Hyperparathyroidism
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Definition
Hyperparathyroidism is excessive production of parathyroid hormone by the parathyroid glands.
Causes, incidence, and risk factors
The parathyroid glands are located at the front and base of the neck around the thyroid gland. They produce parathyroid hormone, which regulates calcium, phosphorus, and magnesium levels within the blood and bone.
When calcium levels are too low, the body responds by increasing production of parathyroid hormone. This increase in parathyroid hormone causes more calcium to be taken from the bone and more calcium to be reabsorbed by the intestines and kidney. When the calcium level returns to normal, parathyroid hormone production slows down.
Excess parathyroid hormone can be produced for a variety of reasons. In some cases, parathyroid hormone is produced without regard to the calcium levels. This is called “primary hyperparathyroidism” and is caused by enlargement of one or more of the parathyroid glands. It is a common disorder affecting about 1 in 1,000 people. The high levels of calcium and parathyroid hormone affect several body systems, including the skeletal, gastrointestinal, renal, muscular, and central nervous system.
“Secondary hyperparathyroidism” is when the body produces extra parathyroid hormone because the calcium levels are too low. This is seen when vitamin D levels are low or when calcium is not absorbed from the intestines. Correcting the calcium level and the underlying problem will bring the parathyroid levels in the normal range.
If the parathyroid glands continue to produce too much parathyroid hormone even though the calcium level is back to normal, this is called “tertiary hyperthyroidism” and occurs especially in patients with kidney problems.
The term “hyperparathyroidism” generally refers to primary hyperparathyroidism.
Related topics:
- Parathyroid related hypercalcemia
- Primary hyperparathyroidism
- Secondary hyperparathyroidism
- Tertiary hyperparathyroidism
Symptoms
- Fatigue
- Back pain
- Joint pain
- Fractures of long bones
- Decreased height
- Increased urine output
- Increased thirst
- Upper abdominal pain
- Loss of appetite
- Nausea
- Muscular weakness
- Muscle pain
- Depression
- Personality changes
- Stupor and possibly coma
- Itching of the skin
- Blurred vision (because of cataracts)
- Bone pain or tenderness
Signs and tests
- Serum calcium is increased.
- Serum phosphorus is decreased.
- Serum alkaline phosphatase may be increased.
- Intact parathyroid hormone (PTH) in the blood is increased.
- Bone X-ray shows bone reabsorption or fractures.
- Imaging of the kidneys or ureters may show calcification or obstruction.
- Reduced bone mineral density on bone desitometry (DEXA), particularly of the forearm.
- Urinary calcium may be increased.
Treatment
Treatment depends upon the severity and cause of the condition. In primary hyperparathyroidism, mild hypercalcemia may be followed medically unless impaired renal function, bone demineralization, mental status changes or High Blood Pressure is present. Otherwise, if the calcium level is very high or symptoms are present, surgery may be necessary to take out the gland that is overproducing the hormone.
Secondary hyperparathyroidism is treated by restoring the calcium back into the normal range, usually by giving calcium and vitamin D alone or in combination, depending on the underlying disorder.
See the specific type of hyperparathyroidism.
Expectations (prognosis)
The outlook varies depending on the specific type of hyperparathyroidism.
Complications
Complications that result from excess calcium deposits within the body:
- Skeletal damage
- Urinary tract infection due to kidney stones and obstruction
- Peptic ulcer disease and pancreatitis
- Pseudogout
Calling your health care provider
Call for an appointment with your health care provider if symptoms indicate that primary hyperparathyroidism may be present.
Call your health care provider if signs of complications develop.
Prevention
Maintaining an adequate intake of calcium may reduce risk of secondary hyperparathyroidism.
by Brenda A. Kuper, M.D.
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