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Anemia in infancy presents a critical health risk, as the reduced erythrocyte count impairs the adequate delivery of oxygen to all bodily cells, resulting in chronic hypoxemia. Prolonged tissue hypoxia can profoundly disrupt both physical and cognitive developmental trajectories, potentially leading—at its most severe—to permanent cognitive impairments, delays in achieving developmental milestones, or even irreversible neurological damage.

Within the scope of pediatric hematology, three primary classifications of infantile anemia are recognized, each underpinned by distinct pathophysiological mechanisms. The first category comprises **hypoproliferative anemias**, characterized by **diminished erythropoietic activity**—a reduction in red blood cell production within the bone marrow—directly attributable to **chronic deficiencies in essential hematinic micronutrients and vitamins**. Key deficiencies include **iron** (a constitutive element of hemoglobin), **folic acid** (a coenzyme critical for DNA synthesis in hematopoietic cells), **B-complex vitamins**—particularly **B6 (pyridoxine)** and **B12 (cobalamin)**—which serve as cofactors in nucleotide biosynthesis, as well as **vitamin C** (enhancing intestinal iron absorption) and **vitamin E** (protecting erythrocyte membranes from oxidative damage). Of equal importance is the **deficiency of erythropoietin**, a glycoprotein synthesized in the kidneys that governs the proliferation and maturation of erythroid precursors. The second classification encompasses **hemolytic anemias**, among which **hereditary spherocytosis** predominates as the most common genetic disorder. This condition is defined by **structural abnormalities in erythrocyte membrane proteins** (e.g., spectrin, ankyrin, protein 4.1), leading to **premature erythrocyte destruction** within the spleen. Inheritance typically follows an **autosomal dominant pattern**, conferring a 50% transmission risk to offspring when one parent carries the mutation. The third group consists of **posthemorrhagic or iatrogenic anemias**, arising from **acute or chronic blood loss**—whether due to **internal hemorrhage** (e.g., gastrointestinal bleeding), **external bleeding** (e.g., traumatic injury), or **excessive phlebotomy** for diagnostic purposes. **Preterm infants** exhibit heightened vulnerability owing to **depleted iron and folate reserves**, a consequence of truncated fetal accumulation periods, and may additionally experience **transient erythropoietin deficiency** during the early neonatal phase. A further risk factor is the **delayed introduction of complementary foods** after six months of age—per **ESPGHAN 2016 guidelines**, postponing the inclusion of **iron-rich foods** (e.g., meat, organ meats) or **vitamin C sources** (which facilitate non-heme iron absorption) can precipitate **progressive depletion of ferritin stores**. Additionally, the **premature administration of cow’s milk** (prior to 12 months) is contraindicated, as it not only contains **low iron concentrations** but also **inhibits iron absorption** via phosphate and calcium content, which forms insoluble complexes.

Iron-deficiency anemia in infants primarily presents with alarming pallor of the skin, marked psychomotor lethargy, and a pronounced disinterest in feeding, which collectively result in failure to thrive—manifesting as both growth retardation and inadequate weight gain. Additional clinical findings include atrophy of the lingual papillae, giving the tongue a smooth, "glazed" appearance, alongside recurrent angular cheilitis (perleche) and persistent xerosis that remains refractory to even consistent emolient therapy. Megaloblastic anemia, arising from folate or vitamin B12 deficiency, may mimic certain leukemic features: the skin adopts a pale-yellow (subicteric) hue, while oral mucosal surfaces become atypically smooth, lose their normal vascular pattern, and develop an ominous deep-red discoloration. Affected infants often exhibit behavioral disturbances ranging from inconsolable crying to unexplained somnolence, with significant delays in psychomotor development. Hemolytic anemia, characterized by premature erythrocyte destruction, is marked by profoundly low hemoglobin concentrations and concomitant hyperbilirubinemia, potentially exacerbating neonatal jaundice or precipitating later cholestatic manifestations.

The maternal diet—both preconception and during pregnancy—plays a pivotal role in preventing micronutrient deficiencies in the developing fetus and, subsequently, in the infant. Inadequate intake of critical nutrients such as folic acid, iron, or vitamin B12 in a pregnant woman’s diet can lead to fetal deficiencies that may manifest as anemia in early infancy. Health authorities emphasize that women planning pregnancy, as well as those already pregnant, should consistently incorporate folate-rich foods into their meals, including lean pork, eggs, leafy greens (such as spinach, lettuce, and kale), citrus fruits, freshly squeezed orange juice, and fermented dairy products like kefir or plain yogurt. Additionally, following individualized consultation with an obstetrician, targeted folic acid supplementation should be initiated at a dosage tailored to the body’s requirements. Optimal folic acid levels in the maternal diet ensure that the fetus accumulates sufficient reserves of this vitamin to sustain the infant during the first months of life. In cases where an infant is diagnosed with folic acid-deficiency anemia, consultation with a pediatrician or hematologist is essential to implement oral supplementation with folic acid, often combined with vitamin C and a B-vitamin complex. Particular attention must be given to vitamin B12, as deficiencies are more prevalent among women adhering to vegan or vegetarian diets devoid of animal-derived products. For breastfed infants diagnosed with iron, folic acid, or vitamin B12 deficiency anemia, controlled supplementation with appropriate preparations is mandatory. Iron is typically administered in drop form, mixed with a small quantity of expressed breast milk or prepared formula to minimize gastrointestinal irritation. The ideal timing for administration is between feedings, significantly enhancing its bioavailability. Fiber intake should also be monitored, as iron supplements may induce constipation. Supportive administration of vitamin C is recommended, as it not only facilitates the absorption of non-heme (plant-based) iron in the small intestine but also participates in folic acid metabolism. For formula-fed infants, iron-fortified, folic acid-enriched, and vitamin B12-supplemented formulas are preferable. Infantile anemia is a fully reversible condition provided that appropriate supplementation is implemented alongside a diet rich in hematinic nutrients. Upon reaching six months of age, the infant’s diet should be gradually diversified, ensuring daily intake of iron (from meat, fish, legumes), folic acid (from leafy greens, whole-grain cereals), vitamin B12 (primarily from animal products), and vitamin B6 (from bananas, nuts, seeds). To enhance iron absorption from plant-based foods, meals can be fortified with lemon juice or bell pepper, both natural sources of vitamin C. Heme iron, which is more readily absorbed, is predominantly found in red meat and organ meats, while folic acid is abundant in green vegetables (e.g., broccoli, asparagus, parsley). Vitamin C can be sourced from berries, kiwi, strawberries, or—once introduced—citrus fruits.