The parathyroids are four glands in the neck that produce parathyroid hormone (PTH) to help control calcium use by the body.

Too much production of PTH caused by increased activity of these glands is known as hyperparathyroidism. When this occurs in response to low blood calcium that is caused by another condition, the hyperparathyroidism condition is called secondary hyperparathyroidism.

Parathyroid hormone helps maintain blood calcium by regulating bone turnover, absorption of calcium from the gut, and release of calcium in the urine.

Many disorders may lead to secondary hyperparathyroidism by causing hypocalcemia (low levels of calcium in the blood), a phosphate imbalance, or both. These include the following:

• Disorders of vitamin D
  • Rickets (osteomalacia)
  • Vitamin D deficiency
  • Vitamin D malabsorption
  • Abnormal vitamin D metabolism, induced by drugs

At-risk populations include children with malnutrition and elderly people with little sun exposure.

• Disorders of phosphate metabolism
  • Malnutrition
  • Malabsorption
  • Aluminum toxicity
  • Kidney disease
  • Some types of cancer
  • 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:

• Not enough phosphate is cleared from the body.
• Phosphate is released from bone.
• Vitamin D is not produced.
• Absorption of calcium in the gut is low.
• Blood levels of calcium are lowered.

Bone is broken down in an attempt to regulate abnormal levels of the above chemicals, and the high levels of phosphates in the blood rise higher. These conditions cause further secondary hyperparathyroidism.

Symptoms generally relate to the underlying cause of secondary hyperparathyroidism.

In children, rickets may cause the following:

• Weakness
• Poor growth
• Bowed limbs
• Swollen joints
• Bone pain and fractures
• Delayed tooth development

Patients with kidney failure may have osteomalacia, osteoporosis, or both. Bone pain or fractures may occur.

Symptoms of malabsorption (such as diarrhea) or of an underlying cancer may occur in patients with those disorders.

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 (breakdown)
• Low bone mineral density
• Abnormal urine calcium levels
  • Low -- if the problem is with absorption in the gut
  • High -- if the problem is with the kidneys

Treatment involves correcting the underlying cause of the secondary hyperparathyroidism.

Patients with vitamin D deficiency are treated with vitamin D, or with other 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.

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.

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 comprising osteomalacia, osteoporosis, secondary hyperparathyroidism, or osteosclerosis. Bone pain, weakness, and fractures are part of the syndrome.

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

Early detection of rickets or vitamin D deficiency may prevent secondary hyperparathyroidism.

Treatment of patients with kidney failure helps minimize secondary hyperparathyroidism.