Hyperparathyroidism occurs when overactive parathyroid glands cause levels of parathyroid hormone (PTH) in the blood to become elevated. An elevated PTH level then leads to a high level of calcium in the blood (hypercalcemia).
- Symptoms are due to the high level of calcium in the blood and include weakness and fatigue, constipation, loss of appetite, memory loss, poor concentration, confusion and increased urination.
- Diagnosis is by measuring levels of parathyroid hormone and calcium in the blood.
- Surgery may be done to remove one or more overactive glands.
The parathyroid glands are located near the thyroid gland. Their exact location, and even the total number of glands, is quite variable. These glands secrete parathyroid hormone (PTH), which regulates calcium levels in the blood and tissues through its effects on bones, the kidneys, and the intestine. (See also Overview of Parathyroid Function.)
Hyperparathyroidism is most commonly caused by a parathyroid adenoma (a type of noncancerous tumor). Parathyroid adenomas are usually isolated and solitary. However, parathyroid adenomas may be part of certain hereditary disorders in which people have tumors of several endocrine glands (multiple endocrine neoplasia syndromes).
Hyperparathyroidism can also be the result of hyperplasia of the parathyroid glands. Hyperplasia is when there is an overall increase in size of an organ or tissue. With parathyroid hyperplasia, each parathyroid gland is enlarged. The cells of the gland appear normal when examined under a microscope, so it is not considered a type of cancer, but medical treatment or surgery is needed to reduce the amount of parathyroid tissue and restore the overactive parathyroid to normal.
The Parathyroid Glands
There are three types of hyperparathyroidism:
- Primary hyperparathyroidism, due to a disorder of one or more parathyroid glands
- Secondary hyperparathyroidism, due to a disorder elsewhere in the body that decreases the level of calcium in the blood (which makes the parathyroid gland increase PTH secretion in order to raise the calcium level)
- Tertiary hyperparathyroidism, due to oversecretion of PTH that is not related to the level of calcium in the blood and is not caused by a parathyroid adenoma
Primary hyperparathyroidism results from excessive secretion of PTH due to a disorder of one or more parathyroid glands. About 85% of people with primary hyperparathyroidism have a parathyroid adenoma (a noncancerous tumor) involving just one parathyroid gland. About 15% of cases are due to hyperplasia or enlargement of all the parathyroid glands. Parathyroid cancer, which usually involves just one parathyroid gland, occurs in less than 1% of cases.
The incidence of primary hyperparathyroidism increases with age and is higher in postmenopausal women. It also frequently occurs three or more decades after receiving radiation to the neck.
Primary hyperparathyroidism causes hypercalcemia (high level of calcium in the blood), hypophosphatemia (low level of phosphate in the blood), and excessive bone resorption (transfer of calcium from bone tissue to the blood). Excessive bone resorption, in turn, leads to osteoporosis.
Secondary hyperparathyroidism occurs when hypocalcemia (low level of calcium in the blood) due to a non-parathyroid disorder leads to chronic oversecretion of PTH. Secondary hyperparathyroidism occurs most commonly in people with advanced chronic kidney disease when decreased formation of active vitamin D in the kidneys and other factors lead to hypocalcemia and chronic stimulation of PTH secretion. Hyperphosphatemia (excess phosphate in the blood) that develops in response to chronic kidney disease also contributes.
Tertiary hyperparathyroidism results when PTH is secreted regardless of the calcium level in the blood. Tertiary hyperparathyroidism generally occurs in people with long-standing secondary hyperparathyroidism and in those who have had chronic kidney disease for several years.
Hyperparathyroidism often has no symptoms. Symptoms, when they occur, are due to hypercalcemia (excess calcium in the blood) and include weakness and fatigue, constipation, loss of appetite, poor concentration, memory loss, confusion, and increased urination.
Hypercalcemia frequently causes high levels of calcium in the urine (hypercalciuria), which can lead to kidney stones. Chronic hypercalcemia may also cause weakness and wasting of muscles.
Excess PTH stimulates activity in bone cells (osteoclasts), which over time can cause the bones to weaken from loss of calcium.
- Blood tests
It is common for a person with hyperparathyroidism to have no symptoms. Doctors often first recognize that hyperparathyroidism may be a problem when a blood test, usually done for another reason, shows an elevated level of calcium in the blood (hypercalcemia).
Once hypercalcemia is diagnosed, doctors usually then check the PTH level in the blood. The finding of an elevated PTH level in a person with hypercalcemia confirms hyperparathyroidism. Normally, PTH regulates calcium in the blood. When calcium is low, the parathyroid glands secrete more PTH to increase calcium in the blood. When calcium in the blood is high, the parathyroid glands slow PTH secretion. Thus, having a high or even high normal PTH level at the same time as a high calcium level, is not normal.
Sometimes imaging tests of the neck (for example,ultrasonography, magnetic resonance imaging, or computed tomography) are done to pinpoint the location of an abnormal parathyroid gland.
- Measures to lower blood calcium level
- Often surgery
Treatment for hyperparathyroidism depends on its severity.
For people with primary hyperparathyroidism who have no symptoms and for whom surgery is not indicated, the underlying hypercalcemia may be treated with measures designed to lower the level of calcium in the blood. Doctors encourage people to remain active because inactivity could worsen hypercalcemia. Doctors may also recommend that people follow a low-calcium diet, drink plenty of fluid to minimize the chance of kidney stones, and avoid drugs that can raise the blood calcium level (for example, thiazide diuretics, which may be used to treat high blood pressure or heart failure).
For people with severe hypercalcemia caused by primary hyperparathyroidism who are unable to undergo surgery, doctors sometimes prescribe drugs that lower PTH and calcium levels, such as cinacalcet or etelcalcetide.
Surgery to remove the parathyroid glands (parathyroidectomy) is indicated for people with symptoms and for those with worsening hyperparathyroidism. Whether people with primary hyperparathyroidism who have no symptoms need surgery is unclear.
Many experts, however, recommend surgery when
- Laboratory values in the blood and urine (for example, abnormalities in calcium and creatinine) reach certain levels.
- Bone density at the hip and/or lumbar spine is low.
- The person is younger than 50 years old.
- The person may not follow up appropriately with the prescribed treatment.
During surgery, a parathyroid gland that has an adenoma is removed. The parathyroid hormone (PTH) level in the blood is measured before and after removal of the abnormal gland(s). If PTH levels fall by 50% or more 10 minutes after the adenoma is removed, the treatment is considered a success.
In people with hyperplasia of all parathyroid glands, surgery involves removal of each gland. A small portion of a normal-appearing parathyroid gland is reimplanted in one of the sternocleidomastoid muscles on either side of the neck or under the skin in the forearm. Reimplantation is done to prevent hypoparathyroidism, a deficiency of PTH. Occasionally, parathyroid tissue is set aside and frozen (called cryopreservation) to allow for later transplantation in the same person in case persistent hypoparathyroidism develops.
When hyperparathyroidism has been mild, blood calcium levels drop to just below normal within 24 to 48 hours after surgery. In moderate and severe hyperparathyroidism, calcium levels must be monitored closely for the first several days after surgery to make sure calcium does not go too low.
Hyperparathyroidism in kidney failure
Hyperparathyroidism in people with kidney failure is due to a complex set of problems involving vitamin D, calcium, phosphate, and parathyroid hormone. Treatment is with active forms of vitamin D, restriction of phosphate in the diet, and the use of oral phosphate binders (drugs that reduce the absorption of phosphate from food) and drugs that lower PTH and calcium levels, such as cinacalcet or etelcalcetide.
Hyperphosphatemia (excess phosphate in the blood) should be prevented or treated if present in people with kidney failure. Doctors restrict the amount of phosphate in the person's diet and prescribe phosphate-binding agents, such as calcium carbonate, calcium acetate, lanthanum, or sevelamer to be take with each meal. Both approaches are usually needed, especially in patients with kidney failure who are on dialysis.
People with kidney failure frequently need vitamin D supplements to improve calcium absorption, but the improved calcium absorption can increase phosphate absorption too and contribute to hyperparathyroidism (see also Hypercalcemia (High Level of Calcium in the Blood)). People with advanced kidney disease, especially those with kidney failure, require close monitoring of their calcium and phosphate levels and frequent adjustment of the dosages of the drugs they are taking.
Doctors can also give cinacalcet or etelcalcetide to people receiving dialysis to decrease the level of PTH when vitamin D, phosphate restriction, or phosphate binders are ineffective or unable to be used safely.
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