Rickets
Disorder of bone mineralization in children caused by vitamin D, calcium, or phosphate deficiency, characterized by growth plate widening, bowing of long bones, rachitic rosary, and craniotabes.
Nutritional rickets is reemerging in dark-skinned and exclusively breastfed infants without vitamin D supplementation (AAP recommends 400 IU/d from birth). Hypophosphatemic rickets (X-linked, autosomal dominant) is FGF23-mediated and not vitamin D-responsive. Treatment of nutritional rickets is vitamin D (cholecalciferol 2,000-6,000 IU/d for ≥12 weeks per Endocrine Society) plus adequate calcium. Adult equivalent is osteomalacia.
How each textbook covers it
Advanced Nutrition and Human Metabolism, 8th ed. (Gropper) — Glossary
Defective mineralization of growing bone causing skeletal deformities (bowed legs, rachitic rosary), growth failure, and hypocalcemic complications. Adult counterpart is osteomalacia.
Modern Nutrition in Health and Disease, 12th ed. — Ch 18: Vitamin D
Nutritional rickets is reemerging in dark-skinned and exclusively breastfed infants without vitamin D supplementation (AAP recommends 400 IU/d from birth). Hypophosphatemic rickets (X-linked, autosomal dominant) is FGF23-mediated and not vitamin D-responsive. Treatment of nutritional rickets is vitamin D (cholecalciferol 2,000-6,000 IU/d for ≥12 weeks per Endocrine Society) plus adequate calcium. Adult equivalent is osteomalacia.
Related terms
Calcium, FGF23, Hypocalcemia, Osteomalacia, Vitamin D