Parathyroid Abnormality

Edmund A. Pribitkin and Jeffrey L. Miller

Parathyroid abnormalities may result in a broad range of symptoms secondary to a disruption in the body’s calcium ion homeostasis. Primary increases in parathyroid hormone (PTH) secretion typically result in hypercalcemia, whereas secondary increases in PTH secretion may occur as a physiological response to response to depleted vitamin D stores or as a result of severe chronic renal failure. Similarly, primary decreases in PTH secretion (such as those occasionally seen following thyroid or parathyroid surgery) result in hypocalcemia, whereas secondary decreases in PTH secretion may be an appropriate physiological response to the hypercalcemia of malignancy and to hypercalcemia associated with excess ingestion of calcium carbonate (milk-alkali syndrome) or vitamin D intoxication.

Primary Hyperparathyroidism

This is caused by elevated PTH, from parathyroid adenoma or parathyroid hyperplasia—usually of all four glands, although the degree of enlargement may be asymmetric. With the increased prevalence of serum calcium screening and the availability of serum PTH assays, the majority of parathyroid abnormalities are detected through serological testing rather than as a result of the classic clinical triad of “bones, stones, and groans.” The number and severity of signs and symptoms experienced vary with the patient’s age at presentation, the rapidity of the change in calcium homeostasis, and the body’s compensating mechanism. Although asymptomatic hyperparathyroidism has become the rule, many patients note improvements in quality of life following treatment, indicating that subtle signs and symptoms may have been underappreciated. Conversely, 10 to 20% of hyperparathyroid patients may initially exhibit normal serum calcium concentrations, but they come to the clinician’s attention through evaluations for low bone mineral density or other symptoms listed following here.

Elevated serum calcium concentration: Found on routine health screening or during evaluation for an unrelated medical problem leads to discovery of hyperparathyroidism in at least 75% of patients diagnosed with pri mary hyperparathyroidism. As previously noted, classic symptoms and signs of hypercalcemia, such as radial band keratopathy (deposition of calcium phosphate in the exposed areas of the cornea) are rarely seen. The hypercalcemia of malignancy can be readily distinguished from that of primary hyperparathyroidism through the finding of depressed levels of intact PTH. Other common causes of hypercalcemia include the milk-alkali syndrome seen in postmenopausal women due to excessive calcium carbonate intake and familial hypocalciuric hypercalcemia, which is characterized by a defective calcium sensing detector in the parathyroid glands and kidneys.