune hemolytic anemia                                 5. Hereditary spherocytosis
  6. Marked reticulocytosis                                        6. HbE
  7. Fragmentation of RBC                                        7. Sickle cell disease.
Important Points: There is not known cause for decreased RDW.

Pathogenic classification of Microcytic Anemia
  1. Disorders of iron metabolism
    1. Iron deficiency anemia                                  
    2. Anemia of chronic disorders (Advance stage)
  2. Disorders of Globin synthesis
    1. Alpha and beta thalassemia                        
    2. Hemoglobin E syndromes.
    3. Hemoglobin C syndromes                              
    4. Unstable hemoglobin disease
  3. Sideroblastic anemias        
    1. Lead intoxication (usually normocytic)
  1. Blood loss in excess of 10–20 mL of red cells per day is greater than the amount of iron that the gut can absorb from a normal diet.
  2. Under these circumstances the iron deficit must be made up by mobilization of iron from RE storage sites. During this period, iron stores—reflected by the serum ferritin level or the appearance of stainable iron on bone marrow aspirations—decrease.
  3. As long as iron stores are present and can be mobilized, the serum iron, total iron-binding capacity (TIBC), and red cell protoporphyrin levels remain within normal limits. At this stage, red cell morphology and indices are normal.
  4. By definition, marrow iron stores are absent when the serum ferritin level is <15 g/L. As long as the serum iron remains within the normal range, hemoglobin synthesis is unaffected despite the dwindling iron stores.
  5. Once the transferrin saturation falls to 15–20%, hemoglobin synthesis becomes impaired. This is a period of iron-deficient erythropoiesis.
  6. In the peripheral blood smear the first appearance of microcytic cells.
  7. Gradually, the hemoglobin and hematocrit begin to fall, reflecting iron-deficiency anemia. The transferrin saturation at this point is 10–15%.
Serum Iron and Total Iron-Binding Capacity
  1. The serum iron level represents the amount of circulating iron bound to transferrin. The TIBC is an indirect measure of the circulating transferrin.
  2. The normal range for the serum iron is 50–150 g/dL; the normal range for TIBC is 300–360 g/dL. Transferrin saturation, which is normally 25–50%, is obtained by the following formula: serum iron x 100 ÷ TIBC.
  3. Iron-deficiency states are associated with saturation levels below 20%.
  4. A transferrin saturation >50% indicates that a disproportionate amount of the iron bound to transferrin is being delivered to non erythroid tissues. If this persists for an extended time, tissue iron overload may occur.
  5. As iron stores are depleted, the serum ferritin falls to <15 g/L are diagnostic of absent body iron stores.
Red Cell Protoporphyrin Levels
  1. Protoporphyrin is an intermediate in the pathway to heme synthesis. Under conditions in which heme synthesis is impaired, protoporphyrin accumulates within the red cell.
  2. This reflects an inadequate iron supply to erythroid precursors to support hemoglobin synthesis. Normal values are <30 g/dL of red cells. In iron deficiency, values in excess of 100 g/dL are seen.
  3. The most common causes of increased red cell protoporphyrin levels are absolute or relative iron deficiency and lead poisoning.
Serum Levels of Transferrin Receptor Protein:
  1. Because erythroid cells have the highest numbers of transferrin receptors of any cell in the body, and because transferrin receptor protein (TRP) is released by cells into the circulation, serum levels of TRP reflect the total erythroid marrow mass.
  2. Another condition in which TRP levels are elevated is absolute iron deficiency. Normal values are 4–9 g/L determined by immunoassay.
  3. This laboratory test is along with the serum ferritin, has been proposed to distinguish between iron deficiency and the anemia of chronic inflammation.
Changes in lab values in iron deficiency anemia
Change Parameter
  1. Ferritin,        
  2. Hb,                                      
  3. MCV
  1. TIBC,              
  2. Serum transferrin,              
  3. RDW

Comparison of IDA & thalassemia anemia

  1. Iron deficient anemia and thalassemia minor present with many of the same lab results. It is very important not to treat a patient with thalassemia with an iron supplement as this can lead to hemochromatosis (accumulation of iron in various organs especially liver).
  2. Hb electrophoresis provides useful evidence in distinguishing these two conditions, along with iron studies
Important Points:
  1. Bone marrow iron is decreased earlier than serum iron.
  2. As long as iron stores are present (serum ferritin, bone marrow iron), and can be mobilized, The serum iron, TIBC and RBC protoporphyrin levels remains within normal limits.


  1. Iron replacement by ferrous sulphate Continue until hemoglobin is normal and for 6 –8 months to   replenish stores.(MCQ)
  2. Parenteral iron therapy: It is given for those who are unable to absorb iron from the GI tract or to those who have intolerance to oral iron.
    100 mg of iron (IM) are required to increase the hemoglobin level by 4% but the total dose of iron should not exceed 2.5 gm.

Iron Requirement

The amount of iron needed by an individual patient is calculated by the following formula:
Body weight (kg) x 2.3 x (15–patient's hemoglobin, g/dL) + 500 or 1000 mg (for stores).
  1. Total dose = Hb deficit (gm/dl) X lean body weight (lb) + 1000 mg of iron needed for storage.
  2. Each 2 ml of iron dextran contains 100 mg of iron.
  3. 7 days of oral therapy raises Hb by 1 gm%
  4. Parenteral iron (100 mg), raises Hb by 4%
  5. If the Hb deficit is 7 gm, oral iron replacement should be continued for at least 7 weeks; Therapy should be continued For 4 to 6 months for replacing iron stores.
  6. Newer iron preparation for parenteral use
    1. IV route – sodium ferric gluconate, iron sucrose
    2. IM route – Iron dextran, iron sorbitol citrate  
Important Points: Oral therapy for iron deficiency anemia
  1. A dose of 300mg of elemental iron is given per day in divided doses
  2. 300mg of elemental iron gives about 50mg of absorbed iron per day (and not 100 mg of absorbed iron)
  3. Typically the reticulocyte count should begin to increase in 4-7 days after initiation of therapy and peak at 1½ weeks (not at 3-4 weeks)
  4. Typically the Hb levels should be fully corrected within 1 month of initiating therapy in the absence of continuing blood loss (and not after six months).
  5. Treatment should not be stopped after normalizing of Hb, but continued for an additional 4 to 6 months to replenish body iron stores.
Important Points:                                      Male                                      Female
  1. Iron present in diet                                10-20mg                                  10-20mg
  2. % of iron absorbed in normal state        6-10%                                     10-12%
  3. % of iron absorbed in iron def anaemia  20%                                        20%
  4. Max % of iron intestine can absorbed     20%                                        20%
Endocrine Deficiency causing anemia
  1. Testosterone and anabolic steroids augment erythropoiesis.
  2. Castration and estrogen administration to males decrease erythropoiesis.
  3. ​Anemia occurs in hypothyroid, deficits in pituitary hormones, Addison's disease, hyperparathyroidism.                                          

Atransferrinemia, also known as familial hypotransferrinemia,
  • Autosomal recessive metabolic disorder
  • Absence of transferrin (plasma protein that transports iron through the blood.)
  • Characterized by microcytic hypochromic anemia and hemosiderosis in the heart and liver.
  • The iron damage to the heart can lead to heart failure.
  • The anemia is typically microcytic and hypochromic
  1. Serum ferritin – increased (since transferrin is low and mostly not carried by transferrin)
  2. So serum ferritin (overload) will be deposited in other organs and bone marrow and as a result bone marrow ferritin is also increased.
  3. Due to increase bone marrow ferritin (a saturated state will decrease iron absorption) --- so serum iron is decreased (microcytic hypchromic anemia)
  4. 4) Due to low transferrin and increased serum ferritin ---- very high serum transferrin saturation is seen
DMT1- deficiency anaemia:
  • Divalent metal transporter 1 (DMT1) is a duodenal apical iron transporter encoded by the SLC11A2 gene.
  • Mutations in SLC11A2 leads to an anemia-iron overload syndrome
  • Autosomal recessive
  • DMT1 is a key mediator of iron absorption and iron transfer from endosomes into the cytosol of developing erythroid cells.
  • DMT1 deficiency leads to severe microcytic hypochromic anaemia present from birth.
  1. Due to lack of DMTI –mutation----serum iron is increased ( due to defective absorption by duodenal epithelial cells)
  2. Liver DMTI mutation causes increased iron uptake but defective release into blood as a result suppression of serum ferritin ------decreased ferritin mostly.
  3. So more TRANSFERRIN IS formed but lack of absorption and conversion into fe3+ by duodenal epithelial cells----- saturation of serum transferrin is high.

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