Concept:
Preterm infants are born with significantly reduced body stores of iron because approximately two-thirds of fetal iron accretion occurs during the third trimester of pregnancy.
Anemia in low-birth-weight preterm infants results from early iron depletion combined with rapid postnatal growth and iatrogenic phlebotomy blood losses.
Explanation:
• Preterm infants weighing $<1.5\text{ kg}$ (Very Low Birth Weight, VLBW) exhaust their meager transplacental iron stores by $6\text{ to }8\text{ weeks}$ of life due to rapid post-natal body growth and expanded blood volume.
• Iron deficiency is the most prevalent nutritional deficiency leading to early-onset microcytic anemia in preterm infants if prophylactic iron supplementation is not initiated by 2--4 weeks of chronological age.
• In response to declining hemoglobin levels and tissue hypoxia, endogenous erythropoietin secretion increases, stimulating active erythropoiesis in the bone marrow that manifests with marked reticulocytosis.
• Copper deficiency can also produce anemia and neutropenia but typically manifests later ($>3\text{--}6\text{ months}$) with associated skeletal changes (osteopenia, cupping of metaphyses).
• Vitamin B12 deficiency causes megaloblastic anemia with inappropriately low reticulocyte counts.
• Standard guidelines recommend daily enteral elemental iron supplementation ($2\text{--}4\text{ mg/kg/day}$) for all VLBW infants starting at 2 to 4 weeks of life through the first year.
Final Answer:
Iron deficiency is the most common nutrient deficiency causing anemia with compensatory reticulocytosis in very low birth weight preterm infants.