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A dysfunction of the body’s normal regulatory feedback mechanisms resulting in excess production of parathyroid hormone (PTH)
- Primary hyperparathyroidism (HPT): intrinsic parathyroid gland dysfunction resulting in excessive secretion of PTH with a lack of response to feedback inhibition by elevated calcium
- Secondary HPT: excessive secretion of PTH in response to hypocalcemia, which can be caused by vitamin D deficiency or renal failure
- Tertiary HPT: autonomous hyperfunction of the parathyroid gland in the setting of long-standing secondary HPT
- Predominantly postmenopausal females
- Female > male (3:1)
Primary HPT is 1 in 500 to 1 in 1,000 in the United States
Etiology and Pathophysiology
- PTH is synthesized by the four parathyroid glands, which are located behind the four poles of the thyroid gland (locations can vary).
- Ectopic (abnormal locations and most common is the thymus) or supernumerary glands (more than four glands)
- PTH releases calcium from bone by osteoclastic stimulation (increasing bone resorption).
- PTH increases reabsorption of calcium in the distal tubules of the kidneys.
- PTH stimulates conversion of 25-hydroxycholecalciferol (25[OH]-Vit D) to 1,25-dihydroxycholecalciferol (1,25[OH]2-Vit D or active vitamin D) in the kidneys. 1,25(OH)2-Vit D increases calcium and phosphate absorption from the GI tract and kidneys, and stimulates osteoclastic activity and bone resorption.
- Primary HPT: unregulated PTH production and release due to the loss of normal feedback control by extracellular calcium, causing increase in serum calcium
- Solitary adenoma (80–85%)
- Diffuse hyperplasia (10–15%) of the four parathyroid glands, either sporadically or in association with multiple endocrine neoplasia (MEN) types I or II
- Parathyroid carcinoma (<1%), a very rare and severe form
- Secondary HPT: adaptive parathyroid gland hyperplasia and hyperfunction
- Dietary: vitamin D or calcium deficiency
- Chronic renal disease resulting in the following:
- Renal parenchymal loss causing hyperphosphatemia
- Impaired calcitriol production causing hypocalcemia
- General skeletal and renal resistance to PTH
- Tertiary HPT: autonomous oversecretion of PTH following prolonged parathyroid stimulation
- MEN types I and II: Patients with multiple gland hyperplasia in the absence of renal disease should be screened for MEN-I gene mutation.
- Neonatal severe primary HPT
- HPT—jaw tumor syndrome
- Familial hypocalciuric hypercalcemia (FHH)
- Familial isolated HPT
Chronic kidney disease, increasing age, poor nutrition, radiation, and/or family history
Adequate intake of calcium and vitamin D may help prevent secondary HPT.
Commonly Associated Conditions
- Vitamin D deficiency
- Chronic renal failure
- MEN syndromes types I and II