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[Vitamin D poisoning in infants: a preventable cause of hypercalciuria and nephrocalcinosis]
Insights
Vitamin D "stoss" prophylaxis in infants is not recommended due to risks of intoxication, hypercalcemia, and nephrocalcinosis. Standard daily vitamin D3 is a safer alternative for preventing rickets.
Area of Science:
- Pediatrics
- Endocrinology
- Nephrology
Background:
- The standard prophylaxis for vitamin D-deficient rickets involves daily administration of 400 IU vitamin D3.
- Vitamin D intoxication is rare with the established regimen.
Observation:
- Four infants developed vitamin D intoxication following high-dose
- stoss
- (7.5 mg) vitamin D3 prophylaxis within 4 weeks.
- Symptoms included failure to thrive, hypercalcemia, nephrocalcinosis, hypercalciuria, and gross hematuria.
Findings:
- Elevated plasma 25(OH) vitamin D3 levels (270 and 158 nmol/l) were observed.
- Hypercalciuria and nephrocalcinosis were strongly linked to the high-dose vitamin D prophylaxis.
- While urinary calcium normalized with dietary changes, nephrocalcinosis persisted in some patients.
Implications:
- High-dose vitamin D
- stoss
- prophylaxis is not indicated for vitamin D-deficient rickets in infants.
- Vitamin D intoxication should be considered in infants presenting with hypercalciuria and nephrocalcinosis.
- Safer, standard vitamin D prophylaxis regimens should be maintained.
Abstract:
The established prophylaxis for vitamin D-deficient rickets today is 400 IU vitamin D3 given daily during the first year of life. With this regimen, vitamin D intoxication is a rare event. Nevertheless, we have recently seen 4 infants with vitamin D intoxication after a so called "stoss" prophylaxis, i.e. twice 300,000 units (7.5 mg) vitamin D3 orally within 4 weeks. One patient presented with failure to thrive due to marked hypercalcemia (3.9 mmol/l) and nephrocalcinosis, 2 patients showed medullary nephrocalcinosis on ultrasonography and one patient had gross hematuria and spontaneous passage of a calculus. Three patients had massive hypercalciuria (calcium/creatinine ratio 1.8-4.8 mol/mol, normal less than 1). The 25 (OH) vitamin D3 plasma levels, measured only in 2 patients, were strikingly increased (270 and 158 nmol/l, respectively, normal 25-80). Urinary calcium excretion slowly decreased to normal values on a low calcium diet and high fluid intake. Nephrocalcinosis, however, persisted in 2 patients and showed a slight progression ultrasonographically in one patient. The short time interval between vitamin D administration and onset of symptoms and the subsequent clinical course provide strong evidence that hypercalciuria and nephrocalcinosis were due to vitamin D "stoss" prophylaxis in all four cases. In conclusion, there is no indication for vitamin D "stoss" prophylaxis for vitamin D-deficient rickets in infants. Vitamin D intoxication still has to be considered as a possible cause of hypercalciuria.