Anemia is a common clinical and public health condition characterized by reduced oxygen-carrying capacity of blood and is associated with impaired growth, neurocognitive development, reduced work capacity, pregnancy complications, and increased morbidity and mortality in hospitalized adults.1–3 Global analyses consistently demonstrate that anemia affects a substantial proportion of children and adults worldwide, with disproportionate burden in low- and middle-income countries.1,2 While iron deficiency remains a central cause, anemia is now understood as a multifactorial syndrome driven by nutritional deficits, infections, inflammation, genetic hemoglobin disorders, chronic organ disease, and blood loss.1,3

Patterns of anemia differ significantly between children and adults. In children, rapid growth, inadequate dietary iron intake, parasitic infections, recurrent inflammation, and inherited disorders (e.g., thalassemia traits) contribute to high prevalence.1,2,15 Iron has crucial roles in early brain development—impacting myelination, neurotransmitter function, and energy metabolism—making pediatric iron deficiency clinically important even before severe anemia develops.11,12 In contrast, adults more commonly develop anemia from chronic inflammation and comorbidity (e.g., chronic infections, autoimmune disease, cancer), gastrointestinal blood loss, renal insufficiency, and iatrogenic causes.3–8

Anemia of inflammation (also termed anemia of chronic disease) is mediated by cytokine-driven iron sequestration and restricted erythropoiesis, largely through hepcidin upregulation and impaired ferroportin-mediated iron export.3–6 This produces a typical phenotype of normocytic or mildly microcytic anemia with low serum iron, reduced transferrin saturation, and normal/high ferritin.3–6 Differentiating anemia of inflammation from iron deficiency (and recognizing overlap) is essential because management differs: treating underlying inflammation, considering iron repletion strategies, and using erythropoiesis-stimulating agents in select contexts (e.g., CKD).3,7

Severity also varies by age and cause. Children may present with moderate-to-severe anemia due to nutritional deficiency, chronic parasitosis, or hemoglobinopathies; adults may have mild-to-moderate anemia that signals serious underlying disease such as occult gastrointestinal malignancy or chronic kidney disease.7–9 Evidence-based approaches recommend structured diagnostic pathways: confirm anemia, classify by red cell indices and reticulocyte response, assess iron status with appropriate cutoffs, and pursue focused etiologic testing.7–9 Additionally, severity influences clinical outcomes and transfusion decisions; restrictive transfusion thresholds are recommended in most stable hospitalized adults, balancing benefit and harm.10

Therefore, comparative evaluation of anemia patterns across children and adults is clinically valuable: it informs age-appropriate diagnostic algorithms, anticipates likely etiologies, guides resource allocation, and improves outcomes through timely targeted treatment.1–3,7,8

A comparative, hospital-based observational study (cross-sectional with short-term outcome assessment) conducted in Pediatric and General Medicine departments of a tertiary-care teaching hospital.

Study population

Two groups were evaluated:

• Children: 6 months to 17 years
• Adults: ≥18 years

Inclusion criteria

Children:

1. Age 6 months–17 years
2. Hemoglobin below age-adjusted laboratory reference range (as per institutional standards) at presentation or during admission
3. Consent from parent/guardian (and assent where applicable)

 Adults:

1. Age ≥18 years
2. Hemoglobin below sex-adjusted laboratory reference range at presentation or during admission
3. Informed written consent

Exclusion criteria (both groups)

1. Recent blood transfusion within prior 4 weeks (alters indices/iron studies)
2. Acute major hemorrhage or trauma requiring immediate transfusion before evaluation
3. Known hematologic malignancy on active chemotherapy (unless the aim includes this subgroup)
4. Refusal of consent
5. Inadequate sample or incomplete key investigations

Data collection

A structured proforma recorded demographics, diet history (iron intake), deworming status (children), menstrual and obstetric history (adults), bleeding symptoms, chronic illness, drug exposure, and infection/inflammation markers.

Laboratory evaluation

All participants underwent:

• CBC with indices (Hb, MCV, MCH, RDW), platelet count, WBC count
• Peripheral smear morphology
• Reticulocyte count
• Iron profile: serum ferritin, serum iron, transferrin saturation (TSAT)
• C-reactive protein (CRP) to interpret ferritin in inflammatory states (as per guideline principles)7
  Additional tests based on clinical suspicion:
• Stool ova/parasite, stool occult blood (adults)
• Vitamin B12/folate (macrocytosis)
• Serum creatinine/eGFR (CKD)
• Hemoglobin electrophoresis/HPLC for suspected hemoglobinopathy (microcytosis disproportionate to anemia, family history)
• Endoscopic evaluation in adults with IDA where indicated7–9

Definitions (operational)

Anemia severity was categorized using institutional/standard clinical cutoffs suitable for local policy and practice, and etiology was assigned using a predefined algorithm (IDA; anemia of inflammation; hemoglobinopathy; B12/folate deficiency; CKD-related; mixed/other).3,7,8

 Outcomes

Short-term outcomes recorded: length of stay, need for transfusion, ICU transfer (if applicable), and discharge status. Transfusion decisions followed restrictive guideline principles for stable adults.10

Statistical analysis

Continuous variables: mean ± SD; categorical variables: n (%). Group comparisons: t-test/χ² test. Multivariable logistic regression identified predictors of moderate-to-severe anemia and transfusion requirement (p<0.05 significant).

Table 1. Baseline characteristics of anemic children vs anemic adults

Children had higher malnutrition proxies and recent infection; adults had substantially higher chronic disease burden—supporting age-specific etiologic differences (nutritional/infective vs chronic inflammation/organ disease).1–3

Table 2. Severity distribution of anemia

Severe anemia was more frequent in children, consistent with nutritional deficiency, parasitosis, and hemoglobinopathy contributions; adults more often had mild anemia that may still reflect significant underlying pathology.1,7,8

Table 3. Morphological pattern by RBC indices/peripheral smear

Microcytosis predominated in children (suggesting IDA/hemoglobinopathy), while normocytic anemia was common in adults—often aligning with anemia of inflammation or CKD.3,7,8

Table 4. Etiology of anemia (final assigned diagnosis)

IDA remained the leading cause in both groups, but children showed higher hemoglobinopathy contribution, while adults had higher anemia of inflammation and CKD-related anemia—mechanistically consistent with hepcidin-driven iron restriction and comorbidity load.3–8,15

Table 5. Iron profile and inflammatory markers

Lower ferritin and TSAT in children supports predominant absolute iron deficiency. Higher ferritin in adults—often with elevated CRP—supports inflammation-related iron sequestration and the need for careful interpretation of ferritin using guideline-based approaches.3,5,7

Table 6. Outcomes and resource use

Adults had longer hospital stays and slightly worse discharge status, reflecting comorbid illness and chronic inflammation contexts. Restrictive transfusion practice is generally supported in stable adults, with individualized decisions based on symptoms and clinical context.10

This comparative analysis highlights clear age-related differences in anemia phenotype, etiology, and outcomes. Globally, anemia continues to impose a high burden, especially in children, and multi-cause frameworks increasingly replace older “iron-only” explanations.1,2 In the present comparison, severe anemia and microcytosis were more common in children, while adults showed a higher proportion of normocytic anemia and anemia of inflammation—findings consistent with established mechanistic understanding of pediatric nutritional vulnerability and adult comorbidity-driven anemia.3–6

Iron deficiency anemia was the leading diagnosis in both groups, aligning with global evidence that iron deficiency remains the dominant contributor to anemia in many settings.1,2 Pediatric predominance of low ferritin and low TSAT supports absolute iron deficiency and emphasizes early detection and treatment, given iron’s role in neurodevelopment.11,12 The literature increasingly links iron deficiency to neurodevelopmental vulnerabilities and behavioral/cognitive outcomes; systematic syntheses emphasize the biological plausibility and potential benefit of correction in appropriate contexts.11,12 Additionally, pediatric hemoglobinopathies (e.g., thalassemia trait) contributed meaningfully to microcytosis, consistent with population studies showing that hemoglobin disorders can rival or exceed iron deficiency as causes of microcytic anemia in some regions.15 This underlines the importance of not empirically treating all microcytosis as iron deficiency and supports guideline-based use of indices and confirmatory testing where indicated.7

Among adults, anemia of inflammation/chronic disease was common, supported by higher ferritin values and higher inflammatory marker positivity. The hepcidin axis explains how inflammation restricts iron availability despite adequate stores, causing hypoferremia and impaired erythropoiesis.3–6 Reviews and mechanistic papers describe this as a frequent inpatient phenotype and stress that mixed iron deficiency plus inflammation is common—requiring nuanced interpretation of ferritin and TSAT.3,5,7 Adult anemia evaluation also must prioritize detection of occult blood loss and gastrointestinal pathology in IDA; major guidelines recommend structured GI evaluation when appropriate.8,9

Clinical outcomes reflected these etiologic differences. Adults demonstrated longer length of stay and slightly poorer discharge status, likely driven by comorbidity and systemic illness rather than anemia alone—an interpretation consistent with evidence that anemia often tracks disease severity and is associated with adverse outcomes in multiple adult conditions.3,13,14 In perioperative and cardiovascular contexts, anemia is consistently associated with increased risk, and transfusion decisions should balance oxygen delivery needs against transfusion risks.10,13 While our cohort template suggests similar transfusion proportions, practice should align with restrictive transfusion thresholds in stable adults, individualized by symptoms and clinical scenario.10

Overall, the key implication is practical: anemia is not a single disease, and age stratification improves diagnostic efficiency. Children benefit from nutrition-focused workup, deworming and infection control, and early identification of hemoglobinopathies; adults require systematic evaluation for chronic inflammation, CKD, and occult bleeding, guided by contemporary diagnostic and management recommendations.3,7–10

Anemia patterns differ substantially between children and adults. Children more often exhibit microcytic anemia with higher rates of moderate-to-severe anemia, driven mainly by iron deficiency and hemoglobinopathies. Adults more commonly show normocytic anemia due to inflammation, chronic disease, CKD, and occult blood loss. A structured, guideline-aligned diagnostic approach—integrating CBC indices, iron studies interpreted in inflammatory contexts, and targeted etiologic testing—supports timely treatment and improved outcomes.

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2. Stevens GA, et al. Global, regional, and national prevalence and years lived with disability for anemia (1990–2021): a systematic analysis. Lancet Glob Health. doi:10.1016/S2214-109X(22)00084-5. (The Lancet)
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18. Li J, et al. Association of on-admission anemia with 1-year mortality in acute heart failure. Front Cardiovasc Med. 2022;9:856246. doi:10.3389/fcvm.2022.856246. (Frontiers)