MON-848 - Hyperparathyroid Crisis Presenting with Acute Pancreatitis and Severe Hungry Bone Syndrome in A Young Patient with Benign Primary Hyperparathyroidism

Introduction:
Primary hyperparathyroidism (PHPT) is a common endocrine disorder, most frequently caused by a single parathyroid adenoma. Rare complications include acute pancreatitis; hyperparathyroid crisis (HPTC), a life-threatening condition marked by severe hypercalcemia and end-organ dysfunction that is typically described in older patients with malignant pathology, large adenomas, or ectopic glands; and Hungry Bone Syndrome (HBS), a postoperative complication characterized by rapid, profound hypocalcemia with hypophosphatemia and hypomagnesemia following parathyroidectomy. HBS is most commonly observed in secondary hyperparathyroidism and is relatively uncommon in PHPT, particularly in patients without underlying renal disease or radiographic skeletal involvement. Risk factors include markedly elevated preoperative PTH, large adenoma size, high bone turnover, and vitamin D deficiency. We present a rare case of PHPT in a young, otherwise healthy male complicated by HPTC, acute pancreatitis, and severe postoperative HBS.

Case Report:
A 34-year-old man with no significant medical history presented with one week of epigastric pain, nausea, and vomiting and was found to have acute pancreatitis and acute kidney injury. Laboratory evaluation revealed severe hypercalcemia (calcium 16.4-17.8 mg/dL, ionized calcium >1.9 mmol/L) and markedly elevated intact parathyroid hormone (PTH 947 pg/mL). Imaging demonstrated a 2.5 cm left inferior parathyroid mass consistent with adenoma. Despite aggressive intravenous hydration and calcitonin, hypercalcemia and renal dysfunction persisted, necessitating hemodialysis prior to definitive surgical management. The patient underwent urgent parathyroidectomy with intraoperative PTH decline. Pathology confirmed a benign parathyroid adenoma with focal nuclear atypia and no features of malignancy.
Postoperatively, the patient developed severe symptomatic hypocalcemia with associated hypophosphatemia and hypomagnesemia, consistent with HBS, requiring intensive intravenous and oral electrolyte replacement and calcitriol therapy. He was discharged on postoperative day five. At the one-month follow-up, calcium and electrolyte levels had normalized, symptoms had resolved, and genetic testing for hereditary PHPT was negative.

Conclusion:
This case demonstrates that hyperparathyroid crisis can occur in young, otherwise healthy individuals with benign parathyroid disease and may initially present with acute pancreatitis. It further highlights that severe Hungry Bone Syndrome can develop in atypical patient populations without underlying renal disease when profound PHPT and high bone turnover are present. Early recognition of PHPT, prompt surgical management, and anticipation of postoperative HBS are essential to optimize outcomes and prevent significant morbidity.

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