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Hyperparathyroidism

 
Medical Encyclopedia: Hyperparathyroidism

Definition

Parathyroid glands are four pea-sized glands located just behind the thyroid gland in the front of the neck. The function of parathyroid glands is to produce a hormone called parathyroid hormone (parathormone), which helps regulate calcium and phosphorous in the body. Hyperparathyroidism is the overproduction of this hormone.

Description

Thyroid glands and parathyroid glands, despite their similar name and proximity, are entirely separate, and each produces hormones with different functions. Hyperparathyroidism may be primary or secondary. It most often occurs in those over age 30, and most commonly in patients 50 to 60 years old. It rarely occurs in children or the elderly. Women are affected by the disease up to three times more often than men. It is estimated that 28 of every 100,000 people in the United States will develop hyperparathyroidism each year.

Normally, parathyroid glands produce the parathormone as calcium levels drop and lower to meet the demands of a growing skeleton, pregnancy, or lactation. However, when one or more parathyroid glands malfunctions, it can lead to overproduction of the hormone and elevated calcium level in the blood. Therefore, a common result of hyperparathyroidism is hypercalcemia, or an abnormally high level of calcium in the blood. Primary hyperparathyroidism occurs as a malfunction of one of the glands, usually as a result of a benign tumor, called adenoma. Secondary hyperparathyroidism occurs as the result of a metabolic abnormality outside the parathyroid glands, which causes a resistance to the function of the parathyroid hormones. Primary hyperparathyroidism is one of the most common endocrine disorders, led only by diabetes and hyperthyroidism.

— Teresa Norris



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Sci-Tech Dictionary: hyperparathyroidism
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(′hī·pər′par·ə′thī′röid′iz·əm)

(medicine) Condition caused by increased functioning of the parathyroid glands.


Dental Dictionary: hyperparathyroidism
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(hīpurper'e-thī'roid-iz-əm)
n

(generalized osteitis fibrosa cystica, von Recklinghausen’s disease of bone), 1. increased parathyroid function resulting from primary hyperplasia, a functioning neoplasm of the parathyroid glands, or secondary hyperplasia related most often to chronic renal insufficiency. Manifestations are related to abnormalities of the bones, kidneys, and blood vessels. Skeletal changes are referred to as generalized osteitis fibrosa cystica or von Recklinghausen’s disease. Brown tumors, which are essentially giant cell tumors, may develop generally, as well as in the jaws. Kidney changes include renal stones and nephrocalcinosis. Calcification of muscles in arteries occurs. Renal rickets is associated with secondary hyperparathyroidism in children with chronic renal disease. Laboratory findings include a high serum calcium level, low phosphorus level, and a normal or high alkaline phosphatase level. Renal impairment, such as occurs in secondary hyperparathyroidism, tends to nullify hypercalcemia because of an increased loss of calcium in the urine. n 2. an abnormal increase in activity of the parathyroid glands, causing loss of calcium from the bones and resulting in tenderness in bones, spontaneous fractures, muscular weakness, and osteitis fibrosa. 3. excessive production of parathormone by the parathyroid gland (as in parathyroid hyperplasia and/or adenoma), resulting in H increased renal excretion of phosphorus by lowering of the renal threshold for this substance. The pathologic changes produced are osteoporotic or osteodystrophic in nature as a consequence of withdrawal of calcium and phosphorus from osseous tissues.

Alternative Medicine Encyclopedia: Hyperparathyroidism
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Definition

Hyperparathyroidism is the overproduction by the parathyroid glands of a hormone called parathyroid hormone (parathormone). Parathyroid glands are four pea-sized glands located just behind the thyroid gland in the front of the neck. Parathyroid hormone (parathormone) helps regulate the levels of calcium and phosphorus in the body.

Description

Thyroid glands and parathyroid glands, despite their similar names and proximity, are entirely separate, and each produces hormones with different functions.

Hyperparathyroidism may be primary or secondary. It most often occurs in patients over age 30, and most commonly in patients 50 to 60 years old. It rarely occurs in children or the elderly. Women are affected by the disease up to three times more often than men. It is estimated that 28 of every 100,000 people in the United States will develop hyperparathyroidism each year.

Normally, parathyroid glands produce the parathormone as calcium levels drop and lower to meet the demands of a growing skeleton, pregnancy, or lactation. However, when one or more parathyroid glands malfunction, it can lead to overproduction of the hormone and elevated calcium level in the blood. Therefore, a common result of hyperparathyroidism is hypercalcemia, or an abnormally high level of calcium in the blood.

Primary hyperparathyroidism occurs as a malfunction of one of the glands, usually as a result of a benign tumor called an adenoma. Secondary hyperparathyroidism occurs as the result of an abnormality outside the parathyroid glands related to the body's metabolism, or chemical changes in living cells that help provide the body's energy. These changes cause a resistance to the function of the parathyroid hormones. Primary hyperparathyroidism is one of the most common endocrine disorders, led only by diabetes and hyperthyroidism.

Causes & Symptoms

Often, there are no obvious symptoms to give rise to suspicion of hyperparathyroidism, and it is first diagnosed when a patient is discovered to be hypercalcemic during a routine blood chemistry profile. Patients may believe they have been feeling fine, but realize improvements in sleep, irritability, and memory following treatment. When symptoms are present, they may include development of gastric ulcers or pancreatitis because high calcium levels can cause inflammation and pain in the linings of the stomach and pancreas.

Most of the symptoms of hyperparathyroidism are those present as a result of hypercalcemia, such as kidney stones, osteoporosis, or bone degradation resulting from the bones giving up calcium. Muscle weakness, central nervous system disturbances such as depression, psychomotor and personality disturbances, and even coma can occur. Patients also may experience heartburn, nausea, constipation, or abdominal pain. In secondary hyperparathyroidism, patients may show such signs of calcium imbalance as deformities of the long bones. Symptoms of the underlying disease also may be present.

Most commonly, hyperparathyroidism occurs as the result of a single adenoma, or benign tumor, in one of the parathyroid glands. About 90 percent of all cases of hyperparathyroidism are caused by an adenoma. The tumors seldom are cancerous. They will grow to a much larger size than the parathyroid glands, often to the size of a walnut. Genetic disorders or multiple endocrine tumors also can cause a parathyroid gland to enlarge and oversecrete hormone. In 10 percent or fewer of patients with primary hyperparathyroidism, there is enlargement of all four parathyroid glands. This condition is called parathyroid hyperplasia.

Diagnosis

Diagnosis of hyperparathyroidism most often is made when a blood test (radioimmunoassay) reveals high levels of parathyroid hormone and calcium. A blood test that specifically measures the amount of parathyroid hormone has made diagnosis simpler. Hypercalcemia is mild or intermittent in some patients, but persistent hypercalcemia is an excellent indicator of primary hyperparathyroidism. Dual energy x-ray absorptiometry (DEXA or DXA), a tool used to diagnose and measure osteoporosis, may be used once the diagnosis is made to show reduction in bone mass for primary hyperparathryroidism patients. Once a diagnosis of hyperparathyroidism is reached, the physician will probably order further tests to evaluate complications. For example, abdominal radiographs might reveal kidney stones.

For secondary hyperparathyroidism, normal or slightly decreased calcium levels in the blood and variable phosphorous levels may be visible. A patient history of familial kidney disease or convulsive disorders may suggest a diagnosis of secondary hyperparathyroidism. Other tests may reveal a disease or disorder that is causing the secondary hyperparathyroidism.

Treatment

Nutritional Therapy

Limiting intake of soft drinks can help to prevent hyperparathyroidism. Soda drinks contain high levels of phosphorus. High phosphorus intake can cause hypocalcemia that leads to secondary hyperparathyroidism. In patients with hyperparathyroidism, forcing fluids and reducing intake of calcium-rich foods can help decrease calcium levels prior to surgery or if surgery is not necessary. These patients should not take any supplements that contain calcium without a doctor's approval.

Allopathic Treatment

Hyperparathyroidism cases will usually be referred to an endocrinologist, who is a physician specializing in hormonal problems, or a nephrologist, who specializes in kidney and mineral disorders.

Patients with mild cases of hyperparathyroidism may not need immediate treatment if they have only slight elevations in blood calcium level and normal kidneys and bones. These patients should be regularly checked, probably as often as every six months, by physical examination and measurement of kidney function and calcium levels. A bone densitometry—a test to diagnose and monitor osteoporosis or thinning of bones—measurement should be performed every one or two years. After several years with no worsened symptoms, the length of time between tests may be increased.

Patients with more advanced hyperparathyroidism usually will have all or half of the affected parathyroid gland or glands surgically removed. This surgery is relatively safe and effective. The primary risks are those associated with general anesthesia. There are some instances in which the surgery can be performed with the patient under regional, or cervical (neck) block, anesthesia. Often such studies as ultrasonography—a test with high-frequency sound waves (ultrasound) that are bounced off tissues and echoes are converted to pictures called sonograms—prior to surgery help pinpoint the affected areas.

Treatment of secondary hyperparathyroidism involves removing or treating the underlying cause. In 2004, a new drug therapy was shown to lower parathyroid levels and improve calcium and phosphorus function in patients receiving dialysis (a blood-purifying treatment often performed on people with kidney diseases) who had uncontrolled secondary hyperparathyroidism. The drug, called cinacalcet, was approved by the U.S. Food and Drug Administration for people who have chronic kidney disease with secondary hyperparathyroidism.

Expected Results

Removal of the enlarged parathyroid gland or glands (parathyroidectomy) cures the disease 95 percent of the time. Relief of bone pain may occur in as few as three days. In 2004, a study showed that parathyroidectomy improved depression in patients with hyperparathyroidism. As many as 54 percent of patients who had the procedure no longer needed antidepressant medications after having the surgery. In up to five percent of patients undergoing surgery, chronically low calcium levels may result, and these patients will require calcium supplements or vitamin D treatment.

Damage to the kidneys as a result of hyperparathyroidism is often irreversible. Prognosis is generally good; however, complications of hyperparathyroidism such as osteoporosis, bone fractures, kidney stones, peptic ulcers, pancreatitis, and nervous system difficulties may worsen prognosis.

Prevention

Secondary hyperparathyroidism may be prevented by early treatment of the disease causing it. Early recognition and treatment of hyperparathyroidism may prevent hypercalcemia. Since the cause of primary hyperparathyroidism, the adenoma which causes parathyroid enlargement, is largely unknown, there are no prescribed prevention methods.

Resources

Books

Murray, Michael T. "Calcium." In Encyclopedia of Nutritional Supplements: The Essential Guide for Improving Your Health Naturally. Rocklin, CA: Prima Publishing, 1996.

Trattler, Ross. Better Health Through Natural Healing. New York, NY: McGraw-Hill Book Company, 985.

Periodicals

Allerheiligen, David A., Joe Schoeber, Robert E. Houston, Virginia K. Mohl, and Karen M. Wildman. "Hyperparathyroidism." American Family Physician 58 (April 15, 1998): 1795–1803.

"Parathyroidectomy Improves Depression in Patients with Hyperparathyroidism." Drug Week (April 23, 2003): 161.

"Positive New Data for Amgen's Sensipar for Secondary Hyperparathyroidism." Pharma Marketletter (April 12, 2004).

Taniegra, Edna D. "Hyperparathyroidism." American Family Physician (January 15, 2004): 333.

Organizations

Osteoporosis and Related Bone Diseases-National Resource-Center. 1150 17th S. NW, Ste. 500, Washington, DC 20036. (800) 624-BONE.

The Paget Foundation. 200 Varick Street, Suite 1004, New York, NY 10014-4810. (800) 23-PAGET.

Other

"Endocrine disorder and endocrine surgery." Endocrine Web. .

[Article by: Mai Tran; Teresa G. Odle]

Veterinary Dictionary: hyperparathyroidism
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Abnormally increased activity of the parathyroid gland. Primary hyperparathyroidism is associated with either neoplasia (chiefly adenomas) or hyperplasia.
An excess of parathyroid hormone leads to resorption of bone, increased resorption of calcium and increased excretion of phosphorus by the renal tubules, and increased absorption of calcium by the gastrointestinal mucosa. It may result in kidney stones and calcium deposits in the renal tubules; in generalized decalcification of bone (osteoporosis), resulting in pain and tenderness of bones and spontaneous fractures; and in hypercalcemia, leading to muscular weakness and gastrointestinal signs.
Secondary hyperparathyroidism develops as a compensatory mechanism when the serum calcium level is persistently below normal or serum phosphorus is elevated, as in chronic renal disease, insufficient calcium or excessive phosphorus in the diet, vitamin D deficiency, low-level soluble oxalate intoxication in horses, and intestinal malabsorption syndromes causing insufficient absorption of calcium and vitamin D.
See also pseudohyperparathyroidism.

  • nutritional secondary h. — a disease of horses, pigs, goats, dogs, cats, and rarely cattle. It is most commonly caused by an excessive dietary intake of phosphorus in the absence of adequate calcium, which in horses is likely to be the result of a diet mainly of grain and in dogs and cats one predominantly of meat, but it may also result from other dietary causes of secondary hyperparathyroidism. In most species there is swelling of the maxillae and mandibles which is most marked in horses, loosening of teeth, shifting lameness, and particularly in dogs and cats, weight-bearing skeletal deformities (angel wings) and folding or compression fractures. Called also miller's disease, bran disease, bighead, Siamese cat disease, paper-bone disease.
  • renal secondary h. — caused by chronic renal dysfunction, mostly in dogs, sometimes in cats, in which there is a secondary hyperparathyroidism, caused by the retention of phosphates. There is demineralization of bones, particularly the maxillae and mandibles, with loosening of teeth and facial swelling. Clinical signs are often overshadowed by the effects of the renal failure. Called also rubber jaw, renal rickets, renal osteitis fibrosa.
Word Tutor: hyperparathyroidism
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pronunciation

IN BRIEF: n. Excess of certain hormone in the body resulting in disturbance of calcium metabolism

Wikipedia: Hyperparathyroidism
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Hyperparathyroidism
Classification and external resources

Thyroid and parathyroid.
ICD-10 E21.
ICD-9 252.0
DiseasesDB 20710
MedlinePlus 001215
eMedicine emerg/265 med/3200
MeSH D006961

Hyperparathyroidism is overactivity of the parathyroid glands resulting in excess production of parathyroid hormone (PTH). The parathyroid hormone regulates calcium and phosphate levels and helps to maintain these levels. Excessive PTH secretion may be due to problems in the glands themselves, in which case it is referred to as primary hyperparathryroidism and which leads to hypercalcemia (raised calcium levels). It may also occur in response to low calcium levels, as encountered in various situations such as vitamin D deficiency or chronic kidney disease; this is referred to as secondary hyperparathyroidism. In all cases, the raised PTH levels are harmful to bone, and treatment is often needed.[1] Recent evidence suggests that Vitamin D deficiency/insufficiency plays a role in the development of hyperparathyroidism.[2]

Contents

Classification

Primary hyperparathyroidism

Primary hyperparathyroidism results from a hyperfunction of the parathyroid glands themselves. There is oversecretion of PTH due to adenoma, hyperplasia or, rarely, carcinoma of the parathyroid glands.

Secondary hyperparathyroidism

Secondary hyperparathyroidism is the reaction of the parathyroid glands to a hypocalcemia caused by something other than a parathyroid pathology, e.g. chronic renal failure.

Tertiary hyperparathyroidism

Tertiary hyperparathyroidism result from hyperplasia of the parathyroid glands and a loss of response to serum calcium levels. This disorder is most often seen in patients with chronic renal failure.

Symptoms and signs

Asymptomatic hyperparathyroidism

Many patients presenting with hyperparathyroidism will have no signs or symptoms, with diagnosis being made on further investigation after a coincidental finding of hypercalcemia. It is, however, reported that many patients will report that they feel better after treatment for hyperparathyroidism.[citation needed]

Symptomatic hyperparathyroidism

Of those patients who do present with symptoms, they are commonly associated with the effects of an increased level of calcium. Since calcium is involved in trans-synaptic communication in the nervous system, high blood calcium levels have a direct effect on the nervous system. Thus, most of the symptoms of parathyroid disease are "neurological" in origin. Common manifestations of hyperparathyroidism include weakness and fatigue, depression, aches and pains, decreased appetite, feelings of nausea and vomiting, constipation, polyuria, polydipsia, cognitive impairment, kidney stones and osteoporosis.[3] Surgical removal of a parathyroid tumor will eliminate the symptoms in most patients.

Osteoporosis

Osteoporosis associated with hyperparathyroidism is caused by the high parathyroid hormone secreted by overactive parathyroid gland(s). Excess parathyroid hormone (PTH) acts directly on osteoclasts to remove calcium from the bones. Thus, the high calcium in the blood comes from the bones. Removing the offending parathyroid gland will restore normal bone density over several years.

Laboratory tests

Serum calcium

In cases of primary hyperparathyroidism or tertiary hyperparathyroidism heightened PTH leads to increased serum calcium (hypercalcemia) due to:

  1. increased bone resorption, allowing flow of calcium from bone to blood
  2. reduced renal clearance of calcium
  3. increased intestinal calcium absorption

By contrast, in secondary hyperparathyroidism effectiveness of PTH is reduced.

Serum phosphate

In primary hyperparathyroidism, serum phosphate levels are abnormally low as a result of decreased renal tubular phosphate reabsorption. However, this is only present in about 50% of cases. This contrasts with secondary hyperparathyroidism, in which serum phosphate levels are generally elevated because of renal disease.

Alkaline phosphatase

Alkaline phosphatase levels are not elevated in all types of hyperparathyroidism. Kumar and Clark 6th edition states that alkaline phosphatase levels do not increase in primary hyperparathyroidism but may increase in secondary hyperparathyroidism.

Etiology

Primary hyperparathyroidism

  • The most common cause is a benign parathyroid adenoma that loses its sensitivity to circulating calcium levels. Usually, only one of the four parathyroid glands is affected.
  • A less common cause is from multiple endocrine neoplasia (MEN).

Secondary hyperparathyroidism

Secondary hyperparathyroidism is due to excessive secretion of parathyroid hormone (PTH) by the parathyroid glands in response to hypocalcemia (low blood calcium levels) and/or hyperphosphatemia (high blood phosphate levels), usually due to chronic renal failure. The bone disease in secondary parathyroidism along with renal failure is termed renal osteodystrophy.

Tertiary hyperparathyroidism

Tertiary hyperparathyroidism, quartary and quintary hyperparathyroidism are rare forms that are caused by long lasting disorders of the calcium feedback control system. In cases of long-standing secondary hyperparathyroidism, the hypertrophied parathyroid glands can become autonomously functioning and continue to secrete PTH independent of whether the original stimuli to secrete PTH are still present.

Diagnosis

The gold standard of diagnosis is the Parathyroid immunoassay. Once an elevated Parathyroid hormone has been confirmed, goal of diagnosis is to determine whether the hyperparathyroidism is primary or secondary in origin by obtaining a serum calcium level:

PTH serum calcium likely type
high high primary hyperparathyroidism
high low or normal secondary hyperparathyroidism

Tertiary hyperparathyroidism has a high PTH and a high serum calcium. It is differentiated from primary hyperparathyroidism by a history of chronic kidney failure and secondary hyperparathyroidism.

Treatment and monitoring

Endocrinologists diagnose diseases affecting glands and should be consulted for hyperparathyroidism. Treatment for the three different types of hyperparathyroidism vary. Generally treatment is first and foremost directed at hypercalcemia; if symptomatic, patients are sent for surgery to remove the parathyroid tumor (parathyroid adenoma) or parathyroid gland (see hypercalcemia). Most experts now believe that almost all patients with hyperparathyroidism should be evaluated for surgery. If hyperparathyroidism is caused by a tumour, it will almost always progress as the tumor grows.

Testing for hyperparathryroidism:

  • Calcium level
  • Bone density
  • Vitamin D
  • Phosphorus

Calcimimetics

A calcimimetic (cinacalcet) is a new type of drug for people with primary and secondary hyperparathyroidism on dialysis. It is recognised by the body as if it is calcium, in other words, it mimics the effect of calcium in your tissues. This tricks your body into thinking there is more calcium in the blood which reduces PTH release from parathyroid glands, leading to lower calcium and phosphorus levels in your blood. Calcimimetics control PTH release from parathyroid glands without increasing calcium and phosphorus levels. The most common side effects of calcimimetics are mild or moderate nausea and vomiting.

History

Hyperparathyroidism was first described and treated in the 1930s by Fuller Albright of Massachusetts General Hospital, working at the Mallinckrodt General Clinical Research Center. The oldest known case was found in a cadaver from an Early Neolithic cemetery in southwest Germany.[4]

See also

References

  1. ^ Fraser WD (July 2009). "Hyperparathyroidism". Lancet 374 (9684): 145–58. doi:10.1016/S0140-6736(09)60507-9. PMID 19595349. 
  2. ^ Zink AR, Panzer S, Fesq-Martin M, Burger-Heinrich E, Wahl J, Nerlich AG (2001). "Vitamin D deficiency and secondary hyperparathyroidism in the elderly: consequences for bone loss and fractures and therapeutic implications.". Endocr Rev. 22 (4): 477-501. PMID 11493580. 
  3. ^ Hyperparathyroidism. National Endocrine and Metabolic Diseases Information Service. May 2006.
  4. ^ Zink AR, Panzer S, Fesq-Martin M, Burger-Heinrich E, Wahl J, Nerlich AG (2005). "Evidence for a 7000-year-old case of primary hyperparathyroidism". JAMA 293 (1): 40–2. doi:10.1001/jama.293.1.40-c. PMID 15632333. 

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