PE12.3 | Vitamin D — Summary & Reflection

KEY TAKEAWAYS

Nutritional rickets results from Vitamin D deficiency (most commonly) or dietary calcium deficiency, causing failure of growth plate mineralisation in children aged 6 months–3 years. Vitamin D undergoes hepatic 25-hydroxylation (to calcidiol) followed by renal 1-alpha-hydroxylation (to calcitriol, the active form). Principal causes in India: exclusive breastfeeding without supplementation, limited sun exposure, dark skin, prematurity.

Clinical features: rachitic rosary, Harrison's sulcus, craniotabes, frontal bossing, wrist and ankle widening, genu varum, hypocalcaemic seizures and tetany. Biochemistry: low calcium, low phosphate, markedly elevated ALP, elevated PTH, low 25(OH)D. X-ray: cupping, fraying, splaying of metaphysis with widened growth plate.

Treatment: stoss therapy 600,000 IU oral single dose (>3 months), followed by 400 IU/day maintenance; daily therapy 2,000–4,000 IU × 6–8 weeks; always add calcium 500–1,000 mg/day. Prophylaxis: 400 IU/day from the first days of life for all breastfed infants.

Hypervitaminosis D: 25(OH)D >150 ng/mL, causes hypercalcaemia (vomiting, polyuria, nephrocalcinosis). Treatment: stop supplement, hydrate, glucocorticoids. Vitamin D toxicity does NOT occur from sun exposure alone.

REFLECT

Consider the urban middle-class family where both parents work indoors, the child attends a creche, and the family is vegetarian. What factors converge to make this child at risk for rickets despite an apparently adequate diet? Reflect on how the '400 IU from birth' recommendation could be incorporated into the existing immunisation contact at birth in India — what would need to change in the current Universal Immunisation Programme to make this happen? What barriers do you anticipate, and how would you counsel a mother who is reluctant to give 'drops' to her newborn?