Nutritional Rickets in Children

Vitamin D-deficiency rickets remains the most common form of calcipenic rickets worldwide and is caused by insufficient vitamin D leading to impaired calcium and phosphate homeostasis. The disorder results in defective mineralization of the growth plate and newly formed bone, particularly during periods of rapid growth. Risk factors include exclusive breastfeeding without supplementation, limited sunlight exposure, dark skin pigmentation, use of sunscreen or clothing covering most of the body, malabsorptive disorders, chronic liver or kidney disease, and diets low in vitamin D and calcium. Clinical manifestations vary with severity but often include delayed motor milestones, growth retardation, bone pain, frontal bossing, widening of wrists and ankles, bowing of the legs, and rachitic rosary along the costochondral junctions. Severe hypocalcemia may present with seizures, tetany, or cardiomyopathy. Diagnosis is established by measuring serum ۲۵-hydroxyvitamin D (the best indicator of vitamin D status). Levels ۱۲ ng/mL (۳۰ nmol/L) are considered deficient; ۱۲-۲۰ ng/mL indicates insufficiency. Typical laboratory findings include elevated alkaline phosphatase, secondary hyperparathyroidism, low or low-normal calcium and phosphate, and radiographic evidence of metaphyseal cupping and fraying. Treatment focuses on correcting vitamin D deficiency and replenishing calcium stores. For most children, vitamin D۳ is preferred. Therapeutic regimens vary but generally include a "loading" or high-dose course, followed by maintenance therapy. A common approach is oral vitamin D ۲,۰۰۰-۶,۰۰۰ IU daily for almost ۸ weeks, until biochemical and radiologic healing occur. An alternative is a single high-dose ("stoss therapy"), though divided daily dosing is often preferred to minimize adverse effects. After repletion, long-term maintenance with ۴۰۰-۶۰۰ IU/day is recommended, along with ensuring adequate dietary calcium and sunlight exposure.