The parathyroids are four glands in the neck that produce parathyroid hormone to help control calcium metabolism.

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.

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
• 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 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.

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

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

Treatment of patients with kidney failure helps minimize secondary hyperparathyroidism.