Vitamin K is a fat-soluble vitamin essential for the activation of vitamin K-dependent proteins involved in coagulation and other physiological processes. Neonates are particularly vulnerable to vitamin K deficiency due to limited placental transfer, low hepatic stores, immature liver function, and insufficient dietary intake, especially in exclusively breastfed infants. This review summarizes the biochemistry and pharmacokinetics of vitamin K, focusing on their role in the pathogenesis of late vitamin K deficiency bleeding (VKDB), including intracranial hemorrhage in early infancy. The limitations of conventional coagulation tests are discussed, highlighting the importance of functional biomarkers such as PIVKA-II (Proteins Induced by Vitamin K Absence or Antagonist-II) for the early detection of subclinical deficiency. Despite effective prophylaxis at birth, late VKDB cases still occur, likely due to declining vitamin K levels over time and nutritional factors. These findings underscore the need for prolonged vitamin K supplementation following adequate prophylaxis at birth, particularly to protect high-risk newborns from late VKDB. Strategies may include vitamin K-containing multivitamin supplementation in preterm infants, as well as daily oral vitamin K supplementation (150 µg/day) in exclusively breastfed infants, in order to ensure adequate vitamin K status during early infancy.

Objective: Very low birth weight (VLBW) preterm infants are at increased risk of neurodevelopmental impairment. Although human milk may promote brain development, the association between type of feeding at discharge and neurodevelopmental outcomes remains uncertain. This study evaluated neurodevelopment at 12 months' corrected age according to type of feeding at discharge in VLBW infants. Methods: This prospective single‐center study included 40 VLBW infants (GA < 32 weeks) born at the University Hospital of Parma. Type of feeding at discharge was classified as exclusive human milk, formula feeding or mixed feeding. Neurodevelopment was assessed at 12 months' corrected age using the Bayley Scales of Infant and Toddler Development, Third Edition (BSID‐III), evaluating cognitive, motor, language, socioemotional and adaptive behaviour domains. Time of full enteral feeding achievement and duration of parenteral nutrition were analyzed as continuous variables. Correlation and ANOVA analyses were performed. Results: Type of feeding at discharge was not significantly associated with neurodevelopmental scores. Earlier achievement of enteral nutrition was associated with better cognitive, motor, and language outcomes, while longer duration of parenteral nutrition was associated with lower motor and language scores ( p < 0.05). Conclusions: In VLBW infants, type of feeding at discharge was not associated with neurodevelopmental outcomes at 12 months' corrected age. However, shorter time to full enteral feeding and shorter duration of parenteral nutrition were associated with more favorable neurodevelopmental performance, particularly in motor and language domains. These findings support the importance of optimizing early nutritional management and warrant confirmation in larger prospective studies.

Reactive oxygen and nitrogen species participate in physiological signaling and adaptation during fetal and neonatal development, whereas excessive, prolonged, or spatially dysregulated production may contribute to oxidative and nitrosative tissue injury. Redox dysregulation has been extensively investigated in neonatal conditions, including bronchopulmonary dysplasia (BPD), hypoxic‐ischemic encephalopathy, retinopathy of prematurity (ROP), necrotizing enterocolitis (NEC), congenital heart disease (CHD), and hyperbilirubinemia. Its relationship with bone metabolism is well established in adult and pediatric disorders, including osteoporosis, inflammatory bone loss, and iron‐overload‐related bone disease. However, the potential contribution of perinatal redox imbalance to early skeletal development remains comparatively underexplored. This narrative review critically examines the biochemical mechanisms of reactive species generation, their interaction with inflammatory pathways, and the experimental and clinical evidence linking redox dysregulation to neonatal organ injury. Particular attention is given to the developing skeleton as a potentially underrecognized target. Experimental studies indicate that excessive reactive species can impair chondrogenesis, alter osteoblast and osteoclast activity, disrupt collagen and osteogenic signaling, and interfere with skeletal growth. Human evidence is predominantly observational. Preliminary longitudinal data show inverse associations between cord‐blood markers of oxidative DNA and protein modification and REMS‐derived skeletal Z‐scores during the first year of life. These findings suggest that early redox imbalance may impair bone quality and growth trajectories in newborns. Prospective studies integrating standardized redox biomarkers, bone‐metabolism indices, imaging, nutrition, medication exposure, growth, and fracture outcomes are needed to determine whether redox dysregulation independently contributes to impaired skeletal development.