European Journal of Cardiovascular Medicine

Anaemia affects roughly a quarter of the global population, with the highest burden in preschool children and women of reproductive age. Recent Global Burden of Disease (GBD 2021) estimates reported a 24.3% all-age prevalence in 2021, with particularly high rates in South Asia and sub-Saharan Africa.²,³ Iron deficiency remains the commonest cause worldwide, but the aetiology of childhood anaemia is multifactorial—encompassing inadequate dietary iron, infection/inflammation, haemoglobinopathies, micronutrient deficiencies (B12, folate), chronic kidney or inflammatory disorders, and, in some regions, malaria and helminths.⁴,⁵,¹¹

In 2024, WHO issued updated guidance on haemoglobin cut-offs and best practices for measuring anaemia, emphasising population-appropriate thresholds and quality-assured Hb assessment.¹ The guidance builds on evidence that Hb requires context (e.g., altitude/smoking) and that programme evaluation should consider both iron deficiency and non-iron causes, so interventions extend beyond iron pills alone.¹,⁷,¹¹ In India, large-scale surveys (e.g., NFHS-5, 2019–21) continue to show a sizeable prevalence of anaemia in children 6–59 months, underscoring the need for robust facility-level data to guide local clinical care and public-health actions.⁸,¹⁰

Frontline haematological tools—CBC, RBC indices (MCV/MCH/MCHC), RDW, and peripheral smear—often allow first-pass classification into microcytic-hypochromic (classically iron deficiency or thalassaemia traits), normocytic (anaemia of inflammation/chronic disease, early iron deficiency), and macrocytic patterns (B12/folate deficiency, marrow disorders). Diagnostic accuracy improves by integrating ferritin (interpreted with inflammatory status), transferrin saturation, and where available, newer parameters such as reticulocyte haemoglobin content/equivalent (Ret-He/CHr), which reflect real-time iron available for erythropoiesis and can aid early diagnosis and monitoring. ⁶,¹²,¹⁸–²²

Public-health initiatives (e.g., WHO daily iron supplementation for infants/young children in settings with high anaemia prevalence; India’s Anaemia Mukt Bharat) emphasise a multi-component package: prophylactic/therapeutic iron-folic acid (IFA), deworming, malaria control where endemic, dietary counselling and fortification, and screening for non-nutritional causes.⁶,⁹–¹¹ Against this backdrop, hospital-based profiles remain valuable to characterise the clinical spectrum, severity, and laboratory patterns presenting to care, and to identify gaps (e.g., under-recognised B12 deficiency or haemoglobinopathies).

We therefore aimed to describe the clinico-haematological profile of paediatric anaemia in a tertiary-care setting, including clinical features, severity by WHO criteria, RBC index patterns, and distribution of aetiologies, and to discuss implications vis-à-vis contemporary evidence and guidelines. ¹–⁶,⁸–¹³

This is a Cross-sectional observational study at a tertiary-care teaching hospital (Department of Paediatrics and Clinical Haematology) over 12 consecutive months.

Participants: Children aged 6 months to 14 years attending OPD/ED/wards with clinical suspicion of anaemia (pallor, fatigue, poor feeding, pica, exertional intolerance, syncope), laboratory-detected low haemoglobin, or referral for anaemia work-up.

Inclusion criteria: (i) Age 6 months–14 years; (ii) Hb below WHO age- and sex-specific thresholds for anaemia¹ (capillary or venous sample measured on a quality-assured analyser); (iii) caregiver consent/assent as applicable.

Exclusion criteria: (i) Recent transfusion (<12 weeks); (ii) ongoing chemotherapy; (iii) acute massive haemorrhage/trauma; (iv) known chronic renal failure on EPO; (v) unwillingness to participate.

Clinical assessment: Demographics, socioeconomic indicators, diet diversity/iron-rich food frequency, pica, deworming history in last 6 months, prior iron therapy, infection history, chronic disease, family history of haemoglobinopathy. Examination for growth parameters, glossitis/koilonychia, lymphadenopathy, hepatosplenomegaly, bleeding stigmata, and cardiac decompensation.

Laboratory investigations: CBC with RBC indices (MCV, MCH, MCHC), RDW; reticulocyte count and Ret-He/CHr where available; peripheral smear morphology; serum ferritin (with CRP where available to account for inflammation), transferrin saturation; serum B12 and folate in macrocytosis or neuro-gastrointestinal symptomatology; G6PD screen where haemolysis suspected; HPLC for haemoglobinopathies as indicated. Classification of severity used WHO 2024 haemoglobin cut-offs; altitude/smoking adjustments not applicable in our low-altitude, non-smoking paediatric cohort.¹,⁷ Quality control followed manufacturer and EQAS standards.

Aetiological assignment:

• Iron deficiency anaemia (IDA): microcytosis/hypochromia ± high RDW with low ferritin (<12–15 µg/L; higher thresholds if CRP elevated) and/or low transferrin saturation; supportive Ret-He < reference.⁶,¹²,¹⁸–²²
• Anaemia of inflammation/chronic disease (AI/ACD): normocytic or microcytic with low serum iron, low/normal transferrin, normal/high ferritin with clinical evidence of chronic inflammation/infection.
• Haemoglobinopathies: HPLC-confirmed β-thalassemia trait/major or sickle haemoglobin variants.
• Megaloblastic deficiency: macrocytosis with low B12/folate and smear features.
• Haemolytic/other: positive haemolysis profile or marrow pathology.

Sample size & statistics: Assuming an IDA proportion of ~55% with 6% absolute precision and 95% confidence, the minimum sample required was ~265; we enrolled 300 to account for exclusions. Descriptive statistics (means±SD, proportions), χ² for categorical comparisons, t/ANOVA for continuous variables; p<0.05 considered significant. Analysis performed in R.

Table 1. Baseline Demographics and Clinical Features (n=300)

Table 2. Anaemia Severity by WHO Criteria

Table 3. RBC Indices & Morphology

Table 4. Biochemical Iron Parameters (subsample tested)

Table 5. Aetiological Distribution

Table 6. Clinical Correlates of Severe Anaemia (multivariable)

This hospital-based profile mirrors global and national patterns: iron deficiency is the leading cause of paediatric anaemia, but non-iron aetiologies are substantial.²–⁵,¹⁰,¹³ Our IDA proportion (~59%) aligns with multi-setting reviews that position iron deficiency as the principal driver while emphasising the sizable contribution of inflammation and haemoglobinopathies.⁴,¹³,¹⁶ The predominance of microcytosis with high RDW and low ferritin/TSAT is consistent with pathophysiology and prior hospital series.¹³,¹⁹–²²

The updated WHO 2024 recommendations underscore careful haemoglobin measurement and context-appropriate cut-offs for defining anaemia.¹ Although altitude/smoking adjustments were not required in our cohort, the principle of contextual interpretation is important when comparing across sites.¹,¹⁵ NFHS-5 continues to show high childhood anaemia prevalence in India, reinforcing the public-health relevance of our findings and the need for integrated strategies.⁸,¹⁰,¹٧

Our data also highlight the practical value of Ret-He/CHr (where available) in early identification and monitoring of iron-restricted erythropoiesis, complementing ferritin which may be confounded by inflammation. The paediatric literature supports Ret-He as a rapid, reliable marker and, in resource-appropriate contexts, a cost-effective adjunct.¹²,¹٨–²³ RDW likewise aids differentiation between IDA and thalassemia traits, although definitive diagnosis of haemoglobinopathies relies on HPLC.¹٩,²⁶

Policy implications align with WHO/IAP guidance: (i) dietary diversification and iron fortification; (ii) routine prophylactic/therapeutic IFA where indicated; (iii) regular deworming and infection control; and (iv) targeted screening for haemoglobinopathies in high-prevalence communities.⁶,⁹–¹¹,¹³ Programmes such as Anaemia Mukt Bharat operationalise multi-component packages with demonstrable improvements in IFA coverage, though gaps remain (e.g., deworming uptake).¹⁰

Strengths of this work include comprehensive clinico-haematological characterisation and explicit aetiological categorisation. Limitations are inherent to single-centre, hospital-based sampling; inflammatory markers were not uniformly available; Ret-He was limited to a subset; and causal inference is precluded by cross-sectional design. Future studies should integrate longitudinal follow-up to track haematological response to therapy and functional outcomes (growth, neurocognition), and incorporate standardized inflammatory adjustment for ferritin.

In summary, our findings reaffirm that while IDA drives the majority of paediatric anaemia, one in ~4–5 cases involves non-iron causes, mandating a diagnostic approach that goes beyond empiric iron to include context-specific testing and prevention bundles.¹–⁶,⁸–¹³

Iron deficiency remains the dominant, preventable driver of paediatric anaemia; however, a meaningful minority have haemoglobinopathies, inflammation-related anaemia, or vitamin deficiencies. Programmes should couple iron strategies with deworming, infection control, dietary improvement, and haemoglobinopathy screening, and clinicians should leverage simple indices (MCV, RDW), ferritin/TSAT (with inflammatory context), and Ret-He where available to tailor care and monitor response.

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