Hyperparathyroidism is a situation where there is excessive production of parathyroid hormone (PTH) by parathyroid glands.


Parathyroid glands are four little bodies located within the thyroid gland. The cells are important because of production of PTH hormone. This hormone plays an irreplaceable role in calcium and bone metabolism. The main objective of PTH is to maintain normal level of calcium in the blood (calcemia). PTH can increase serum calcium by decalcification of bones and releasing calcium into the blood. In addition, PTH stimulates the production of vitamin D, which also increases calcium blood level (mainly by supporting calcium absorption from the gut). Excessive secretion of PTH may arise primarily or in response to other disorders.


Parathyroid glands
Schema - parathyroid glands (red)



Primary hyperparathyroidism

In this case, the problem is directly in the parathyroid gland. It is usually a benign tumor (adenoma), whose cells produce excessive amount of PTH. Much rarer malignant tumors of parathyroid gland with retained ability to produce PTH can have similar effect.

Secondary hyperparathyroidism

In this case, hyperparathyroidism is just a reaction to low level of calcium in the blood (hypocalcemia). It is a part of complex body reaction to normalize calcium concentration, and therefore the serum level calcium is in this case normal or even low (when the PTH action is not sufficient). Secondary hyperparathyroidism is typical in chronic renal failure.

Tertiary hyperparathyroidism

This state may follow the above mentioned secondary hyperparathyroidism when the situation gets out of control. Parathyroid glands are stimulated to produce excessive amounts of PTH, their cells multiply and they may cease to hang on control mechanisms of the body.


In primary hyperparathyroidism we usually find hypercalcemia (high blood calcium level). This condition manifests with weakness, fatigue, apathy, tendency to constipation and some ECG changes including arrhythmias or (in the worst case) even sudden cardiac arrest. In addition, there may be symptoms of bones decalcification. The bones are soft, easily deform, break and so-called pathologic fractures occur. In secondary (and tertiary) hyperparathyroidism the cause is low calcium level, which more or less normalizes due to actions of PTH and therefore, bone symptoms dominate. In chronic renal failure this is referred to as renal osteodystrophy (kidney-related disorders of bone metabolism).


Note: Once again, elevated level of parathyroid hormone (i.e. hyperparathyroidism) does not automatically correspond with elevation of blood calcium level. It may be increased, normal, or decreased. It depends on the type and the underlying cause of hyperparathyroidism!


Suspicion of primary hyperparathyroidism can arise when there is an incidental finding of hypercalcemia in the blood tests. Direct evaluation of PTH blood level is advisable. A patient with elevated PTH level of an unknown cause should have a neck ultrasound to exclude any parathyroid tumors. When evaluating calcium metabolism, it is always important to know vitamin D blood level, phosphate blood level and renal parameters to exclude chronic kidney failure.


It is necessary to treat the underlying cause, if possible. In primary hyperparathyroidism we try to remove the tumor producing PTH. In secondary (and tertiary) hyperparathyroidism, it is necessary to treat the underlying disease that led to hypocalcemia (e.g. renal failure) and regularly administer the patient calcium and vitamin D as dietary supplement.