Non‐autonomy of parathyroid hormone secretion in acute primary hyperparathyroidism

Abstract

A patient with acute primary hyperparathyroidism treated with mithramycin preoperatively, underwent neck exploration and two enlarged parathyroid glands were excised: one huge adenoma (6g) and another smaller gland. Mithramycin was administered preoperatively to lower life-threatening hypercalcaemia, and parathyroid slices from the huge adenoma removed at surgery were submitted in vitro to various calcium concentrations in the media to determine the influence of calcium on parathyroid adenoma secretory pattern in acute primary hyperparathyroidism. Mithramycin induced a significant decline in calcium levels and significant elevations of calciotrophic hormones (intact PTH, mid-region specific PTH, calcitonin and calcitriol). Significant suppression in PTH output in vitro was achieved by increasing calcium levels in the media. These results exclude autonomous PTH secretion (non-calcium dependent) as a possible aetiology of acute primary hyperparathyroidism. We suggest that a sudden increase in the set-point of the diseased parathyroid cells in the presence of a huge cell mass accounts, in large part, for both the marked hypercalcaemia and elevated PTH levels in this patient.

Severe symptomatic hypercalcaemia

“…Remarkable increases of PTH are characterisitc of acute primary hyperparathyroidism, up to values 30 times normal levels 67 It has excluded autonomous PTH secretion as a possible cause of acute primary hyperparathyroidism, and it has been suggested that a sudden increase in the set point of the diseased parathyroid cells in the presence of a huge cell mass accounts in large part for both the marked hypercalcaemia and elevated PTH levels in these patients 9. Infections, recent surgery, immobilisation, dehydration, and trauma appear to play a prominent part in the acute primary hyperparathyroidism 6…”