6940 Thrombotic Events in Primary Hyperparathyroidism: Association or Coincidence?
Authors: Guatemala Funes Irving Alexis , Zavgorodneva Zhanna , EL-Soufi Yahya , Khan Abdullah , Zahedi Tooraj , Zhang Fan 
Published: October 2024

Abstract
Disclosure: I.A. Guatemala Funes: None. Z. Zavgorodneva: None. Y. EL-Soufi: None. A. Khan: None. T. Zahedi: None. F. Zhang: None.
Introduction: The classical manifestations of primary hyperparathyroidism are nephrolithiasis, osteoporosis, and hypercalcemia-related symptoms, such as abdominal pain, constipation, polydipsia, and polyuria. Parathyroid crisis is a rare and life-threatening presentation of primary hyperparathyroidism characterized by calcium levels above 14-15 mg/dl and marked symptoms of hypercalcemia. Here, we describe a rare case of bilateral pulmonary embolism in a patient with severe hypercalcemia secondary to parathyroid adenoma. Case Report The patient is a 70-year-old female with a past medical history of primary hyperparathyroidism, who presented with profound fatigue, shortness of breath, polyuria and constipation. The patient denied any trauma, immobilization, or long-distance travel. On physical exam patient was confused, dehydrated, and nonhypoxic but with increased work of breathing. Initial labs showed severe hypercalcemia with calcium 19.2 mg/dL, significant elevated PTH 1113.9 pg/mL from her baseline PTH 380.8 pg/mL, normal 25 VitD, and acute kidney injury with creatinine increased from 0.9 mg/dL to 2.8 mg/dL. The calcium level in 24-hour urine collection was 323 mg/24 hours. CT chest angiogram revealed a bilateral lower lobe pulmonary embolism. The lower extremity duplex was negative for venous thrombosis. Thyroid ultrasound demonstrated suspected left parathyroid adenoma 2.1 x 2.1 x 1.4 cm. Renal ultrasound was negative for renal calculi. Following treatment with intravenous fluids, Calcitonin, and Denosumab, her calcium level improved to 10.1 mg/dL. The patient’s symptoms improved and underwent parathyroidectomy. PTH levels decreased significantly after parathyroidectomy. Pathology report confirmed parathyroid adenoma. Discussion The association between hypercalcemia and venous or arterial thrombosis has been rarely reported. Calcium participates directly in the platelet activation, platelet aggregation, and coagulation cascade. However, the true correlation between hypercalcemia and thrombosis is not well understood. It is believed that indirect factors such as vasoconstriction, dehydration, and cytotoxic effects due to hypercalcemia and the direct effects over platelet function and coagulation, may act together to induce thrombosis. Unfortunately, much of the evidence between hypercalcemia and hypercoagulability is based on case reports and our case could be one more evidence that this correlation exists. The patient’s age, absence of other risk factors of hypercoagulability, simultaneous manifestation of hypercalcemic crisis, and acute PE make hypercalcemia as a more likely pathogenetic origin of thrombus formation. Conclusion: Physicians should be cautious of the hypercalcemia-induced thrombotic events caused by dehydration and calcium-triggered vasoconstriction, clotting system activation, or platelet aggregation.
Presentation: 6/3/2024