Mediastinal Parathyroid Adenoma Causing Hypercalcemic Crisis, Acute Kidney Injury, and Hungry Bone Syndrome

A recent case report examined an unusual presentation of primary hyperparathyroidism driven by an ectopic mediastinal parathyroid adenoma. The patient, a 61-year-old man, was admitted with fatigue and severe hypercalcemia, with serum calcium reaching 6.16 mmol/L and parathyroid hormone (PTH) levels exceeding 5000 pg/mL. These values are far beyond typical laboratory ranges and underscore how ectopic parathyroid tissue can produce a biochemical crisis. For researchers studying calcium homeostasis and PTH regulation, the case illustrates the extreme end of the spectrum and the downstream consequences for renal function, as serum creatinine rose from 150 to 266 μmol/L, indicating acute kidney injury.

The diagnostic approach combined standard and functional imaging. Neck ultrasound identified only a small nodule in the left parathyroid region, which was insufficient to explain the severity of the presentation. 99mTc-MIBI imaging then revealed a focal area of increased radiotracer uptake within the mediastinum, pointing to an ectopic location. After multidisciplinary consultation, the patient underwent thoracoscopic resection of a mediastinal mass. Pathology confirmed an ectopic parathyroid adenoma measuring 3.2 × 2.8 × 1.5 cm.

Postoperatively, PTH levels fell sharply to 56.17 pg/mL, and the patient developed severe hypocalcemia, with a nadir of 1.85 mmol/L, along with numbness in the extremities. These findings were consistent with hungry bone syndrome, a state of rapid skeletal calcium uptake after removal of a long-standing PTH excess. Management included intravenous and oral calcium supplementation plus calcitriol. Serum calcium gradually recovered, and renal function improved significantly over the same period.

The authors note that while each element of this case has been reported individually, the combination of extreme biochemical values, acute kidney injury, and a well-documented postoperative course is uncommon. The report highlights two practical points: functional imaging can be decisive for localizing ectopic parathyroid adenomas when neck ultrasound is inconclusive, and hungry bone syndrome should be anticipated and managed proactively after resection of a large, hyperfunctioning adenoma.

This is a single case report, so the findings cannot be generalized to all patients with hyperparathyroidism or ectopic adenomas. The observations are descriptive and do not establish treatment protocols or dosing strategies. For laboratory and metabolic researchers, the case provides a detailed example of the biochemical trajectory from severe hypercalcemia through postoperative hypocalcemia, and it reinforces the value of correlating imaging, pathology, and serial laboratory measurements. The material is intended for research and educational use only and does not constitute medical advice.