MON-257 A Case of Primary Hyperparathyroidism Complicated by Vitamin D Deficiency

Abstract

Background: Primary hyperparathyroidism is a relatively common disorder caused by the inappropriate autonomous secretion of parathyroid hormone which subsequently leads to hypercalcemia. There is increased prevalence of vitamin D deficiency in patients with primary hyperparathyroidism. As these patients are already hypercalcemic, there is reluctance within the medical community to provide vitamin D supplementation due to fear of exacerbating hypercalcemia. Clinical Case: A 17 year old African American male was referred to the pediatric endocrinology clinic for hypercalcemia (total serum calcium level 11.2 mg/dL, 8.6-10.6). His past medical history was significant for a diagnosis of membranoproliferative glomerulonephritis type 2 which was in remission. His most recent blood tests showed normal renal function. A review of his hospital chart showed that his calcium levels had been on the upper end of the reference range or above it for at least a year prior to his presentation to the clinic. He had no signs or symptoms concerning for hypercalcemia. He was not taking any calcium supplements or other medications which are known to be associated with elevated calcium levels. There was no known family history of hypercalcemia. He denied any history of renal stones, adrenal disease, weight loss, or osteoporosis but did report a wrist and knee fracture both of which occurred during competitive wrestling matches. His vital signs and physical exam were unremarkable. On laboratory analysis his serum calcium was 11.0 mg/dL, intact PTH 112 pg/mL (ref range 12-88), 25 hydroxyvitamin D was 10 ng/mL (ref range 20-80), Alk Phos 145 U/L (ref range 100-300), Albumin 4.8 g/dL (3.4-5.0), TSH 1.97 mcIU/mL (0.35-4.0), Free T4 0.8 ng/dL (0.6-1.7), Cr 0.94 mg/dL (0.5-1.3), 24 hour urine calcium excretion was 228 mg and calculated calcium to creatinine ratio was 0.07. Ultrasound of the neck and nuclear parathyroid scan and did not definitively show a parathyroid adenoma but could also not rule out the presence of an adenoma. Given patient’s low 25 OH vitamin D level he was given a 4 week course of supplemental vitamin D (1,000 units daily) with resultant 25 OH vitamin D level of 21 ng/mL. His serum calcium and intact PTH level remained elevated at 10.9 mg/dL and 108 pg/mL respectively. The patient was sent to otolaryngology for evaluation should the need arise in the future for surgical intervention and genetic testing to definitively rule out familial hypocalciuric hypercalcemia was sent. As he is asymptomatic with mild hypercalcemia currently, we will continue to monitor yearly per guideline recommendations. Conclusion: Supplementation with modest doses of vitamin D did not significantly raise our patient’s calcium level and led to an improvement in the 25 hydroxyvitamin D level. Vitamin D repletion should be considered in cases of asymptomatic primary hyperparathyroidism associated with mild hypercalcemia.