Most people with primary hyperparathyroidism have one or more enlarged, overactive parathyroid glands that secrete too much parathyroid hormone. In secondary hyperparathyroidism, a problem such as kidney failure makes the body resistant to the action of parathyroid hormone. Here we deal mainly with primary hyperparathyroidism, which develops in about 100,000 people in the U.S. each year.
The parathyroid glands are normally located on the thyroid gland in the neck. Occasionally, a person is born with one or more of the parathyroid glands embedded in the thyroid, the thymus, or somewhere in the chest. In most such cases, however, the glands function normally.
Although their names are similar, the thyroid and parathyroid glands are entirely separate glands, each producing distinct hormones with specific functions. The parathyroid glands secrete parathyroid hormone (PTH), a substance that helps maintain the correct balance of calcium and phosphorous in the body. PTH regulates release of the calcium from bone, absorption of calcium in the intestine, and excretion of calcium in the urine. When the amount of calcium in the blood falls too low, the parathyroid glands secrete just enough PTH to restore the balance.
If the glands secrete too much hormone, as in hyperparathyroidism, the balance is disrupted: blood calcium rises. This condition, called hypercalcemia, is what usually signals the doctor that something may be wrong with the parathyroid glands. In 85% of people with this disorder, a benign tumor (adenoma) has formed on one of the parathyroid glands, causing it to become overactive. In most other cases, the excess hormone comes from two or more enlarged parathyroid glands, a condition called hyperplasia. Very rarely, hyperparathyroidism is caused by cancer of a parathyroid gland.
Excess PTH triggers the release of too much calcium into the bloodstream. The bones may lose calcium, and too much calcium may be absorbed from food. The levels of calcium may increase in the urine, causing kidney stones. PTH also acts to lower blood phosphorous levels by increasing excretion of phosphorus in the urine.
In most cases the cause is unknown, occurring in people with no family history of the disorder. Only about 3-5% of cases can be linked to an inherited problem. Familial endocrine neoplasia type I is one rare inherited syndrome that affects the parathyroids as well as the pancreas and the pituitary gland. Another rare genetic disorder, familial hypocalciuric hypercalcemia, is sometimes confused with typical hyperparathyroidism.
A person with hyperparathyroidism may have severe symptoms, subtle ones, or none at all. Increasingly, routine blood tests that screen for a wide range of conditions including high calcium levels are alerting doctors to people who, though symptom-free, have mild forms of the disorder.
Hyperparathyroidism is diagnosed when tests show that blood levels of calcium as well as parathyroid hormone are too high. Other diseases can cause high blood calcium levels, but only in hyperparathyroidism is the elevated calcium the result of too much parathyroid hormone. A blood test that accurately measures the amount of parathyroid hormone has simplified the diagnosis of hyperparathyroidism.
Once the diagnosis is established, other tests may be done to assess complications. Because high PTH levels can cause bones to weaken from calcium loss, a measurement of bone density may be done to assess bone loss and the risk of fractures. Abdominal radiographs may reveal the presence of kidney stones and a 24-hour urine collection may provide information on kidney damage and the risk of stone formation.
Some patients who have mild disease may not need immediate treatment, according to a panel of experts convened by the National Institutes of Health in 1990. Patients who are symptom-free, whose blood calcium is only slightly elevated, and whose kidneys and bones are normal, may wish to discuss long-term monitoring. In the panel's recommendation, monitoring would consist of clinical evaluation and measurement of calcium levels and kidney function every 6 months, annual abdominal X-ray, and bone mass measurement after 1 to 2 years. If the disease shows no signs of worsening after 1 to 3 years, the interval between exams may be lengthened. Immobilization and gastrointestinal illness with vomiting or diarrhea can cause calcium levels to rise, and if these conditions develop, patients with hyperparathyroidism should seek medical attention.
The prognosis is excellent for persons with primary hyperparathyroidism who have no symptoms, as well as those who have surgery to remove one or more parathyroid glands.
Possible complications include skeletal damage, urinary tract infections, kidney damage or kidney stones, peptic ulcers, inflammation of the pancreas, high blood pressure, nervous system disorders, and rare complications from surgery.
A person with primary hyperparathyroidism who also has borderline nutritional status may develop deficiencies in the following substances that are necessary for normal bone formation: Vitamin C, Vitamin K, Manganese.
Patients may have thinning of the bones without symptoms, but with risk of fractures.
Patients may have thinning of the bones without symptoms, but with increased risk of fractures.
Horsetail is rich in minerals and has been used in traditional remedies to support normal bone integrity.
Oat straw is rich in minerals and has been used in traditional remedies to support normal bone integrity.
Ginkgo biloba extract contains substances similar to isoflavone in soy, raising the theoretical possibility that this herb may also have some degree of bone protection; studies regarding this potential use had not been conducted at time of writing.
Black cohosh is reported to have estrogen-like effects and may enhance estrogen's role in the body, such as reducing the breakdown of bone; more research is needed to determine the value of this use.
If the patient and doctor choose long-term follow-up over surgery, the patient should try to drink lots of water, get plenty of exercise, and avoid certain diuretics, such as the thiazides.
Surgery to remove the enlarged gland (or glands) is the only treatment for the disorder and cures it in 95% of cases when performed by surgeons experienced with this condition. About 1% of patients undergoing surgery have damage to the nerves controlling the vocal cords, which can affect speech. Some 1-5% develop chronic low calcium levels, which may require treatment with calcium and/or vitamin D. The complication rate is slightly higher for hyperplasia than it is for adenoma since more extensive surgery is needed.
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