Category: Calcium/Bone Disorders
Treatment goals in hypoparathyroidism include maintaining low-normal calcium levels in addition to avoiding complications such as hypercalciuria. These are achieved with supplementation with calcium and active vitamin D. Use of vitamin D precursors such as ergocalciferol or cholecalciferol (D3) at high doses are no longer recommended given the safety and wide availability of active metabolites.
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An 87 year-old woman presented with weakness, malaise and constipation. She had undergone a total shoulder arthroplasty 1 month ago and was discharged to a skilled facility. She has a history of surgical hypoparathyroidism following total thyroidectomy for benign nodular disease in the 1970s. Her hypoparathyroidism had been managed with calcium carbonate 600 mg 2 tablets 3-4 times a day and D3 at 50,000 IU twice a week. Her transfer record indicated that she had inadvertently received 50,000 IU three times a week for the first two weeks of her stay, and then reduced to twice a week. Her admission labs reveal a non-PTH mediated hypercalcemia with a corrected serum calcium of 13.2 mg/dL, creatinine 1.2 mg/dL, PTH <0.6 pg/mL, PTHrP 0.9 pmol/L (normal <2.0), 1,25-vitamin D 34 pg/mL and total 25-hydroxyvitamin D (25-OH-D) 197 ng/mL (D3 fraction was 192 ng/mL and D2 5.4 ng/mL).
Review of her record indicated that her serum calcium ranged between 8.5 and 10.7 mg/dL over the past 15 years; including 4 other episodes of hypercalcemia (>10.2 mg/dL) none of which were symptomatic. Her D3 dose had been up to 50,000 IU three times a week several years ago but was subsequently decreased to twice a week given the recurrent hypercalcemia. Following intravenous hydration she received an infusion of 5 mg of zoledronate as well as prednisone 40 mg daily for 3 days. Her serum calcium normalized and she was discharged to the skilled facility. Her serum calcium remained in the low-normal range at 1-month follow-up.
This case of symptomatic hypercalcemia was likely multifactorial, including poor patient handoff during transfers. In addition, it illustrates one of the main concerns regarding use of vitamin D precursors in the treatment of hypoparathyroidism. In the absence of PTH, large doses of vitamin D precursors are needed to allow appropriate hydroxylation to the active metabolite. D3 has a long half-life; thus, dose titration takes several weeks to show effect on serum calcium, allowing for potential prolonged hypercalcemia. This leads to hypercalciuria and increases the risk of neprhocalcinosis, nephrolithiasis and soft tissue calcifications. Use of the active metabolite allows for better dose titration and closer monitoring, maintaining serum calcium at goal.
Assistant Professor of Medicine
Jad G. Sfeir, M.D. is an Assistant Professor of Medicine at the Mayo Clinic College of Medicine and Science in Rochester, Minnesota. After completing his training in Endocrinology and Metabolism, he is currently training in Geriatric Medicine and studying the effects of aging on bone and mechanisms of targeting cell senescence to prevent age-related bone loss at the Robert and Arlene Kogod Center on Aging.