Hypervitaminosis A causing hypercalcemia in cystic fibrosis. Case report and focused review
Khalid H Safi1, Amy G Filbrun, Samya Z Nasr
1Department of Pediatric Pulmonology, University of Michigan, Ann Arbor, Michigan.
Insights
Hypervitaminosis A can cause hypercalcemia in pediatric cystic fibrosis patients. Regular monitoring of vitamin A is crucial for early detection and management of this rare complication.
Area of Science:
- Pediatric Endocrinology
- Nephrology
- Nutritional Science
Background:
- Cystic Fibrosis (CF) with pancreatic insufficiency often requires vitamin supplementation.
- Hypervitaminosis A is a rare but serious complication of vitamin A intake.
- Hypercalcemia can lead to significant renal complications like nephrocalcinosis.
Observation:
- A pediatric patient with CF presented with symptoms of hypercalcemia, including fatigue and increased urination.
- Laboratory results revealed elevated vitamin A levels, hypercalcemia, and signs of renal impairment.
- Renal ultrasound confirmed bilateral nephrocalcinosis.
Findings:
- The patient was diagnosed with chronic hypervitaminosis A leading to hypercalcemia, nephrocalcinosis, and renal insufficiency.
- Treatment involved discontinuing vitamin A supplements, diuresis, and prednisolone.
- This case highlights the potential for vitamin A toxicity in CF patients with malabsorption issues.
Implications:
- Emphasizes the critical need for routine vitamin A level monitoring in pediatric CF patients.
- Suggests that vitamin A toxicity can occur even with inconsistent supplement intake.
- Underscores the importance of individualized vitamin supplementation and monitoring protocols in chronic conditions.
Abstract:
Hypercalcemia is a rare complication of hypervitaminosis A. We report a pediatric patient with cystic fibrosis (CF) and pancreatic insufficiency who was found to have hypervitaminosis A causing hypercalcemia, complicated by nephrocalcinosis and renal impairment. The patient is a 4-year-old girl with pancreatic-insufficient CF, gastroesophageal reflux, oral aversion, and failure to thrive requiring gastrostomy tube placement. She was prescribed Source CF vitamins, but rarely received the full dose, due to emesis and intolerance. She had routine annual labs that revealed hypercalcemia with elevated blood urea nitrogen and creatinine, which were not present in her previous annual labs. Upon further questioning, her mother reported that she seemed more fatigued for a few weeks, had abdominal pain, and was urinating more frequently. Upon admission to the hospital, laboratory results revealed elevated HCO3, while serum levels of potassium, phosphorus, and albumin were within normal limits. Vitamin D (25-hydroxy) level was low, and vitamin A level was elevated. Extensive metabolic and hormonal workup for the etiology of the hypercalcemia revealed evidence of chronic renal insufficiency and elevated vitamin A levels. She had a renal ultrasound that revealed bilateral nephrocalciosis. Diagnosis of chronic hypervitaminosis A complicated by hypercalcemia was made and was managed by holding vitamin A supplements, aggressive diuresis, and prednisolone. This case emphasizes the importance of regular vitamin A monitoring in patients with CF. There is a wide variability for the lowest intake required to cause toxicity, and the lower limit to cause toxicity has not been determined.
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