SUN-813 - Refractory Hypercalcemia Caused by an Intrathyroidal Parathyroid Adenoma Associated with Distal Renal Tubular Acidosis Treated with Zoledronic Acid: A Diagnostic and Surgical Challenge

Primary hyperparathyroidism (PHPT) is usually due to a single parathyroid adenoma and is mostly cured with resection. Ectopic parathyroid glands, including intrathyroidal parathyroid adenomas, represent a diagnostic challenge and are an important cause of refractory hypercalcemia post parathyroidectomy. Intrathyroidal parathyroid glands are rare, accounting for 1-6% of adenomas and are routinely mistaken as thyroid nodules. Distal renal tubular acidosis (dRTA) is a rare complication of hypercalcemia and the use of Zoledronic acid (ZA) to treat symptomatic hypercalcemia in these cases can be challenging given the added risk of nephrotoxicity. In this case we describe the diagnostic approach and management of a patient with persistent severe hypercalcemia due to an intrathyroidal parathyroid adenoma complicated by dRTA, with prior ZA use for the treatment of hypercalcemia.

A 73-year-old female with PHPT and osteoporosis complicated by vertebral compression fractures was found on ultrasound to have a suspected left-sided parathyroid adenoma. An outside sestamibi scan was negative; subsequent 4D-CT showed a lesion posterior to the left thyroid mid pole. Prior to surgery, she was hospitalized with severe hypercalcemia: calcium (Ca)16.2 mg/dL (8.7–10.3 mg/dL), and acute kidney injury (AKI), with PTH 706 pg/mL (15–65 pg/mL). Hypercalcemia improved with intravenous fluids, calcitonin, and ZA. At surgery, three parathyroid glands were resected, and two auto transplanted in the left forearm; fourth gland was not identified. Postoperatively, PTH remained elevated (up to 1167 pg/mL), with recurrent hypercalcemia, AKI, hypophosphatemia, and new dRTA, raising concern for ectopic PTH secretion or carcinoma. Repeat high resolution sestamibi scan revealed a heterogenous lesion posterior-inferior to the left thyroid lobe; initially suggestive of a thyroid nodule. FNA with PTH washout demonstrated PTH >5,000 pg/mL, consistent with an intrathyroidal parathyroid gland. After an exhausted work up and multiple admissions for electrolyte abnormalities associated to dRTA, the patient underwent a curative intrathyroidal parathyroidectomy with left thyroid lobectomy, resulting in normalization of PTH (17 pg/mL) and Ca (8.7 mg/dL).

We outline the challenges in managing persistent severe hypercalcemia caused by intrathyroidal parathyroid adenomas. This case brings awareness to the risk of developing dRTA in patients with persistent PHPT, which is an uncommon complication. Treatment with ZA for management of hypercalcemia also plays an important role, as ZA has been rarely associated with proximal RTA and even fewer cases have attributed dRTA to ZA use. A multidisciplinary approach and prompt recognition of the intrathyroidal parathyroid adenoma, along with appropriate management of severe renal complications was critical in optimizing our patient prior to surgery.

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