Vitamin D is essential for calcium-phosphorus homeostasis and normal skeletal growth in childhood, while its receptors and metabolic enzymes are also expressed in immune and other tissues. This thesis summarizes current evidence on pediatric vitamin D deficiency, emphasizing bone metabolism, immune regulation, growth and neurodevelopment, diagnosis, risk stratification and prevention. Severe deficiency may cause hypocalcemia, secondary hyperparathyroidism, impaired mineralization and nutritional rickets. Observational data also link low vitamin D status with infections, autoimmune and allergic conditions, but causal relationships and the benefits of supplementation for non-skeletal outcomes remain inconsistent. Prevention should prioritize adequate nutrition, age-appropriate supplementation when indicated, safe sunlight exposure, food fortification and targeted assessment of high-risk children. (1,2,3)
No takes yet. Share an insight, caveat, or question.
Soliyev Abduboriy Sattorjon o'g'li (2026) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: