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SAT-510 Hypercalcemia Secondary to Vitamin D Intoxication and Nephrocalcinosis in 2 Children

Background: Hypercalcemia secondary to Vitamin D intoxication is rare; however, over the past years vitamin D supplementation has become frequent due to the changes on recommended levels proposed by some academies, and frequent evaluation of vitamin D25 levels in otherwise healthy children. Toxic le...

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Detalles Bibliográficos
Autores principales: Diaz, Alejandro, Velasquez, Sara
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Endocrine Society 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6570712/
http://dx.doi.org/10.1210/js.2019-SAT-510
Descripción
Sumario:Background: Hypercalcemia secondary to Vitamin D intoxication is rare; however, over the past years vitamin D supplementation has become frequent due to the changes on recommended levels proposed by some academies, and frequent evaluation of vitamin D25 levels in otherwise healthy children. Toxic levels of vitamin D have been defined by the Endocrine Society as ≥150 ng/mL and by the former Institute of Medicine as ≥100 ng/mL. Case reports: We present two cases of hypercalcemia due to vitamin D intoxication. A 4-year-old male with past medical history of vitiligo, presented to the emergency department after 2 days of emesis. His calcium level was 16.4 mg/dL (8.5-10.2 mg/dL), phosphorus 3.4 mg/dL (2.5 to 4.5 mg/dL), intact PTH <1.0 pg/ml (12-88 pg/mL), and 25-OH vitamin D was 397 ng/mL (<100 ng/mL). When interviewed, his maternal grandmother administered a vitamin D preparation obtained in Ecuador, which contained 600,000 IU of vitamin D3 per vial. She gave him one vial monthly for 4 months. On physical examination, he had ataxic gait. A renal ultrasound showed bilateral medullar nephrocalcinosis. He was treated with pamidronate and calcitonin. Calcium levels normalized after four days on treatment. Clinical symptoms resolved. Vitamin D level normalized after a few weeks. A kidney ultrasound 6 years later showed resolution of nephrocalcinosis. The second case is a 3-month-old girl who presented to the emergency department with constipation, weight loss, and increased urination. Her calcium level was 17.4 mg/dL, intact PTH 0.3 pg/mL, vitamin D25 439 ng/mL, vitamin D1.25 147 pg/mL (24-86 pg/mL). She was treated with calcitonin, pamidronate, and a low calcium formula. A kidney ultrasound showed marked bilateral nephrocalcinosis and mild bilateral pelviectasis. When interviewed, her nanny gave her 1 mL of vitamin D3, which contained 24,000 IU of Vitamin D3 daily, since first week of life, instead of the recommended 1 drop (400 IU), for a total of 6 weeks. After 6 days of treatment the calcium levels normalized (9.6 mg/dL). She was followed after discharge. Her vitamin D25 levels normalized after 3 months: vitamin D25 was 92 ng/mL, and vitamin D1,25 was 68 pg/mL. Kidney ultrasounds for the next 4 years showed stable bilateral nephrocalcinosis and mild left pelviectasis. Renal function tests have been normal. Conclusions: Hypercalcemia due to Vitamin D intoxication is becoming more common after modification of normal values of vitamin D25 and increased supplementation in otherwise healthy children. Vitamin D intoxication has serious acute complications and, in some cases, persistent nephrocalcinosis several years after hypercalcemia is resolved.