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The many faces of primary hyperparathyroidism
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Primary hyperparathyroidism has long ceased to be a disease of “stones, bones, abdominal groans, with psychic overtones,� but more usually presents as an incidental finding of hypercalcemia in asymptomatic patients. There are many recognized complications of primary hyperparathyroidism (PHPT) that dictate the need for curative surgery (eg, low bone mass, kidney stones) and there are a number of associated findings (eg, hypertension, diabetes) that are more prevalent in PHPT, but have not yet been demonstrated to improve following surgery.
The first patient I want to discuss is a 62-year-old woman in whom the referring physician was unsure of the diagnosis. Her calcium was 10.6 mg/dL (reference interval 8.6-10.2), a parathyroid hormone (PTH) of 35 pg/mL (12-88), and a Sestamibi scan that did not demonstrate any parathyroid tissue. The concern was that this patient did not have PHPT because the PTH was still within the normal range and the scan was negative. The error here is that the normal range for PTH in a patient with hypercalcemia is not the stated 12-88 but <20 since non-parathyroid hypercalcemia should suppress the PTH. Additionally, although many of my colleagues disagree with me, parathyroid localizing studies (Sestamibi scan or ultrasound) are not diagnostic procedures and should only be considered by the surgeon once a decision has been made that parathyroidectomy is indicated. After discussion about her disease, she agreed to a referral to the surgeon.
The second is a 64-year-old woman with a long history of mental illness treated with lithium, a drug known to cause parathyroid gland hyperplasia. Her calcium had been stable at 10.5-10.7 for four years, the PTH 58-72, and she too had a negative Sestamibi scan. The negative scan was not a surprise because this woman most likely has parathyroid hyperplasia and the scan is usually negative in that situation. After two years off lithium therapy her mental health had been stable and she was free of symptoms of hypercalcemia. Her bone density T-score at all sites (forearm, spine, and proximal femur) was >–2.0, renal function was normal, as was urine calcium excretion. Lithium-induced parathyroid hyperplasia does regress in some patients once therapy is discontinued, but not in all, as in my patient. Whether to recommend parathyroidectomy in asymptomatic patients with hyperplasia is an unanswered question because the surgery is substantially more involved than removal of a solitary adenoma and restoration of normocalcemia is not always achieved. In this case, after discussion with the patient and her treating physician it was elected not to refer her to surgery for now.