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MON-336 Presumed Parathyroid Infarction Leading to Remission of Primary Hyperparathyroidism: A Rare Clinical Occurrence

Background: Infarction of a parathyroid adenoma, also known as ‘parathyroid auto-infarction’ or ‘parathyroid apoplexy,’ is a rare condition that can present and lead to acute and dramatic reduction of calcium (Ca2+) and parathyroid hormone (PTH) levels and spontaneous remission of primary hyperparat...

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Detalles Bibliográficos
Autores principales: Nguyen, Tiffany, Narla, Radhika Rao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7209212/
http://dx.doi.org/10.1210/jendso/bvaa046.838
Descripción
Sumario:Background: Infarction of a parathyroid adenoma, also known as ‘parathyroid auto-infarction’ or ‘parathyroid apoplexy,’ is a rare condition that can present and lead to acute and dramatic reduction of calcium (Ca2+) and parathyroid hormone (PTH) levels and spontaneous remission of primary hyperparathyroidism (PHPT). Some patients may experience neck pain, dysphagia, hoarseness, anterior neck swelling or ecchymoses, while others are asymptomatic. Ultrasound can show the lesion getting larger due to hemorrhage, but weeks to months later, there can be a size decrease of the adenoma due to loss of blood supply and necrosis. Sestamibi scans can also show non-localization on serial exams. Few case reports have evidence of infarction on pathology. Clinical Case: A 38 year old man with no significant past medical history presented after a pedestrian-motor vehicle accident with polytrauma, including a cervical spine injury requiring tracheostomy and immobilization of his neck. Over the first week of his hospitalization, his Ca2+ rose as high as 14.0 mg/dL (8.9-10.2 mg/dL). Concurrent PTH level was 233 pg/mL (12-88 pg/mL) and 25-OH vitamin D level was 14.8 ng/mL (20.1-50.0 ng/mL). A neck ultrasound showed a hypoechoic nodule measuring 1.4 x 1.2 x 1.6 cm posterior to the superior aspect right thyroid lobe. A sestamibi scan with SPECT-CT showed a persistent focal activity in the region of right thyroid bed. He was treated with aggressive intravenous (IV) hydration, 7 doses of intranasal calcitonin 500 units, multiple doses of furosemide 40-80 mg IV, pamidronic acid 90 mg IV, and eventually transitioned to cinacalcet 30 mg twice daily. Due to his C-spine injury, parathyroid surgery was deferred. Four months later, the patient developed acute muscle spasms. He denied anterior neck pain, dysphagia, bruising, or swelling. Ca2+ level was checked and found to be 7.0 mg/dL. Cinacalcet was decreased, and eventually had to be discontinued. His serial Ca2+ and PTH levels normalized to 9.8 mg/dL and 55 pg/mL, respectively. A repeat 25-OH vitamin D level was replete at 31.1 ng/mL. A follow up ultrasound redemonstrated a slightly ill-defined hypoechoic nodule, now only measuring 0.9 x 0.9 x 1.4 cm along the the right thyroid. A sestamibi scan was also obtained and did not localize any lesion. The biochemical and imaging findings were most consistent with a parathyroid infarction resulting in spontaneous remission of PHPT. Now one year following his initial presentation, he remains normocalcemic. Clinical Lesson: The differential diagnosis for a sudden remission of PTH-dependent hypercalcemia is limited. Parathyroid infarction is a rare condition with paucity of data regarding follow up, but these patients likely need to remain under close long term clinical and biochemical surveillance as recurrence has been documented in the literature.