The parathyroid glands are responsible for maintaining normal calcium homeostasis, and surgical resection is most often performed for conditions where hyperparathyroidism disrupts this balance. The production of parathyroid hormone (PTH) by the chief cells of the parathyroid gland leads to a rise in serum calcium levels by three distinct mechanisms: PTH (1) causes bone resorption leading to the release of calcium into the blood; (2) promotes calcium conservation by the kidneys; and (3) increases absorption of calcium by the GI tract via the production of activated vitamin D in the kidneys.

Hyperparathyroidism is classified into primary, secondary, or tertiary according to etiology. Primary hyperparathyroidism is due to an overproduction of PTH, typically from an autonomously functioning adenoma that is not responsive to normal feedback mechanisms. Most cases are caused by a single parathyroid adenoma, with a minority being due to two adenomas or four-gland hyperplasia (Fig. 19.1).

The symptoms of primary hyperparathyroidism are classically described as “painful bones, renal stones, abdominal groans, and psychic moans” corresponding to the arthralgias, osteoporosis, nephrolithiasis, pancreatitis, peptic ulcers, constipation, fatigue, and depression associated with hypercalcemia. Because these conditions are vague, nonspecific, and common, many individuals do not realize they are experiencing symptoms at all. In fact, it is often only in retrospect that the signs of hypercalcemia are elicited by a clinician taking a detailed history.

The presence of a parathyroid adenoma is diagnosed by the finding of elevated levels of serum PTH and calcium. Parathyroidectomy is indicated in all patients who are symptomatic, and also in individuals who are asymptomatic but display sequelae of hypercalcemia including low bone density scores, high urinary calcium levels, and decreased creatinine clearance.

High-resolution ultrasonography of the neck and/or nuclear scintigraphy (e.g., sestamibi scan) can be used to identify the location of the parathyroid adenoma (Fig. 19.2). Preoperative imaging is increasingly being performed to confirm the location of the adenoma, which allows for a targeted, smaller incision over the enlarged gland. If no localization studies are performed, an exploration of all four glands is necessary to rule out multi-gland disease.

Parathyroid carcinoma is a rare malignant tumor of the parathyroid glands that is another potential cause of primary hyperparathyroidism. In contrast to patients with a parathyroid adenoma, patients with parathyroid carcinoma typically have symptoms of marked hypercalcemia and may present with hypercalcemic crisis. On physical exam a palpable neck mass may be appreciable. Patients may also present with change in voice due to recurrent laryngeal nerve involvement by the tumor.

Elevated PTH production can also occur in response to low calcium levels, as is seen in chronic kidney disease. In this situation, known as secondary hyperparathyroidism, the release of PTH is an appropriate physiologic response to low serum calcium levels, and thus there is no role for parathyroidectomy. The hypocalcemia of renal failure occurs as a result of decreased production of activated Vitamin D by the kidneys. Therefore, renal transplantation is the only cure for secondary hyperparathyroidism caused by kidney failure. It is important to note that patients with secondary hyperparathyroidism do not have the same symptoms as those with primary hyperparathyroidism, since calcium levels are not elevated. Most symptoms of secondary hyperparathyroidism are related to the excessive bone resorption that occurs from the body’s efforts to mobilize reserves of calcium and restore normal serum levels.