Wikipedia: Hyperparathyroidism

Hyperparathyroidism is an increased parathyroid hormone (PTH) levels in theblood. This occurs either from the parathyroid glandsinappropriately making too much PTH (primary hyperparathyroidism) or other events triggering increased production by the parathyroid glands (secondary hyperparathyroidism). Most people with primary disease have no symptoms at the time of diagnosis. In those with symptoms the most common is kidney stones with other potential symptoms including weakness, depression, bone pains, confusion, and increased urination. Both types increase the risk ofweak bones.

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Primary hyperparathyroidism in 80% of cases is due to a single benign tumor known as a parathyroid adenoma with most of the rest of the cases due to a multiple benign tumors. Rarely it may be due to parathyroid cancer.Secondary hyperparathyroidism typically occurs due to vitamin D deficiencychronic kidney disease, or other causes oflow blood calcium.Diagnosis of primary disease is by finding a high blood calcium and high PTH levels.

Primary hyperparathyroidism may be cured by removing the adenoma or overactive parathyroid glands. In those without symptoms, mildly increased blood calcium levels, normal kidneys, and normal bone density monitoring may be all that is required. The medication cinacalcet may also be used to decrease PTH levels. In those with very high blood calcium levels treatment may include large amounts of intravenous normal saline. Low vitamin D levels should be corrected.

Primary hyperparathyroidism is the most common form.In the developed worldbetween one and four per thousand people are affected. It occurs three times more often in women than men and is typically diagnosed between the ages of 50 and 60. The disease was first described in the 1700s and in the late 1800s was determined to be related to the parathyroid. Surgery as a treatment was first carried out in 1925.

Signs and symptoms

Symptoms depend on whether the hyperparathyroidism is the result of parathyroid overactivity or secondary.

In primary hyperparathyroidism about 75% of people have no symptoms. The problem is often picked up during blood work for other reasons via a raised calcium. Many other people only have non-specific symptoms. Symptoms directly due to hypercalcemia are relatively rare, being more common in patients with malignant hypercalcemia. If present, common manifestations of hypercalcemia include weakness and fatigue, depression, bone pain, muscle soreness (myalgias), decreased appetite, feelings of nausea and vomiting,constipationpolyuria,polydipsia, cognitive impairment, kidney stones(See Foot Note) andosteoporosis. A history of acquired racquet nails(brachyonychia) may be indicative of bone resorption. Parathyroid adenomas are very rarely detectable on clinical examination. Surgical removal of a parathyroid tumor eliminates the symptoms in most patients.

In secondary hyperparathyroidism the parathyroid gland is behaving normally; clinical problems are due to bone resorption and manifest as bone syndromes such as rickets,osteomalacia and renal osteodystrophy.


Radiation exposure increases the risk of primary hyperparathyroidism. A number of genetic conditions including multiple endocrine neoplasia syndromes also increase the risk.


Normal parathyroid glands measure the ionized calcium (Ca2+) concentration in the blood and secrete parathyroid hormone accordingly: if the ionized calcium rises above normal the secretion of PTH is decreased, whereas when the Ca2+ level falls, parathyroid hormone secretion is increased.

Secondary hyperparathyroidism occurs if the calcium level is abnormally low. The normal glands respond by secreting parathyroid hormone at a persistently high rate. This typically occurs when the 1,25 dihydroxyvitamin D3 levels in the blood are low and there ishypocalcemia. A lack of 1,25 dihydroxyvitamin D3 can result from a deficient dietary intake of vitamin D, or from a lack of exposure of the skin to sunlight, so the body cannot make its own vitamin D from cholesterol. The resultinghypovitaminosis D is usually due to a partial combination of both factors. Vitamin D3 (orcholecalciferol) is converted to 25-hydroxyvitamin D (orcalcidiol) by the liver, from where it is transported via the circulation to the kidneys where it is converted into the active hormone, 1,25 dihydroxyvitamin D3.Thus a third cause of secondary hyperparathyroidism ischronic kidney disease. Here the ability to manufacture 1,25 dihydroxyvitamin D3 is compromised, resulting in hypocalcemia.



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