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29. IRON DEFICIENCY ANEMIA IN CHILDREN
Osmonova G.Zh.
Het Patel
Ishant Nimbalkar
Rochelle Netto
Gaurav Gadge
Faiz Attari.
(1, Teacher., International Medical Faculty , Osh State University , Osh, Kyrgyzstan)
2,3,4,5,6 Student, International Medical Faculty, Osh State University, Osh, Kyrgyzstan.)
Abstract
Iron deficiency anemia (IDA) is the most prevalent nutritional illness in children, affecting physical, cognitive, and immune development. It remains a major public health concern worldwide, particularly in developing countries.To critically analyze the epidemiology, etiopathogenesis, diagnostic markers, management, and preventive strategies for iron deficiency anemia in children, from international data and graphical representation.A descriptive review was conducted using WHO, CDC, and IAP statistics (2015–2024). Data were presented in tabulated form to show regional prevalence. A pie chart shows the proportion of childhood anemia on continents. Globally, ~40% of children aged less than 5 years are anemic, and half of these are due to iron deficiency. Africa and South-East Asia have the highest prevalence. Iron therapy and dietary correction are effective interventions, and public health interventions reduce prevalence when delivered on a large scale.
ID in children is preventable and treatable. Early diagnosis, nutrition education, and fortification programs are the key to reducing global burden
Introduction
Iron deficiency anemia (IDA) is a hypochromic, microcytic anemia caused by the deficiency of iron for the formation of normal red cells. IDA is the most common cause of anemia in childhood and is responsible for nearly half of the global anemia burden. Iron is essential for hemoglobin formation, cell respiration, immune function, and nervous system development. Supply exceeds need in growing children, leading to iron depletion. Early childhood IDA has been linked to cognitive impairment, psychomotor impairment, and reduced school performance.
Iron is a key micronutrient required for diverse biological processes:
Hemoglobin and myoglobin formation (oxygen transport and storage)
Cytochrome enzymes (cell respiration)
DNA synthesis and cell growth
Synthesis of neurotransmitters (dopamine, serotonin)
Kids are the most susceptible to IDA due to fast growth, high requirements for iron, and recurrent dietary deficiencies. Iron deficiency during infancy and early childhood could lead to lifelong neurodevelopmental disabilities, like late psychomotor development, impaired attention, and lower IQ.
Despite medical progress, iron deficiency anemia is still a major global cause of morbidity. WHO places it as a moderate-to-severe public health problem when the prevalence of anemia exceeds 40% in any given group — reached in most developing regions.
Epidemiology
According to WHO (2021), 39.8% of children aged 6–59 months are anemic globally, and approximately half of these are due to iron deficiency.
Region
Prevalence of Anemia in Children (6–59 months)
Main Contributing Factors
Africa 60–65%
Nutritional deficiency, malaria, helminth infections
South-East Asia 55%
Dietary deficiency, rapid growth, parasitic infections
Eastern Mediterranean 45%
Chronic infections, poor diet
Latin America 25–30%
Dietary iron deficiency
Europe <15%
Low prevalence due to fortification programs
Table 1: Regional prevalence and factors contributing to childhood anemia.
Figure 1: Global Distribution of Childhood Anemia (Iron Deficiency and Others).
In India (NFHS-5, 2021):
67.1% of children aged 6–59 months are anemic.
More than 50% among them have laboratory evidence of iron deficiency.
Age and Sex Pattern:
Infants (6–24 months): Most common due to withdrawal from breastfeeding and feeding low-iron complementary foods.
Adolescents: Specifically girls, as a result of loss through menstruation and lack of dietary supervision.
Causes:
1. Nutritional Deficiency: Low intake of heme iron foods.
2. Socioeconomic: Poverty and limited access to iron-containing diets.
3. Parasitic Infections: Hookworm, schistosomiasis.
4. Maternal Anemia: Leads to low iron stores in infants.
5. Cultural Feeding Pattern: Premature exposure to cow's milk or prolonged exclusive breastfeeding.
Methods
This article is a narrative review integrating data from major pediatric and hematology resources (WHO, IAP, Nelson Textbook of Pediatrics). Data were derived from WHO Global Health Database, CDC, IAP Guidelines, and peer-reviewed journals on PubMed and Cochrane Library.
Data Sources
World Health Organization (WHO)
Centers for Disease Control and Prevention (CDC)
National Family Health Survey (NFHS-5)
Indian Academy of Pediatrics (IAP) 2021 Guidelines
PubMed, Medline, and Cochrane Database (2015–2024)
Nelson Textbook of Pediatrics, 22nd Edition
Inclusion Criteria
Child population studies (0–18 years)
Iron deficiency anemia
Clinical trials and reviews regarding diagnosis, therapy, and prevention
Exclusion Criteria
Genetic anemias (thalassemia, sickle cell disease)
Anemia of chronic disease without iron deficiency
Adult-oriented studies
Data Extraction
Variables that were studied included:
Prevalence rates and demographic trends
Classification based on etiology (nutritional, pathological, environmental)
Laboratory diagnostic criteria (Hb, ferritin, iron studies)
Therapeutic effectiveness of parenteral and oral iron solutions
Impact of national prevention programs
Results/Outcome
Aetiology includes poor nutrition, increased requirements, decreased absorption, and blood loss. Clinical presentation ranges from pallor and weakness to mental retardation. Laboratory findings show low Hb, MCV, MCH, serum ferritin, and iron but high TIBC. Treatment is by dietary change, oral or parenteral iron, deworming, and education.
1. Etiopathogenesis
Iron deficiency progresses gradually in three steps:
1. Depletion of iron stores:
Serum ferritin decreases (<12 µg/L)
No anemia yet
2. Iron deficient erythropoiesis:
Decreased serum iron, increased TIBC
Production of RBC is impaired
3. Iron deficiency anemia:
Age-related reference range for hemoglobin drops below
Microcytosis and hypochromia become apparent
2. Clinical Features
System. Manifestations
________________________________________
General. Fatigue, pallor, poor appetite, irritability, pica
Cardiovascular. Tachycardia, systolic murmur, heart failure
Neurological. Delayed milestones, poor concentration, cognitive delay
Gastrointestinal Glossitis, angular cheilitis, dysphagia (Plummer-Vinson syndrome)
Musculoskeletal. Poor growth, reduced endurance
Nails & Skin. Koilonychia (spoon nails), dry skin, brittle hair
________________________________________
3. Laboratory Findings
Parameter. Normal Range. Iron Deficiency Anemia
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Hemoglobin. >11 g/dL. ↓
MCV. 80-100 fL. ↓ (<75 fL)
MCHC 32-36%. ↓
Serum ferritin >12 µg/L. ↓
Serum iron. 50-120 µg/dL. ↓
TIBC. 250-400 µg/dL. ↑
Transferrin saturation. >20%. ↓(<15%)
Reticulocyte count. 0.5-2%. ↓ or normal
Peripheral smear. Normocytic microcytic,
hypochromic cells
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4. Management
a) Dietary Correction
Heme iron: liver, red meat, fish, egg yolk
Non-heme iron: green leafy vegetables, legumes, nuts, cereals
Iron absorption enhanced by vitamin C; inhibited by tea, coffee, calcium, and phytates.
b) Oral Iron Therapy
Dose: 3–6 mg/kg/day elemental iron (ferrous sulfate preferred)
Duration: Continue 3 months after Hb normalization
Expected Response:
Reticulocytosis within 7 days
Hb rise by 1 g/dL every 2–3 weeks
Side Effects: Constipation, epigastric discomfort, dark stools.
c) Parenteral Iron Therapy
Indicated for malabsorption, intolerance, or severe anemia.
Preparations: Iron sucrose, ferric carboxymaltose, iron dextran.
Monitoring: Serum ferritin after 4–6 weeks.
d) Blood Transfusion
Reserved for Hb <5 g/dL or cardiac decompensation.
e) Deworming
Albendazole (400 mg single dose every 6 months) or Mebendazole (100 mg twice daily for 3 days).
Discussion
IDA in children is a multifactorial disorder influenced by diet, infection, and growth dynamics. Despite being preventable, it continues to cause developmental and cognitive delays worldwide.
Pathophysiology:
Iron is stored as ferritin and hemosiderin. When stores are exhausted, erythropoiesis becomes iron-deficient, leading to smaller (microcytic) and pale (hypochromic) RBCs with reduced hemoglobin content.
Impact on Development:
Iron deficiency impairs neurotransmitter synthesis (dopamine and serotonin), alters myelination, and reduces attention and learning capacity. Early-life IDA can lead to permanent neurobehavioral deficits.
Diagnostic Approach:
Ferritin is the most specific test for iron deficiency, though it may rise in infections (as an acute-phase reactant). Hence, concurrent CRP testing helps interpretation.
Public Health Implications:
IDA affects school performance and productivity. In endemic regions, combining iron supplementation, fortification of foods, deworming, and maternal education provides the best outcome.
Modern Approaches:
Recent studies suggest that intermittent iron dosing (every other day) improves absorption and reduces side effects. Intravenous iron formulations such as ferric carboxymaltose are now safer and more efficient for rapid repletion.
Limitations of Current Programs:
Despite supplementation programs like India’s National Iron Plus Initiative, challenges persist — poor compliance, gastrointestinal side effects, and lack of monitoring. Strengthening community-based delivery systems is essential.
Conclusion
Iron deficiency anemia remains a major preventable cause of morbidity in childhood. Its impact extends beyond hematological parameters to cognitive, physical, and immune functions.
Comprehensive management should include:
Early screening in high-risk groups
Nutritional counseling for families
Routine deworming
Fortification of staple foods
Regular monitoring of hemoglobin and ferritin levels
A multidisciplinary approach involving pediatricians, nutritionists, and public health workers is vital to achieve sustainable reduction in the global burden of childhood anemia.
References
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