What is this Condition?
In hyperparathyroidism, one or more of the four parathyroid glands (pea-sized organs located behind the thyroid) are overactive, causing excessive secretion of parathyroid hormone. This results in bone loss and leads to excessive calcium and a shortage of phosphates in the blood. Consequently, the kidneys and gastrointestinal system absorb more calcium.
What Causes it?
Hyperparathyroidism may be classified as primary or secondary. In primary hyperparathyroidism, one or more of the parathyroid glands become enlarged. The most common cause is an adenoma, a type of benign tumor. Other causes include genetic disorders or multiple endocrine neoplasia (a rare disorder that causes the endocrine glands to become overactive). Primary hyperparathyroidism usually occurs between ages 30 and 50 but can also occur in children and the elderly. It affects women two to three times more often than men.
Secondary hyperparathyroidism is marked by excessive production of parathyroid hormone. This type of hyperparathyroidism results from a condition outside the parathyroid glands that decreases the level of calcium in the body. Such conditions include rickets, vitamin D deficiency, chronic kidney failure, or osteomalacia (softening of the bones).
What are its Symptoms?
Symptoms of primary hyperparathyroidism may include:
• kidney: excessive urination (one of the most common effects)
• bones and joints: chronic lower back pain and easy fracturing due to bone degeneration; bone tenderness; pain associated with calcium buildup in joints, erosion of joint surfaces, and cartilage fractures
• digestive tract: severe epigastric pain radiating to the back caused by pancreatitis; abdominal pain, appetite loss, and nausea caused by peptic ulcers
• muscles: marked muscle weakness and wasting, particularly in the legs
• nervous system: psychomotor and personality disturbances, depression, overt psychosis, stupor and, possibly, coma
• other: skin destruction, cataracts, anemia, and calcification under the skin.
In secondary hyperparathyroidism, decreased levels of calcium in the blood may produce the same features of calcium imbalance, with skeletal deformities of the long bones (rickets, for example), as well as symptoms of the underlying disease.
How is it Diagnosed?
A diagnosis of primary disease is confirmed by lab tests revealing high levels of parathyroid hormone and calcium in the blood. X-rays typically show diffuse demineralization of bones, bone cysts, outer cortical bone absorption, and subperiosteal erosion of the phalanges and distal clavicles. Microscopic examination of the bone typically shows increased bone turnover. Lab tests show elevated urine and blood calcium, chloride, and alkaline phosphatase levels and decreased blood phosphorus levels.
In secondary disease, lab findings show normal or slightly decreased serum calcium levels and variable serum phosphorus levels, especially when hyperparathyroidism is due to rickets, osteomalacia, or kidney disease. The person’s history may reveal a family history of kidney disease, seizure disorders, or drug ingestion. Other lab studies and physical exam findings identify the cause of secondary hyperparathyroidism.
How is it Treated?
Treatment varies, depending on the cause of the disease. Treatment for primary hyperparathyroidism may include surgery to remove the adenoma or, depending on the extent of hyperplasia, all but half of one parathyroid gland (necessary to maintain normal parathyroid hormone levels). Such surgery may relieve bone pain within 3 days. However, kidney damage may be irreversible.
If surgery isn’t feasible or necessary, the following treatments can decrease calcium levels:
• forcing fluids
• limiting dietary intake of calcium
• promoting sodium and calcium excretion through forced diuresis using normal saline solution, Lasix, or Edecrin
• administering sodium, potassium phosphate, calcitonin, Mithracin, or biphosphonates.
Treatment of secondary hyperparathyroidism must correct the underlying cause. It consists of vitamin D therapy or, in the person with kidney disease, administration of an oral calcium preparation for hyperphosphatemia. In the person with kidney failure, dialysis is necessary to lower calcium levels and may have to continue for life. In the person with chronic secondary hyperparathyroidism, the enlarged glands may not revert to normal size and function even after calcium levels have been controlled.
What can a Person with Hyperparathyroidism do?
Be sure to receive periodic medical follow-up through lab tests. If your condition wasn’t corrected surgically, make sure you avoid calcium-containing antacids and thiazide diuretics (such as Diuril).