Description
Rickets, caused primarily by vitamin D deficiency, leads to impaired bone mineralization in children, resulting in bone deformities, delayed growth, and skeletal pain. Prevention involves adequate sunlight exposure, a diet rich in vitamin D and calcium, and supplementation in at-risk populations such as exclusively breastfed infants or those with limited sun exposure. Treatment includes vitamin D and calcium supplementation, correction of underlying causes, and monitoring of biochemical markers and bone health. In severe cases, high-dose vitamin D therapy may be required. Early diagnosis and intervention are crucial to prevent long-term complications and support healthy growth and development in children.
Summary Listen
- Vitamin D is a fat-soluble vitamin, functioning more like a prohormone due to its widespread effects on tissues. Natural sources include ergocalciferol (vitamin D2) from plants and cholecalciferol (vitamin D3) from animals. Sunlight is a major source, converting 7-dehydrocholesterol in the skin to vitamin D3. Other sources include fatty fish, liver, and fortified dairy/cereal products.
- The body converts vitamin D into two forms: 25-hydroxy vitamin D (calcidiol), a storage form, and 1,25-dihydroxy vitamin D (calcitriol), the biologically active form. Vitamin D is vital for bone and teeth development, muscle function, immune response, and overall growth. It modulates calcium and phosphate absorption, potentially influences insulin sensitivity, and acts as an antioxidant.
- Rickets is a disease of growing bones characterized by defective mineralization of cartilage and bone. Common causes are vitamin D or calcium deficiency. Less common causes include hypophosphatemia and kidney conditions. Etiology includes nutritional deficiencies, malabsorption, liver/kidney disease, and genetic conditions.
- Clinical features in infancy include craniotabes and delayed milestones. Toddlers may present with rachitic rosary and bowed legs. Older children may experience bone pain, fatigue, knock knees, or pigeon chest. Extra-skeletal manifestations include muscle weakness and abdominal protrusion.
- Diagnosis involves radiological confirmation with X-rays, revealing cupping and fraying of metaphyses and widened growth plates. Biochemical analysis includes vitamin D, calcium, phosphate, alkaline phosphatase, and parathyroid hormone levels. It's crucial to differentiate between calcipenic and phosphopenic rickets.
- Treatment involves high-dose vitamin D supplementation (2000-4000 IU/day for 6-12 weeks), followed by maintenance (400-600 IU/day), alongside calcium supplementation. Renal rickets requires calcitriol. Monitoring includes alkaline phosphatase levels and repeat X-rays. Prevention includes vitamin D supplementation from birth (400 IU/day) and adequate sun exposure (30-45 minutes, 5 times a week, with 40% body surface area exposed).
- Hypervitaminosis D presents with vomiting, polyuria, lethargy, hypotonia, abdominal pain, poor feeding, and nausea. Lab findings include elevated calcium and suppressed PTH. Management involves stopping vitamin D, ensuring adequate hydration, and, in some cases, using diuretics, steroids, or bisphosphonates.
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