Endocrine Abstracts

Introduction: Primary hyperparathyroidism (PHPT) is the most common cause of hypercalcemia, often caused by a single adenoma (85%) or four-gland hyperplasia (15%). Brown tumors are rare erosive bony lesions caused by localised rapid osteoclastic turnover resulting from hyperparathyroidism.

Case presentation: A 28-year-old lady presented to the Emergency Department with a 3-day history of fever, dry cough and generalized body aches. She reported sudden onset lower back pain radiating to her thighs and 1-month history of multiple joints pains predominantly knee joints. Biochemical investigations were consistent with PHPT: corrected calcium (cCa²+) 3.20 mmol/l (2.23–2.50), phosphate 0.60 mmol/l (0.74–1.52) and PTH 160.3 pmol/l (1.6–6.9). Other relevant laboratory findings were: ALP 3259 U/l (40–150), 24 h urine calcium 4.75 g, normal renal and thyroid function. CT neck/chest revealed a right thyroid nodule measuring 2.5 cm and brown tumors on multiple ribs, cervico-thoracic spine and long bones. MRI spine also showed brown tumors in the right sacral alar and iliac bones. Sestamibi SPECT/CT was later performed indicating a possible hyperfunctioning parathyroid lesion on inferior pole of the right thyroid lobe. There was focal increased tracer uptake in the right iliac crest, left distal tibia and left elbow suggestive of brown tumors. Although referred for a parathyroidectomy, an ultrasound guided FNAC of the right thyroid nodule was performed prior to surgery at the request of the surgical team. FNAC findings were suggestive of parathyroid tissue. Following the procedure, the patient reported pain at the site of FNAC, and pins and needles in all limbs. On neck examination, there was a 4 cm right sided hard and tender neck lump. Laboratory tests revealed cCa²+ 1.92 mmol/l and PTH 4.8 pmol/l. Neck ultrasound showed a 3.77×3.07 cm mixed echogenic nodule with cystic changes in the right thyroid lobe. She was treated for hungry bone syndrome requiring calcium and magnesium supplementation. Haemorrhage and apoplexy of the culprit parathyroid adenoma due to FNAC was suspected. Surgery was cancelled and she was discharged on calcium carbonate and calcitriol. At her last Endocrine clinic review, she was well and remained normocalcaemic (cCa²+ was 2.14 mmol/l, phosphate 0.91 mmol/l) on calcium supplementation. She has not attended further endocrine follow-up thereafter.

Conclusion: Our patient with severe PHPT and significant bone disease appears to have resolution of PHPT following apoplexy of parathyroid adenoma secondary to FNAC. Spontaneous remission of PHPT due to necrosis and hemorrhage of a parathyroid adenoma, the so-called “parathyroid auto-infarction”, “auto-parathyroidectomy” or “parathyroid apoplexy” is a very rare, but previously described phenomenon.