Prediction and Prevention of Hungry Bone Syndrome in Secondary Hyperparathyroidism: A Case Report and Review of the Literature

Presentation Number: MON 299
Date of Presentation: April 3rd, 2017

Lisa Ereifej*1 and Christina M Lovato2
1University Of New Mexico Hopsitals, Albuquerque, NM, 2University of New Mexico Health Sciences Center, Albuquerque, NM


Introduction: Hungry bone syndrome is a critical postoperative complication of parathyroidectomy in patients with primary or secondary hyperparathyroidism. It is defined as a profound and prolonged hypocalcemia, which if unrecognized, can lead to significant symptoms of tetany, seizures, cardiac arrhythmias, and laryngospasm that can be life-threatening. We present a case of a patient with secondary hyperparathyroidism who developed severe hungry bone syndrome following subtotal parathyroidectomy.

Clinical Case: A 29-year-old woman presented with a history of end-stage renal disease secondary to autoimmune glomerular nephropathy, livedoid vasculopathy, and secondary hyperparathyroidism, refractory to calcitriol. Preoperatively, her serum PTH was 3479 pg/ml (reference range: 11-80 pg/ml), corrected serum calcium was 9.9 mg/dl (reference range: 8.4 -10.4 mg/dl),serum phosphorous was 6.4 mg/dl (reference range: 2.3-5.6 mg/dl), and alkaline phosphatase was 714 units/L (reference range: 30-150 units/L). She was started on Cinacalcet and her PTH decreased to 1512 pg/ml. Given persistently elevated PTH levels, the patient underwent 3 and ½ gland parathyroidectomy and a portion of one parathyroid gland was autotransplanted. Surgical pathology showed hypercellular parathyroid glands with the largest gland weighing 3.4 grams. Postoperatively, her PTH decreased to 7 pg/ml. In addition, serum calcium decreased to 8.0 mg/dl and ionized calcium decreased to 0.8 mmol/L (referance range:1.15-1.27 mmol/L). She experienced protracted hypocalcemia over the next 7 days, requiring up to 6.5 grams of elemental calcium per day, which was replaced with a combination of oral and IV calcium. She was also started on calcitriol which was titrated up to 1 microgram twice a day. In addition, she was dialyzed against a high calcium bath (3.5 mEq/L) to help treat the severe hypocalcemia. Calcium levels stabilized on postoperative day 8. The patient was discharged on calcitriol and calcium carbonate. PTH levels improved to 50 pg/ml on outpatient follow up, however, the patient continued to require oral calcium and calcitriol to maintain serum calcium levels.

Discussion: Various studies have demonstrated an increased risk of hungry bone syndrome in patients with high preoperative PTH and alkaline phosphatase. In this case report, our patient had significantly elevated PTH and alkaline phosphatase levels that led to the development of hungry bone syndrome. It is crucial for clinicians to recognize the factors that place patients at risk for developing hungry bone syndrome as these patients may develop profound hypocalcemia that will require high calcium doses and frequent, close monitoring. We will review risk factors as well as the treatment approaches for prevention and management of hungry bone syndrome which can reduce the significant morbidity and mortality associated with this syndrome


Nothing to Disclose: LE, CML