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Vitamin D and Risk for Vitamin A Intoxication in an 18-Month-Old Boy
Valentina Talarico1, Massimo Barreca1, Rossella Galiano2
1Department of Pediatrics, "Pugliese-Ciaccio" Hospital, 88100 Catanzaro, Italy.
Insights
Over-treating vitamin D deficiency rickets can lead to vitamin D intoxication. This case highlights the importance of checking 25-hydroxyvitamin D levels before and during treatment to prevent toxicity.
Area of Science:
- Pediatrics
- Endocrinology
- Clinical Nutrition
Background:
- Vitamin D deficiency rickets is common in infants.
- Multivitamin preparations are widely used for prevention and treatment.
- Inappropriate dosing can lead to toxicity.
Purpose of the Study:
- To report a case of vitamin D intoxication in an infant.
- To emphasize the importance of monitoring 25-hydroxyvitamin D levels.
- To discuss the potential for over-treatment in rickets management.
Main Methods:
- Case report of an 18-month-old boy with symptoms of hypercalcemia.
- Laboratory investigations including serum calcium, parathyroid hormone (PTH), and 25-hydroxyvitamin D (25-OHD).
- Renal ultrasound for nephrocalcinosis assessment.
- Treatment with intravenous hydration, furosemide, and prednisolone.
Main Results:
- The patient presented with hypercalcemia, low PTH, and extremely high 25-OHD levels.
- Renal ultrasound revealed nephrocalcinosis.
- Treatment normalized serum calcium and progressively reduced 25-OHD levels.
- No signs of vitamin A intoxication were observed.
Conclusions:
- Diagnosis of vitamin D deficiency rickets without monitoring 25-OHD levels can lead to over-treatment.
- Vitamin D intoxication is a potential risk associated with excessive supplementation.
- Careful monitoring and appropriate dosing are crucial for safe and effective rickets management.
Abstract:
An 18-month-old boy presented with abdominal pain, vomiting, diarrhea, and poor appetite for 6 days. He had been given a multivitamin preparation once daily, containing 50.000 IU of vitamin D and 10.000 IU of vitamin A for a wide anterior fontanelle for about three months. He presented with hypercalcemia, low levels of parathyroid hormone (PTH), and very high serum 25-hydroxyvitamin D (25-OHD) levels. Renal ultrasound showed nephrocalcinosis. He did not have sign or symptom of vitamin A intoxication. Patient was successfully treated with intravenous hydration, furosemide, and prednisolone. With treatment, serum calcium returned rapidly to the normal range and serum 25-OHD levels were reduced progressively. In conclusion the diagnosis of vitamin D deficiency rickets without checking 25-OHD levels may cause redundant treatment that leads to vitamin D intoxication (VDI).
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