Poster Presentation ESA-SRB-APEG-NZSE 2022

Primary hyperparathyroidism manifest (#336)

David Lewis 1 , Patrice Forner 1 , Katherine Samaras 1
  1. Endocrinology Department, St Vincent's Hospital, Sydney, NSW, Australia

Primary hyperparathyroidism is a common endocrine problem characterised by overproduction of parathyroid hormone (PTH) with hypercalcaemia. Solitary parathyroid adenomas account for approximately 80% of cases1. PTH overproduction relates to increased parathyroid cell mass with reduced calcium sensing receptor expression leading to blunted negative feedback2. The majority of patients have mild hypercalcaemia with an elevated or inappropriately normal PTH level3.

A 57-year-old female presented with malaise, altered mental status, a one-week history of nausea and vomiting and a two-week history of left hip pain. Corrected calcium was 4.25 mmol/L (2.1-2.6), phosphate 0.8 mmol/L (0.7-1.5), parathyroid hormone 125.1 pmol/L (2.0-9.0), 25-hydroxy vitamin D 21 nmol/L (50-150) and eGFR 38 ml/mn/1.73m2 (>60). A firm mass was palpated in the region of the left inferior pole of the thyroid. Vigorous intravenous rehydration and calcitonin infusions were delivered with rapid improvement in hypercalcaemia. A CT abdomen pelvis revealed an obstructive 10mm renal calculus at the left vesicoureteric junction. A ureteric stent was placed emergently. Ultrasound of the neck showed two nodules in the left inferior thyroid, one with intensely avid uptake of 99mTc-Sestamibi on Spect-CT. The patient proceeded to a left parathyroid exploration with hemithryoidectomy and central node dissection, histopathology diagnosed an atypical parathyroid tumour with severe cytological atypica without diagnostic features of parathyroid carcinoma. Day 3 postoperative hypocalcaemia developed and was managed with one week of twice daily calcium carbonate and calcitriol.

This case is a florid presentation of primary hyperparathyroidism with both acute and chronic complications. It highlights the utility of the clinical examination in patients with hypercalcaemia. Even in the absence of longer acting anti-resorptives, postoperative hypoparathyroidism with hypocalcaemia was seen, consistent with suppression of the healthy glands. Severe hypercalcaemia with a highly elevated PTH should prompt consideration of parathyroid carcinoma and atypical parathyroid adenomas.

  1. Walker MD, Silverberg SJ. Primary hyperparathyroidism. Nature Reviews Endocrinology. 2018 Feb;14(2):115-25.
  2. Brown EM. Role of the calcium-sensing receptor in extracellular calcium homeostasis. Best practice & research Clinical endocrinology & metabolism. 2013 Jun 1;27(3):333-43.
  3. Silverberg SJ, Shane E, Jacobs TP, Siris E, Bilezikian JP. A 10-year prospective study of primary hyperparathyroidism with or without parathyroid surgery. New England Journal of Medicine. 1999 Oct 21;341(17):1249-55.