Hyperparathyroidism

(Overactive Parathyroid)

by Krisha McCoy, MS

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Definition | Causes | Risk Factors | Symptoms | Diagnosis | Treatment | Prevention

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Definition

The parathyroid glands are four small glands in the neck. They make parathyroid hormone (PTH). PTH raises the level of calcium in the blood.

In hyperparathyroidism too much PTH is secreted. This causes high levels of calcium in the blood. High calcium is known as hypercalcemia. The condition is classified as being:

• Primary hyperparathyroidism—most common form, a benign tumor of the parathyroid gland makes too much PTH on its own
• Secondary hyperparathyroidism—occurs in patients with long-standing kidney failure or a vitamin D deficient state (very common)
• Tertiary hyperparathyroidism—also occurs in patients with very long-standing kidney failure, very often on dialysis

 

Causes

In most cases, the exact cause is not known. Factors that may contribute to hyperparathyroidism include:

• Adenoma (benign tumor) in the parathyroid gland (accounting for 85% of primary hyperparathyroidism)
• Vitamin D deficiency (due to inadequate dietary intake, lack of sunlight exposure, or malabsorption, like celiac disease)
• Hyperplasia (enlargement) of the parathyroid glands (accounting for over 80% of secondary or tertiary hyperparathyroidism)
• Kidney failure or other medical problems that make the body resistant to the action of the parathyroid hormone (called secondary hyperparathyroidism)
• Familial hyperparathyroidism
• Radiation therapy to head or neck during childhood
• Multiple endocrine neoplasia (MEN)
• Parathyroid cancer (very rare)

 

Risk Factors

The following factors increase your chance of developing hyperparathyroidism:

• Sex: female (hyperparathyroidism is three times more common in women, especially after menopause)
• Age: older than 60 years
• Multiple endocrine neoplasia (an inherited disorder that affects the endocrine glands)
• Genetics that make you more likely to have hyperparathyroidism

 

Symptoms

If you experience any of these, do not assume it is due to this condition. The symptoms may be caused by other health conditions. If you have any one of them, see your doctor.

The degree of hypercalcemia, as well as the disease progress, will determine the symptoms. Your blood level of calcium must be elevated to have most cases of hyperparathyroidism. Symptoms commonly seen with primary hyperparathyroidism include the following:

• Constipation
• Nausea
• Vomiting
• Abdominal pain
• Headache
• Loss of appetite
• Thirst
• Frequent and sometimes painful urination due to kidney stones
• Lethargy
• Fatigue
• Muscle weakness
• Joint pain
• Memory loss
• Depression
• Heartburn
• Back pain

 

Diagnosis

Your doctor will ask about your symptoms and medical history. A physical exam will be done. You may be referred to a specialist. An endocrinologist is a specialist that focuses on hormones.

Tests may include the following:

• Blood tests—to measure calcium, phosphorus, magnesium, alkaline phosphatase, vitamin D, and PTH, kidney and liver function tests
• Urine test—a 24-hour urine collection to measure calcium excretion and kidney function (very important test)
• Abdominal x-ray—a test that uses radiation to take a picture of the structures inside the body; can show kidney stones caused by high calcium levels
• Bone density test—a test to measure bone loss and risk of fractures
• Neck ultrasound—a test that uses sound waves, no radiation, to detect a large parathyroid tumor (adenoma)
• Technetium 99m sestamibi scan—a nuclear medicine test that uses safe nuclear molecultes to make pictures of the parathyroid glands to help locate a single parathyroid adenoma in primary hyperparathyroidism

 

Treatment

Talk with your doctor about the best plan for you. Depending on the type of hyperparathyroidism treatment options include the following:

• Primary hyperparathyroidism—surgery is curative, medicine is not indicated and will generally not help
• Secondary hyperaparthyroidism—if due to vitamin D deficiency:
  • Ergocalciferol (vitamin D2) or cholecalciferol (vitamin D3)—for treating secondary hyperparathyroidism due to deficiency of vitamin D.
  • Calcitriol (the most active vitamin D metabolite)—helps to reduce PTH production in secondary hyperparathyroidism in chronic kidney failure
  • Cinacalcet—helps to lower PTH blood levels for secondary and tertiary hyperparathyroidism in chronic kidney disease

 

Prevention

There are no guidelines for preventing this condition.

 RESOURCES:

American Association of Clinical Endocrinologists
http://www.aace.com/

The Hormone Foundation
http://www.hormone.org/

National Institute of Diabetes and Digestive and Kidney Disorders
http://www2.niddk.nih.gov/

 CANADIAN RESOURCES:

Canada Health Portal
http://chp-pcs.gc.ca/CHP/

Canadian Society of Endocrinology and Metabolism
http://www.endo-metab.ca/

REFERENCES:

Bilezikian JP, Khan AA, Potts JT Jr on behalf of the Third International Workshop on the Management of Asymptomatic Primary Hyperthyroidism. Guidelines for the Management of Asymptomatic Primary Hyperparathyroidism: Summary Statement from the Third International Workshop. J Clin Endocrinol Metab. 2009;94:335-339.

Cannella G, Messa P. Therapy of secondary hyperparathyroidism to date: vitamin d analogs, calcimimetics or both? J Nephrol . 2006;19:399-402.

Clark OH. How should patients with primary hyperparathyroidism be treated? (Editorial). J Clin Endocrinol Metab . 2003;88:3011-3014.

Hyperparathyroidism. National Institute of Diabetes and Digestive and Kidney Disorders website. Available at: http://www.niddk.nih.gov/health/endo/pubs/hyper/hyper.htm .

Messa P, Macario F, Yaqoob M, et al. The OPTIMA study: assessing a new cinacalcet (Sensipar/Mimpara) treatment algorithm for secondary hyperparathyroidism. Clin J Am Soc Nephrol. 2008;3:36-45.

Silverberg SJ, Bilezikian JP. The diagnosis and management of asymptomatic primary hyperparathyroidism. Nat Clin Pract Endocrinol Metab . 2006;2:494-503.

Taniegra ED. Hyperparathyroidism. Am Fam Physician . 2004; 69:333-340.

Torpy JM. Glass RM, ed. Hyperparathyroidism. JAMA . 2005;293(14).

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Last reviewed January 2010 by B. Gabriel Smolarz, MD
Last Updated: 1/14/2010