Hyperparathyroidism

Hyperparathyroidism is caused by overactive parathyroid glands. Overactive parathyroid glands produce too much parathyroid hormones, which in turn stimulate increased levels of calcium in the blood stream.

The excess calcium released by the bones leads to osteoporosis and osteomalacia (both bone-weakening diseases). Other results of hyperparathyroidism are kidney stones, because of high levels of calcium excreted into the urine by the kidneys.

Primary hyperparathyroidism is now commonly diagnosed by elevated calcium levels found on laboratory profiles in asymptomatic patients. It affects women two to three times more frequently than men.

Causes

Hyperparathyroidism may be primary or secondary:

• In primary hyperparathyroidism, one or more of the parathyroid glands enlarges, increasing PTH secretion and elevating serum calcium levels. The most common cause is a single adenoma. Primary hyperparathyroidism is also a component of multiple endocrine neoplasia, in which all four glands are usually involved.
• In secondary hyperparathyroidism, excessive compensatory production of PTH stems from a hypocalcemia-producing abnormality outside the parathyroid gland, such as rickets, vitamin D deficiency, chronic renal failure, and osteomalacia due to phenytoin (Dilantin).

Signs and symptoms

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.

When symptoms do appear, they are often mild and nonspecific, such as a feeling of weakness and fatigue, depression, or aches and pains. With more severe disease, a person may have a loss of appetite, nausea, vomiting, constipation, confusion or impaired thinking and memory, and increased thirst and urination. Patients may have thinning of the bones without symptoms, but with risk of fractures. Increased calcium and phosphorous excretion in the urine may cause kidney stones. Patients with hyperparathyroidism may be more likely to develop peptic ulcers, high blood pressure, and pancreatitis.

Diagnosis

Findings differ in primary and secondary disease.

Primary disease

In primary disease, a high concentration of serum PTH on radioimmunoassay with accompanying hypercalcemia confirms the diagnosis. In addition, X-rays 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 with such tests as X-ray spectrophotometry typically demonstrates increased bone turnover. Laboratory tests reveal elevated urine and serum calcium, chloride, and alkaline phosphatase levels and decreased serum phosphorus levels.

Hyperparathyroidism may also raise uric acid and creatinine levels and increase basal acid secretion and serum immunoreactive gastrin. Increased serum amylase levels may indicate acute pancreatitis.

Secondary disease

For secondary hyperparathyroidism, normal or slightly decreased calcium levels in the blood and variable phosphorous levels may be visible. Patient history of familial kidney disease or convulsive disorders may suggest a diagnosis of secondary hyperparathyroidism. Other tests may reveal a disease or disorder, which is causing the secondary hyperparathyroidism.

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.

In cases of secondary hyperparathyroidism, the first goal is to treat the underlying problem. For many adults, that problem is chronic kidney failure. But because treatments for kidney failure won't cure hyperparathyroidism, doctors have traditionally used vitamin D replacement therapies to reduce the production of PTH. Although effective, this can lead to excessively high levels of both calcium and phosphorus in people undergoing dialysis. Now it appears that the drug cinacalcet (Sensipar) may reduce PTH levels without these side effects.

Prevention

Maintaining an adequate intake of calcium may reduce risk of secondary hyperparathyroidism. Early recognition and treatment of hyperparathyroidism may prevent hypercalcemia. Since the cause of primary hyperparathyroidism, or the adenoma which causes parathyroid enlargement, is largely unknown, there are not prescribed prevention methods.