The common disorders of the parathyroid gland fall into two main categories: (a) those associated with poor secretion of PTH or hypoparathyroidism and (b) those associated with excess secretion of PTH or hyperparathyroidism.
Hyperparathyroidism is the most common disorder involving the parathyroid glands. Primary hyperparathyroidism is a disorder of mineral metabolism characterized by a defect in the normal feedback control of PTH secretion by the plasma calcium concentration. Secondary hyperparathyroidism is a disorder characterized by primary disruption of mineral homeostasis, such as impaired production of 1α, 25(OH)2D3 or low dietary intake of calcium, which leads to a low blood calcium level and a compensatory increase in para thyroid gland function, size, and secretion of PTH. Hyperparathyroidism can result from a single adenoma, multiple adenomas, hyperplasia, usually of the chief cells, and carcinoma.
The principal clinical features of hyperparathyroidism are a markedly elevated plasma level of serum calcium (11–13 mg/100 mL) and, when present for pro longed intervals of time, extensive resorption of the skeleton. At the kidney level, the presence of renal kidney stones or calculi can be a consequence. Deposition of calcium in the collecting tubules of the kidney pro duces nephrocalcinosis. The hyperactive parathyroid gland may be removed surgically, resulting in a fall in serum calcium levels and often minimization of the urolithiasis. The principal deleterious consequence of prolonged hyperparathyroidism is the greatly decreased mineral content of the skeleton.
The most common cause of hypoparathyroidism is damage to or removal of the parathyroid glands in the course of an operation on the thyroid gland. Most cases are found in children; approximately twice as many females as males are affected. The most prominent clinical feature of hypoparathyroidism is hypocalcemia, and in extreme instances tetany can be observed.
Pseudohypoparathyroidism is a rare genetic disorder involving bone and mineral metabolism. It is probably inherited as an X-linked dominant trait with variable penetrance and is characterized by signs and symptoms similar to those of hypoparathyroidism. However, in this disease state there is a peripheral resistance to the biological actions of parathyroid hormone and an elevated secretion of PTH. Characteristic clinical features include a round face, short stature, brachydactylia (abnormal shortness of fingers or toes), especially of the metacarpal and metatarsal bones as a result of early epiphyseal closure (see Figure 1).
Fig1. A shortened left third metacarpal bone is evident in the hands of a 26-year-old woman with pseudohypoparathyroidism (PHP). This is diagnostic in patients with PHP. Note that all digits, except the thumbs and index fingers, are shorter than normal.
