IRON DEFICIENCY ANEMIA
Last Updated : 5/3/2010
M R Lokeshwar*, Nitin Shah**
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Anemia is defined as reduction in the oxygen carrying capacity of blood, as observed by reduced levels of hemoglobin concentration and red cell mass (Hematocrit) leading to tissue hypoxia. It reflects the disturbance of the dynamic balance between production and destruction of erythrocytes and hemoglobin. In normal subjects the average life span of red cell i.e. time between the release of red cell from bone marrow and its disappearance from circulation, is between 100 to 120 days. The cells destroyed each day are replaced by new cells released from marrow, with the result the red cell population in the blood consists of cells ranging in the age from 1 to 120 days. Thus approximately 1% or slightly less of body's red cells are destroyed and replaced each day. Any disruption of this balance - such as reduced production or increased destruction leads to anemia. The aged cells are removed from circulation by the reticuloendothelial system, where the flow of blood is slow, particularly in the splenic pulp. Child is said to be anemic when the hemoglobin and or Hematocrit is two standard deviation below mean for that particular age and sex.

Table 1 gives the normal values (normal mean and lower limit of normal) of various hematological parameters at different age groups.

Table 1: AVERAGE NORMAL BLOOD VALUES AT DIFFERENT AGE GROUPS
AGE Hb (gm%) RBC (m/L) HCT % MCV (cu. mm) MCH (pg) MCHC % Reticulocyte %
1 day 18.0 5.14 61 119 36.0 31.6 32
4 weeks 14.2 4.0 43 106 35.5 33.5 0.6
1 year11.64.6357725.033.00.9
10-12 years13.04.8398027.033.01.0
Adult- Men16.05.4478729.034.01.0
Adult- women14.04.8428729.034.01.0


Lower limit of hemoglobin at newborn period is 16 gm%, at 3 months- 9 gm%, 6 months to 6 years- 10 gm%, 7 to 12 years -12 gm%. Thus 9 gm% - 11 gm% Hb is normal for a child around age of 3 months needing no treatment and same will represent severe anemia needing blood transfusion in newborn period.

Classification and Etiology of anemia :
There are four basic causes of anemia - loss, destruction, sequestration and hypoproduction.

Anemia can be further classified by
- RBC size: micro, normo, and macrocytic anemia.
- RBC shape: e.g. Sickle cell.
- Etiology

Etiological Classification of Anemia:
Nutritional Anemia: Anemia is a major nutritional global problem of immense public health significance, affecting persons of all ages, sex and economic group. It is ranked as the commonest chronic malady of mankind affecting approximately 30% i.e. 1500 million people all over the world. It is a pathologic condition where hemoglobin or Hematocrit level becomes abnormally low because of low essential nutrients regardless of the causes of these deficiencies. In developing countries like ours, besides deficiencies of food specific nutrients like iron, folic acid, B12 protein, vitamin C, vitamin E, trace elements, etc, poor health facilities, poor socioeconomic status, faulty dietary patterns, the degree of urbanization, ethnic background, prevalence of hook worm and other worm infestations, repeated bacterial infections, etc also influence the incidence of anemia particularly in children. The nutritional anemia has major consequences not only on the morbidity and mortality in children but also affects growth and intellectual development of these children.

In India, anemia is the most common nutritional problem affecting more than ½ of the total population, particularly in children and pregnant women where the incidence is 50 to 97%. It has been suggested that prevalence of anemia in pre-school children, and pregnant women is sensitive index of the situation in the community.

Iron deficiency anemia

in children occurs most frequently between the age of 6 months to 3 years and 11 to 17 years.

Stages of iron deficiency:

Iron deficiency anemia

is the end stage of a relatively long drawn process of deterioration in the iron status of the individual. It is only tip of iceberg of the iron deficiency state.

- Storage iron depletion (Pre-latent iron deficiency): Iron reserve is decreased or absent in this stage. At this stage, the only abnormalities are decreased iron stores and increased iron absorption from the gastrointestinal tract. It is characterized by reduced serum ferritin, reduced iron concentration in the marrow and liver tissue. Hemoglobin, serum iron, total iron binding capacity and transferrin saturation are within normal limits.

Iron limited erythropoiesis (Latent iron deficiency): As the iron stores gets exhausted, latent iron deficiency state develops. At this stage, in addition to already reduced iron stores (decreased serum ferritin), serum iron and transferrin saturation also are low with increased total iron binding capacity and increased free erythrocyte protoporphyrin. However, hemoglobin levels are still normal.

Iron deficiency anemia: As the negative iron balance continues, now the production of erythroid cells in the marrow is impaired leading to reduction in hemoglobin concentration with development of progressive microcytic, hypochromic anemia. Thus, Hb, MCV, MCH & MCHC are reduced in addition to already decreased serum iron, increased TIBC and decreased transferrin saturation. Transferrin saturation below 12 - 16% is diagnostic of iron deficiency state.

Etiology of Iron deficiency anemia (IDA)
Iron deficiency results when insufficient amount of iron is available to meet body's requirements. This can occur because of:
- Decreased supply of iron due to:
* Inadequate intake of iron
* Reduced bioavailability of dietary iron
- Decreased absorption of iron: Cause of iron malabsorption includes chronic diarrhea, malabsorption syndromes, milk allergy, sprue, partial or total gastrectomy and rarely genetically determined absorptive defect specific for iron. Pica through may be a manifestation of iron deficiency, is also considered to be a predisposing factor for poor iron absorption.
- Increased requirement of iron: as seen in premature babies during first few months (as they have a rapid growth) and during the periods of growth as in infancy and adolescence, lactation, pregnancy.
- Chronic blood loss:
* Gastrointestinal bleeding: The chronic loss of few milliliters of blood daily is sufficient to deplete iron stores and lead to iron deficiency. Often these bleeds are occult and unsuspected. In the western world, milk induced enteropathy is the commonest cause of occult GI bleeding seen in approximately more than 50% of infants with IDA. Hookworm infestation is the other important cause of intestinal blood loss particularly in developing countries. 450 million people all over the world harbor this parasite and about 0.2 cc of blood / worm of ankylostoma per day may be lost and with necator - infestation each worm accounts for loss of about 0.1 - 0.5 ml/day. Female subjects harboring more than 100 worms (5 ml/day blood loss) and male subjects harboring more than 250 worms (12.5 ml/day blood loss) tend to become anemic. The daily blood loss may be as great as 250 cc/day.
* Feto-maternal bleed: It is one of the important causes of anemia in newborn. In about 50% of all pregnancies there is some degree of feto-maternal hemorrhage of which 8% are significant (0.5 - 40 cc fetal blood loss) and 1% severe (>100 cc fetal blood loss).
* Repeated venepunctures for investigations, hemodialysis, regular blood donations are important iatrogenic causes of iron deficiency due to chronic blood loss.

Decreased Supply of Iron
Breast milk, the

primary source of infant nutrition

is poor in iron, containing 0.28 - 0.73 mg/lit as compared. However, the iron in breast milk has a very high bioavailability (20 - 80%) and hence iron deficiency rarely occurs in exclusively breast fed infants till the age of 4 - 6 months. Breast-feeding does not protect against iron deficiency after the age of 6 months, unless iron containing weaning foods are introduced. During adolescence, false concern about the body figure, food fads, ignorance, particularly in girls lead to iron deficiency.

Table 2 : ETIOLGICAL FACTORS IN IRON DEFICIENCY ANEMIA :
Decreased iron assimilationBlood lossIncreased physiologic requirement
  • Iron poor diet & poor bioavailability of Fe in the food
  • * GI bleeding Hookworm infestation,Peptic ulcer,Diverticulitis,
  • Prematurity
  • Iron malabsorption
    • Chronic diarrhea & Malabsorption Syndrome
    • Sprue
    • G. I. Surgery
Milk induced enteropathy
  • Aspirin & other drugs
  • Feto- maternal transfusion
  • Early clamping of cord
  • Bleeding disorders
  • Period of growth
  • Infancy
  • Adolescence
  • Pica
  


Table 4: FACTORS AFFECTING THE BIOAVAILABILITY OF THE DIETARY NON-HEME IRON
Enhance Ascorbic acid, meat, fish, poultry
InhibitTannates (tea, coffee), Bran, Egg Yolk, Calcium Phosphate, EDTA, Antacids, phytates, cholestyramine, clay, starch.


IRON METABOLISM
An average adult has about 3 -5 grams of iron and children have 55 mg /kg/ body weight of iron in the body. It is more in males as compared to females. 70% of iron in the body is in the form of Hb, 26% constitutes the stores and 3.9% is incorporated in myoglobin and various other iron containing enzymes. Plasma iron forms only 0.1% of the body iron.

Iron balance in the body is achieved mainly by control of absorption of iron rather than its excretion. Body iron remains fixed within relatively narrow limits. Most of the iron is recirculated in the body. Only 1-1.5 mg of iron is excreted daily. Thus daily requirement is minimum. Absorption of iron mainly depends upon dietary content of iron. Various foodstuffs with their iron content are listed in Table 3.

Table 3 : IRON CONTENT OF FOOD ARTICLES
Class of Food Iron content
mg/100 g
Articles rich in iron 
> 10 mg / 100 g
Cereals 2.5 - 14.0 Bajra, Wild Barley, Kang Ragi, Rice flakes, whole wheat Flour, Kodra (Harik)
Pulses & Legumes2.7 - 11.0Bengal gram, Cow gram, Soya bean
Leafy Vegetables0.9 - 40.0Amaranth, Beet, Greens,Bengal gram leaves, Coriander, Alu leaves, Pudina, Neem, Radish top, Rajgira leaves, Turnip greens, all types of green bhajis. (Spinach, methi, lettuce, etc.)
Roots & tubers0.4 - 13.9 
Other Vegetables0.2 - 22.2Amaranth seeds,Daincha seeds
Nuts & oil seeds2.5 - 10.0Garden cress, Gingelly, mustard, Pistachio
Fruits
0.1 - 10.0Dates, Karwanda, Raisins
Sea food1.0 - 11.5Most Indian fish, crab
Meat2.0 - 18.8Beef
Milk0.2 - 0.8 
Miscellaneous Jaggery, Yeast


-

Non-vegetarian diet

is richest source of iron containing 10-18 mg of iron per 100 grams.
- Bioavailability of iron: Ultimate absorption of iron into mucosal cells mainly depends upon bioavailability of iron in the various foodstuffs. The non-vegetarian foods have iron (haem) with very high bioavailability and the absorption of this is not affected by any other factor in the lumen including various food ingredients. Absorption of iron from vegetarian sources is affected by various factors as shown in Table no. 4.
- Mucosal cell control: Appropriate iron balance in the body is achieved by mucosal cell control through transferrin and apoferritin receptors. When the serum iron is normal and adequate, the iron gets incorporated into apoferritin in the mucosal cell and this is ultimately excreted after 3 - 4 days, when lifespan of mucosal cells is over. However, if iron deficiency state exists in the body, transferrin is utilized to combine with iron and is transported and stored at storage site.
-

Iron transport and storage:

Transferrin helps in transport of iron from the intestine to the site of its utilization. Iron is stored in the body in the form of ferritin and hemosiderin.
- Transport of iron across the placenta: The transport of iron across placenta occurs against a gradient, thereby protecting fetus against iron deficiency. However, this effective fetal parasitism is limited in cases of severe maternal iron deficiency. Thus babies with low iron stores may be born to mothers who are severely iron deficient during pregnancy. It is important to remember that most of the placental transfer of the iron occurs during the 3rd trimester of pregnancy. As a consequence of this, all preterm babies invariably develop anemia unless supplemented by iron and conversely iron deficiency in the mother may cause preterm labor.

References

Contributor Information and Disclosures

M R Lokeshwar*, Nitin Shah**
*Visiting Pediatrician - P.D.Hinduja National Hospital, Mumbai Pediatrician and Hematologist-Oncologist,Lilavati Hospital, Bandra, Mumbai. **Division of Pediatric Hematology-Oncology, Dept of Pediatrics, LTMG Hospital & LTM Medical College, Sion, Mumbai - 400 022.


First Created : 2/8/2001

References

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