Severe maternal malnutrition during pregnancy, liver or kidney disease, chronic diarrhea, premature birth, or multiple pregnancies can all lead to insufficient vitamin D storage in the infant, resulting in congenital vitamin D deficiency rickets.
Insufficient Sun Exposure
Dehydrocholesterol in human skin converts to vitamin D when exposed to ultraviolet rays from sunlight. Therefore, factors like air pollution, high-rise buildings, and prolonged indoor activities for infants can all impair vitamin D production.
Inadequate dietary vitamin D supplementation
Natural foods contain very little vitamin D. Even with exclusive breastfeeding, infants who have limited outdoor exposure and no supplemental vitamin D are prone to deficiency.
Increased vitamin D requirements
Infancy is a period of rapid growth and development, coinciding with the peak incidence of vitamin D deficiency.Premature infants and twins experience rapid postnatal growth, requiring more vitamin D than their insufficient reserves can provide, making them susceptible to vitamin D-deficient rickets.
Disease or Medication Effects
Gastrointestinal and hepatobiliary diseases impair vitamin D absorption and utilization. Long-term use of antiepileptic drugs or glucocorticoids disrupts vitamin D and calcium metabolism, leading to deficiency.
"Calcium deficiency" is actually "vitamin D deficiency"
Vitamin D deficiency disrupts calcium and phosphorus metabolism, causing a chronic systemic nutritional disorder characterized by epiphyseal lesions. This condition, known as vitamin D-deficient rickets, is one of the most common diseases among infants and young children in China, prevalent nationwide with a higher incidence in northern regions. Commonly referred to by the general public as "calcium deficiency," it is actually "vitamin D deficiency."
Early Symptoms of Vitamin D-Deficiency Rickets
· Irritability, startle response, fussiness, excessive sweating, large fontanelle, and bald patch at the back of the head;
· During the active phase, typical epiphyseal changes emerge, such as "ping-pong head"—a sensation of a ping-pong ball when pressing both sides of the occipital region;· Accumulation of osteoid tissue in the anterior chest, at the rib-cartilage junctions, and along the lower rib margins, forming "chest deformities," "beaded ribs," and rib flaring; kyphosis causing a hunchback; lower limbs presenting as bowlegged ("O-shaped") or knock-kneed ("X-shaped"); and "bracelet-like" swelling at the wrists and ankles;
· Severe hypophosphatemia causes generalized muscle flaccidity and reduced muscle tone, leading to abdominal muscle weakness, bloating, and delayed motor development;
· Vitamin D deficiency also compromises children's immunity, increasing susceptibility to pneumonia and diarrhea.
The key to preventing vitamin D-deficient rickets lies in scientifically supplementing vitamin D.
The principles of vitamin D supplementation are early initiation, appropriate dosage, and full course of treatment. Full-term newborns should begin vitamin D supplementation at 2 weeks postnatal at 400 IU/day;Premature infants, low birth weight infants, and twins should begin supplementation at 1 week of age with 800 IU/day, switching to 400 IU/day after 3 months. Both groups should continue supplementation until age 2. Calcium supplementation is generally unnecessary, except for infants with inadequate milk intake or malnutrition, who may require appropriate micronutrient and calcium supplementation.
Patients with severe vitamin D-deficient rickets (marked by significant epiphyseal deformities or functional impairment), complications, or inability to take oral medication may receive a single high-dose intramuscular injection of 200,000–300,000 IU vitamin D, switching to the prophylactic dose (400 IU vitamin D daily) after 3 months.The standard therapeutic dose for general rickets is 2,000–4,000 IU of vitamin D orally daily, switching to the prophylactic dose after one month.
Excessive vitamin D supplementation can cause toxicity
Vitamin D toxicity may result from short-term repeated high-dose vitamin D therapy for rickets, excessive prophylactic doses, or daily intake exceeding recommended levels.Early signs of vitamin D toxicity include loss of appetite, nausea, vomiting, irritability, low-grade fever, and weight loss. Severe cases may present with convulsions, elevated blood pressure, arrhythmia, frequent urination, nocturia, or even dehydration, potentially progressing to chronic renal failure.