Hypervitaminosis A: A Rare Cause of Hypercalcemia

Abstract

Introduction: Hypercalcemia is a rather common clinical problem and a majority of cases are found to be secondary to primary hyperparathyroidism and malignancy. A rare cause of hypercalcemia is associated with high levels of vitamin A and thought to be secondary to the effect of vitamin A on bone to stimulate osteoclastic resorption or inhibit osteoblastic formation. Clinical Case: A 54 year-old male with a past medical history of CKD stage 3 secondary to medullary sponge kidney presented for hypercalcemia. He complained of chronic constipation, joint pain, mood changes and recurrent kidney stones. Reported multivitamin use (including 1000mcg of vitamin A) for years but was discontinued one year prior to visit. Lab work showed calcium of 11.5 mg/dL (8.7–10.2mg/dL), albumin 4.9 g/dL (3.8–4.9g/dL), elevated 24h urine calcium, eGFR 40 mL/min/1.73, parathyroid hormone 5 pg/mL (15-65pg/mL,) normal 1,25-OH vit D and 25-OH vit D, PTHrP <2.0 pmol/L, serum protein electrophoresis unremarkable. His vitamin A level was elevated to 103 ug/dL (20.1–62.0ug/dL). CT chest showed no findings concerning for sarcoidosis. Bone density scan showed normal bone mineral density. Patient diagnosed with hypercalcemia secondary to elevated vitamin A levels. Current limited literature shows stopping the vitamin A supplement will normalize vitamin A levels and correct the hypercalcemia. This patient had discontinued his multivitamin 1 year prior and vitamin A remained elevated, thought to be due to his poor kidney function. Treatment was targeted at improving his hypercalcemia and reducing his symptoms. He was prescribed a one-week course of prednisone 40 mg daily. His calcium level improved to 10.5 mg/dL. Prednisone was reduced to 20 mg daily with normalization of calcium to 10.3 mg/dL (8.7–10.2mg/dL). Conclusion: Hypercalcemia is a rare but known complication of vitamin D toxicity. The liver, kidney and adrenal glands store vitamin A and it is excreted in the urine. Liver and kidney disease pose higher risk of vitamin A toxicity. We present a unique case of Hypercalcemia secondary to elevated vitamin A levels in a patient with moderate chronic kidney disease who was not taking excessive amounts of vitamin A and whose calcium and vitamin A did not normalize once vitamin A supplements were discontinued. The CKD 3 may have reduced vitamin A clearance and increased its toxicity. Hypercalcemia is not the only concern regarding vitamin A toxicity, the increasing use of dietary supplements and over the counter medications may pose significant risks for osteoporosis and bone fractures. A high clinical suspicion and thorough workup to exclude other causes of hypercalcemia is warranted to diagnose hypervitaminosis A as the etiology. Steroids can reduce gastrointestinal absorption of calcium, however, its role in vitamin A toxicity remains unclear. Further research is needed to investigate the appropriate treatment for these patients.