Secondary hyperparathyroidism

Definition

Secondary hyperparathyroidism is when the parathyroid glands in your neck produce too much parathyroid hormone (PTH) because your calcium levels are too low.

See also:

• Hyperparathyroidism
• Primary hyperparathyroidism

Alternative Names

Hyperparathyroidism - secondary

Causes, incidence, and risk factors

The parathyroid glands help control calcium use and removal by the body. They do this by producing parathyroid hormone, or PTH. PTH helps control calcium, phosphorus, and vitamin D levels within the blood and bone.

When calcium levels are too low, the body responds by increasing production of parathyroid hormone. This increase in parathyroid hormone causes more calcium to be taken from the bone and more calcium to be reabsorbed by the intestines and kidney.

Medical conditions that cause low blood calcium levels or interfere with the body's ability to break down and remove phosphate can lead to secondary hyperparathyroidism. Too much phosphate causes changes in calcium levels.

Kidney failure is a common cause of secondary hyperparathyroidism. Kidney failure can interfere with the body's ability to remove phosphate.

Other causes of secondary hyperparathyroidism may include:

• Calcium deficiency
  • Not enough calcium in the diet
  • Too much calcium loss in the urine
• Conditions that make it hard for the body to breakdown phosphate, including:
  • Aluminum poisoning
  • Certain types of cancer
  • Kidney disease
  • Malnutrition
  • Malabsorption
• Vitamin D disorders (often seen in children with malnutrition and older adults who do not get enough sunlight):
  • Problems absorbing vitamin D into the body (malabsorption)
  • Problems breaking down vitamin D (due to the use of certain drugs)
  • Rickets
  • Too little vitamin D (deficiency)

Symptoms

General symptoms may include:

• Bone deformities
• Broken bones (fractures)
• Swollen joints

Other symptoms relate to the underlying cause of secondary hyperparathyroidism. See the specific article for symptom information:

• Chronic kidney failure
• Malabsorption
• Rickets

Signs and tests

Blood tests will be done to check calcium, phosphorus, and PTH levels. A urine test is done to determine how much calcium is being removed from the body.

Phosphorus levels will be low if you have absorption problems, and high if you have kidney failure.

Bone x-rays and a bone density test can help detect fractures, bone loss, and bone softening.

Treatment

Correcting the calcium level and the underlying problem can bring the PTH levels back to normal.

Treatment may involve:

• A special form of vitamin D (requires a doctor's prescription) if you have low vitamin D levels
• Surgery for cancer

Patients with chronic kidney failure are usually given calcium and vitamin D, and are told to avoid phosphate in their diet. Dialysis, a kidney transplant, or parathyroid surgery may be needed.

Expectations (prognosis)

The outcome depends on the underlying cause.

Complications

Persons with kidney problems may continue to produce too much parathyroid hormone even when their calcium level is back to normal. This is called "tertiary hyperthyroidism." Parathyroid surgery may be needed.

Other complications include:

• Increased risk of broken bones
• Renal osteodystrophy (a condition that causes bone pain, weakness, and fractures)

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 diagnosis and treatment of rickets or vitamin D deficiency may prevent this condition. Proper treatment of kidney failure helps reduce symptoms of secondary hyperparathyroidism.

References

Wysolmerski JJ. Insogna KL. The Parathyroid Glands, Hypercalcemia, and Hypocalcemia. In: Kronenberg HM, Schlomo M, Polansky KS, Larsen PR, eds. Williams Textbook of Endocrinology. 11th ed. St. Louis, Mo: WB Saunders; 2008: chap. 266.

Bringhurst FR, Demay MB, Kronenberg HM. Disorders of Mineral Metabolism. In: Kronenberg HM, Schlomo M, Polansky KS, Larsen PR, eds. Williams Textbook of Endocrinology. 11th ed. St. Louis, Mo: WB Saunders; 2008: chap. 27.