The parathyroids are four glands in the neck that produce parathyroid hormone to help control calcium metabolism. Excessive production of this hormone caused by increased activity of these glands is known as hyperparathyroidism. When this occurs in response to low blood calcium caused by another condition, the condition is called secondary hyperparathyroidism.

Causes, incidence, and risk factors

Parathyroid hormone helps maintain blood calcium by regulating bone turnover, absorption of calcium from the gut, and excretion of calcium in the urine. Many disorders may lead to secondary hyperparathyroidism by causing hypocalcemia (low levels of calcium in the blood), disordered phosphate balance, or both. These include the following:

Bisorders of

vitamin D

osteomalacia

(

rickets )

vitamin D deficiency

vitamin D malabsorption

abnormal vitamin D metabolism induced by drugs

Disorders of phosphate metabolism

malnutrition

malabsorption

aluminum toxicity

kidney disease

cancers

phosphate depletion (may also cause osteomalacia)

Calcium deficiency

not enough calcium in the diet

too much calcium loss in the urine

Chronic renal failure

Chronic renal failure is an important cause of secondary hyperparathyroidism. The disorder is complex:

Phosphate clearance is impaired.

Phosphate is released from bone.

Vitamin D is not produced.

Intestinal calcium absorption is low.

Blood levels of calcium are lowered.

A positive feedback loop leads to increased bone resorption (bone is broken down in an attempt to regulate abnormal levels of these chemicals) and hyperphosphatemia (high levels of phosphates in the blood), which causes further secondary hyperparathyroidism. At-risk populations include children with malnutrition and elderly people with little sun exposure.

Signs and tests

Signs may include bone deformities, swollen joints, or fractures. Tests may show:

Elevated intact PTH

Low serum calcium

Abnormal

serum phosphorus levels

low if due to absorption problems

high if due to kidney failure

Elevated serum alkaline phosphatase

Variable vitamin D levels

X-rays

may show evidence of osteomalacia, fractures, or bone resorption

Low bone mineral density

Abnormal urine calcium levels

low if the problem is with absortion in the gut

high if the problem is with the kidneys

Treatment

Treatment involves correcting the underlying cause of the secondary hyperparathyroidism. Patients with vitamin D deficiency are treated with vitamin D or measures to correct malabsorption. Patients with cancer are usually treated surgically. Patients with chronic kidney failure are usually treated with calcium supplementation, phosphate restriction, and vitamin D analogs. Dialysis, kidney transplantation, or parathyroid surgery may be needed.

Expectations (prognosis)

The outcome for secondary hyperparathyroidism depends on the underlying cause. When treated, rickets generally has a good prognosis. Other causes of secondary hyperparathyroidism have variable outcomes.

Complications

"Tertiary hyperparathyroidism" may occur in some patients with kidney failure. In these cases, hypercalcemia (elevated levels of calcium) may develop with calcium supplementation, and surgery on the parathyroids may become necessary. Renal osteodystrophy is another potential complication. This is a variable syndrome comprised of osteomalacia, osteoporosis, secondary hyperparathyroidism, or osteosclerosis. Bone pain, weakness, and fractures are part of the syndrome.

Calling your health care provider

Call your health care provider if you have symptoms of this disorder, particularly if you are being treated for kidney disease.

Prevention

Early detection of rickets or vitamin D deficiency may prevent secondary hyperparathyroidism. Treatment of patients with kidney failure helps minimize secondary hyperparathyroidism.