Not all elevations in PTH indicate need for surgery

Last week a surgeon whom I work with frequently called me for some advice about a patient who was sent to him for parathyroidectomy.

The patient was a young woman who had low bone mass on DXA. There was no history of glucocorticoid therapy, renal insufficiency, fracture or kidney stones, but she did have muscle and bone pain. As part of the work-up, the primary care physician discovered slightly elevated parathyroid hormone in the 70-80 pg/mL range (normal 18-65 pg/mL). He ordered a technetium sestamibi parathyroid nuclear scan which showed a possible parathyroid adenoma. Neck ultrasound confirmed a probable parathyroid gland in this location. She was referred directly to the surgeon for parathyroidectomy.

However, the surgeon noted that her total calciums had ranged between 8.2 and 8.8 mg/dL (normal range 8.5-10.5 mg/dL). He was appropriately concerned that the PTH was elevated due to something else besides primary hyperparathyroidism, such as vitamin D deficiency.

Indeed, the patient had a history of Roux-en-Y bariatric surgery. I told him that until proven otherwise, she most likely had secondary hyperparathyroidism due to vitamin D deficiency from gastrointestinal malabsorption. She absolutely must not undergo parathyroidectomy.

I have seen cases of primary hyperparathyroidism that were masked by coexisting severe vitamin D deficiency. In those cases, the calcium was usually at least high normal. The calcium increased after treatment of the vitamin D deficiency. However, given the low calcium and elevated PTH along with history of bariatric surgery, this patient most likely has vitamin D deficiency.

I commended him for not proceeding with parathyroidectomy. I have seen a handful of similar cases in the past where surgery was performed with serious consequences afterwards. These patients had severe postoperative hypocalcemia. Most resolved with time. However, at least one had permanent postoperative hypoparathyroidism and hypocalcemia requiring lifelong calcitriol and oral calcium therapy. This unfortunate outcome could have been completely avoided if only her physicians had realized that not every elevation in PTH is due to primary hyperparathyroidism.

Endocrinologists are well aware of this scenario and understand how to manage these patients. The question I have is: How can we more strongly encourage our colleagues in primary care and surgery to realize this? How can we get them to consider having such patients evaluated by endocrinology first instead of proceeding directly with surgery?