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Primary hyperparathyroidism develops spontaneously without apparent cause, but possibly in response to exogenous stimuli. When the normal control of serum calcium is disturbed and there is increased autonomous production of PTH, the state is referred to as primary hyperparathyroidism. In contrast, secondary hyperparathyroidism occurs when there is a defect in mineral homeostasis that leads to a compensatory increase in parathyroid function. This occurs most commonly in response to renal disease, but may also develop as a consequence of the hypocalcemia associated with some diseases of the gastrointestinal tract, bone or other endocrine organs. Occasionally, with prolonged secondary stimulation, the hyperfunctioning glands are no longer physiologically responsive to an increased ionized calcium. This rare, relatively
autonomous state is referred to as tertiary hyperparathyroidism and develops most commonly after renal transplantation when the defect in calcium homeostatis is corrected. The numerical values for calcium and PTH here are consistent with primary hyperparathyroidism.
Relation between serum immunoreactive parathyroid hormone (iPTH) and serum calcium in patients with hypoparathyroidism, pseudohypoparathyroidism, ectopic hyperparathyroidism, and primary, secondary, and tertiary hyperparathyroidism. GP1M, guinea pig antiserum 1M. (After Clark OH, Way LW. Thyroid and parathyroid. In: Current surgical diagnosis and treatment, ed 8. Norwalk, CT, Appleton & Lange, 1989:249)
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