Endocrine Abstracts

JOINT3998

Background: Parathyroid carcinoma is a rare but aggressive cause of primary hyperparathyroidism (PHPT), accounting for <1% of cases. Its delayed diagnosis often results in severe phosphocalcic imbalance, leading to marked hypercalcemia, skeletal destruction, and end-organ damage. Surgical resection is the only curative treatment, but postoperatively hungry bone syndrome (HBS) frequently complicates recovery, prolonging hypocalcemia due to excessive mineral uptake by bones.

Case Presentation: A 36-year-old underweight female (body mass index = 16. 4 kg/m²) with facial dysmorphia and feeding difficulties, presented after four years of progressive, uninvestigated right mandibular and left maxillary swellings, found to be large (10 cm) brown tumors with maxillary sinus invasion on cone beam computed tomography. Laboratory findings revealed severe hypercalcemia (Calcium = 14. 2 mg/dL), markedly elevated parathormone (PTH) (780. 8 pg/mL), and hypercalciuria (779 mg/24h), confirming PHPT. Ultrasonography identified a 1. 52 × 1. 74 × 4 cm hypoechoic, inhomogeneous left superior parathyroid lesion, with intense Technetium -99m MIBI uptake, highly suspicious for malignancy. PHPT complications included forearm osteoporosis and bilateral nephrocalcinosis with stage 3 chronic kidney disease. She underwent emergency total en bloc thyroidectomy with removal of three parathyroid glands. Histopathology confirmed parathyroid carcinoma (pT2N0L0V1Pn1) in the left superior gland, with hyperplasia in the left inferior and right superior glands. Despite preoperative vitamin D supplementation, intensive hydration, andavoiding bisphosphonates, severe HBS developed (Calcium=5, 1 mg/dl; Magnesium=1, 7 mg/dl; Phosphorus=2. 3mg/dl; Alkaline Phosphatase = 467 U/l, after the PTH postsurgical drop (2, 4 pg/ml). She required prolonged high-dose IV and per os calcium (up to 2500 mg calcium element daily), high doses of calcitriol, and magnesium supplementation with multiple dose adjustments for three months. MEN syndromes were excluded. A six-month follow-up is scheduled to assess brown tumor regression and determine if surgical correction for skeletal damage is necessary. Lifelong multidisciplinary follow-upwill monitor forrecurrence, phosphocalcic balance, and end-organ damage.

Conclusion: Delayed diagnosis led to severe pre- and postsurgical phosphocalcic imbalance and severe skeletal and renal complications. Identifying risk factors for malignancy guided the choice of an optimal surgical approach. However, despite close monitoring and intensive management, metabolic rebalancing was prolonged. Long-term multidisciplinary follow-up is essential for bone recovery, and recurrence monitoring.