ECEESPE2025 ePoster Presentations Bone and Mineral Metabolism (142 abstracts)
A case of primary hyperparathyroidism due to an oxyphil cell adenoma
Ghachem Aycha 1 , Imen Halloul 1 , Wiem Saafi 1 , Nassim Ben Hadj Slama 1 , Hamza Elfekih 1 , Ach Taieb 1 & Ghada Saad 1
1Farhat Hached University Hospital, Endocrinology - Diabetology Departement, Sousse, Tunisia
JOINT3617
Introduction: Oxyphil cell parathyroid adenoma were defined as parathyroid tumours containing >75% oxyphilic. They are considered to be an uncommon cause of primary hyperparathyroidism, and were historically thought to be clinically silent cells because they were believed to involuted. Recently these adenomas present more often than previously thought and may manifest a more severe form of primary hyperparathyroidism than classical adenoma. We report the case of a parathyroid adenoma with oxyphilic cells responsible of primary hyperparathyroidism
Observation: This is a 57-year-old patient with a history of fracture of the left foot, who presented with incidentally discovered hypercalcaemia at 2.71 mmol/l. The work-up showed hypophosphaemia at 0.7 mmol/l, hypercalciuria at 7.3 mmol/24h, associated with PTH at 186 pg/ml, with no detectable repercussions. The indication for surgery was based on the presence of a fracture and hypercalciuria. The localised work-up showed a left lower parathyroid adenoma fixed on sestamibi scintigraphy, not visualised on cervical ultrasound. The patient underwent a simple post-operative course, and the patho-anatomical examination concluded that it was an oxyphilic cell adenoma of the left lower parathyroid gland. Post-operative serum calcium was 2.32 mmol/l and serum phosphorus 1 mmol/l.
Conclusion: Oxyphil cell parathyroid are an uncommon cause of primary hyperparathyroidism. Functional oxyphil adenomas occur more frequently than is usually appreciated. Their role still remains controversial, Nevertherless, they could play an important role in hormone secretion.
Volume 110
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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