Parathyroid Crisis as the First Presentation of Hyperparathyroidism: A Case Report

Document Type

Conference Proceeding

Publication Date

10-2025

Publication Title

Journal of the Endocrine Society

Abstract

Background: Parathyroid crisis (PTC) is a rare and life-threatening condition marked by severe symptomatic hypercalcemia usually > 14 mg/dl associated with neurological, gastrointestinal, renal, or cardiac dysfunction. Prompt recognition and timely treatment are essential to prevent complications and optimize outcomes. Case: A 71-year-old female with a history of hypertension presented to emergency with a 1-month history of headache, confusion, dry mouth, generalized weakness, and gait instability. She was asymptomatic at her physical exam 2 months prior and had no history of hyperparathyroidism (HPT). Initial laboratory workup revealed Calcium (Ca) 16.2 mg/dL, ionized Ca 8,72 mg/dL, PTH 1060 pg/mL, Phosphorus (P) 1 mg/dL, vitamin D (VitD) 64 ng/mL, TSH 0.58 mcIU/mL, and Magnesium 2.1 mg/dL. She was promptly prescribed intravenous fluids, Calcitonin 200 units twice daily, and Pamidronate 90mg. Neck US revealed a 4.8 x 2.3 x 2.5 cm cystic mass with thickened septations in the right thyroid lobe and a technetium-99m-sestamibi scan showed persistent radiotracer uptake in the cystic lesion, suspicious for a parathyroid adenoma. Subsequent labs revealed Ca of 9.8, but patient requested to be discharged for personal reasons. 10 days later, she underwent a right superior and complete left parathyroidectomy, and pathology revealed a hypercellular parathyroid gland with locules containing pink-red hemorrhagic thin fluid. She developed post-procedure hypocalcemia of 8.2, which was supplemented. Her most recent labs show PTH 61, Ca 9.7, and VitD 67. Currently, the patient is asymptomatic, follows at the Endocrine clinic, and is supplementing Ca, Mg and VitD. Discussion: PTC is typically triggered by an inciting event, though some cases have no identifiable cause. In such instances, parathyroid gland hemorrhage has been proposed as a potential factor. A recent literature review reported that 5% of PTC cases were associated with parathyroid cancer. Despite our patient’s marked hypercalcemia, extremely high PTH, and hypophosphatemia, pathology findings were negative for malignancy. Instead, the presence of a hypercellular parathyroid gland with locules containing pink-red hemorrhagic fluid suggests that hemorrhage may have contributed to her decompensation. There is no consensus on the optimal treatment for PTC. While urgent parathyroidectomy was previously recommended, recent studies suggest that medical management—including early hydration, furosemide-induced calciuresis, and bisphosphonates— can effectively correct hypercalcemia, serving as a bridge to parathyroidectomy, as seen in our patient. PTC also increases the risk of postoperative hypocalcemia likely due to suppressed normal parathyroid function, bone hunger, and preoperative use of bisphosphonates or calcimimetics. Close monitoring and prompt intervention are essential to improving outcomes.

Volume

9

Issue

Suppl 1

First Page

A268

Comments

ENDO 2025 Endocrine Society Annual Meeting, July 12-25, 2025, San Francisco, CA

Last Page

A269

DOI

10.1210/jendso/bvaf149.500

Link to Full Text

Share

COinS