Hyperparathyroidism is the overproduction by the parathyroid glands of a hormone called parathyroid hormone (parathormone). Parathyroid glands are four pea-sized glands located just behind the thyroid gland in the front of the neck. Parathyroid hormone (parathormone) helps regulate the levels of calcium and phosphorus in the body.
Thyroid glands and parathyroid glands, despite their similar names and proximity, are entirely separate, and each produces hormones with different functions.
Hyperparathyroidism may be primary or secondary. It most often occurs in patients over age 30, and most commonly in patients 50 to 60 years old. It rarely occurs in children or the elderly. Women are affected by the disease
up to three times more often than men. It is estimated that 28 of every 100,000 people in the United States will develop hyperparathyroidism each year.
Normally, parathyroid glands produce the parathormone as calcium levels drop and lower to meet the demands of a growing skeleton, pregnancy, or lactation. However, when one or more parathyroid glands malfunction, it can lead to overproduction of the hormone and elevated calcium level in the blood. Therefore, a common result of hyperparathyroidism is hypercalcemia, or an abnormally high level of calcium in the blood.
Primary hyperparathyroidism occurs as a malfunction of one of the glands, usually as a result of a benign tumor called an adenoma. Secondary hyperparathyroidism occurs as the result of an abnormality outside the parathyroid glands related to the body's metabolism, or chemical changes in living cells that help provide the body's energy. These changes cause a resistance to the function of the parathyroid hormones. Primary hyperparathyroidism is one of the most common endocrine disorders, led only by diabetes and hyperthyroidism.
Causes & symptoms
Often, there are no obvious symptoms to give rise to suspicion of hyperparathyroidism, and it is first diagnosed when a patient is discovered to be hypercalcemic during a routine blood chemistry profile. Patients may believe they have been feeling fine, but realize improvements in sleep, irritability, and memory following treatment. When symptoms are present, they may include development of gastric ulcers or pancreatitis because high calcium levels can cause inflammation and pain in the linings of the stomach and pancreas.
Most of the symptoms of hyperparathyroidism are those present as a result of hypercalcemia, such as kidney stones, osteoporosis, or bone degradation resulting from the bones giving up calcium. Muscle weakness, central nervous system disturbances such as depression, psychomotor and personality disturbances, and even coma can occur. Patients also may experience heartburn, nausea, constipation, or abdominal pain. In secondary hyperparathyroidism, patients may show such signs of calcium imbalance as deformities of the long bones. Symptoms of the underlying disease also may be present.
Most commonly, hyperparathyroidism occurs as the result of a single adenoma, or benign tumor, in one of the parathyroid glands. About 90 percent of all cases of hyperparathyroidism are caused by an adenoma. The tumors seldom are cancerous. They will grow to a much larger size than the parathyroid glands, often to the size of a walnut. Genetic disorders or multiple endocrine tumors also can cause a parathyroid gland to enlarge and oversecrete hormone. In 10 percent or fewer of patients with primary hyperparathyroidism, there is enlargement of all four parathyroid glands. This condition is called parathyroid hyperplasia.
Diagnosis of hyperparathyroidism most often is made when a blood test (radioimmunoassay) reveals high levels of parathyroid hormone and calcium. A blood test that specifically measures the amount of parathyroid hormone has made diagnosis simpler. Hypercalcemia is mild or intermittent in some patients, but persistent hypercalcemia is an excellent indicator of primary hyperparathyroidism. Dual energy x-ray absorptiometry (DEXA or DXA), a tool used to diagnose and measure osteoporosis, may be used once the diagnosis is made to show reduction in bone mass for primary hyperparathryroidism patients. Once a diagnosis of hyperparathyroidism is reached, the physician will probably order further
For secondary hyperparathyroidism, normal or slightly decreased calcium levels in the blood and variable phosphorous levels may be visible. A patient history of familial kidney disease or convulsive disorders may suggest a diagnosis of secondary hyperparathyroidism. Other tests may reveal a disease or disorder that is causing the secondary hyperparathyroidism.
Limiting intake of soft drinks can help to prevent hyperparathyroidism. Soda drinks contain high levels of phosphorus. High phosphorus intake can cause hypocalcemia that leads to secondary hyperparathyroidism. In patients with hyperparathyroidism, forcing fluids and reducing intake of calcium-rich foods can help decrease calcium levels prior to surgery or if surgery is not necessary. These patients should not take any supplements that contain calcium without a doctor's approval.
Hyperparathyroidism cases will usually be referred to an endocrinologist, who is a physician specializing in hormonal problems, or a nephrologist, who specializes in kidney and mineral disorders.
Patients with mild cases of hyperparathyroidism may not need immediate treatment if they have only slight elevations in blood calcium level and normal kidneys and bones. These patients should be regularly checked, probably as often as every six months, by physical examination and measurement of kidney function and calcium levels. A bone densitometry—a test to diagnose and monitor osteoporosis or thinning of bones—measurement should be performed every one or two years. After several years with no worsened symptoms, the length of time between tests may be increased.
Patients with more advanced hyperparathyroidism usually will have all or half of the affected parathyroid gland or glands surgically removed. This surgery is relatively safe and effective. The primary risks are those associated with general anesthesia. There are some instances in which the surgery can be performed with the patient under regional, or cervical (neck) block, anesthesia. Often such studies as ultrasonography—a test with high-frequency sound waves (ultrasound) that are bounced off tissues and echoes are converted to pictures called sonograms—prior to surgery help pinpoint the affected areas.
Treatment of secondary hyperparathyroidism involves removing or treating the underlying cause. In 2004, a new drug therapy was shown to lower parathyroid levels and improve calcium and phosphorus function in patients receiving dialysis (a blood-purifying treatment often performed on people with kidney diseases) who had uncontrolled secondary hyperparathyroidism. The drug, called cinacalcet, was approved by the U.S. Food and Drug Administration for people who have chronic kidney disease with secondary hyperparathyroidism.
Removal of the enlarged parathyroid gland or glands (parathyroidectomy) cures the disease 95 percent of the time. Relief of bone pain may occur in as few as three days. In 2004, a study showed that parathyroidectomy improved depression in patients with hyperparathyroidism. As many as 54 percent of patients who had the procedure no longer needed antidepressant medications after having the surgery. In up to five percent of patients undergoing surgery, chronically low calcium levels may result, and these patients will require calcium supplements or vitamin D treatment.
Damage to the kidneys as a result of hyperparathyroidism is often irreversible. Prognosis is generally good; however, complications of hyperparathyroidism such as osteoporosis, bone fractures, kidney stones, peptic ulcers, pancreatitis, and nervous system difficulties may worsen prognosis.
Secondary hyperparathyroidism may be prevented by early treatment of the disease causing it. Early recognition and treatment of hyperparathyroidism may prevent hypercalcemia. Since the cause of primary hyperparathyroidism, the adenoma which causes parathyroid enlargement, is largely unknown, there are no prescribed prevention methods.
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Teresa G. Odle