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Hyperparathyroidism EDNA D Hyperparathyroidism EDNA D. TANIEGRA, M.D., University of Arkansas for Medical Sciences, Little Rock, Arkansas Primary hyperparathyroidism is the most frequent cause of hypercalcemia in ambula- tory patients. The condition is most common in postmenopausal women, although it O A patient informa- can occur in persons of all ages, including pregnant women. If symptoms are present, tion handout on hyperparathyroidism, they are attributable to hypercalcemia and may include weakness, easy fatigability, written by the author anorexia, or anxiety. However, most persons have no symptoms, and primary hyper- of this article, is pro- parathyroidism usually is diagnosed after an elevated serum calcium level is found vided on page 340. incidentally on multiphasic chemistry panel testing. Persistent hypercalcemia and an elevated serum parathyroid hormone level are the diagnostic criteria for primary hyperparathyroidism. Other causes of hypercalcemia are rare, and usually are associ- ated with low (or sometimes normal) parathyroid hormone levels. Malignancy is the most frequent cause of hypercalcemia in hospitalized patients. Parathyroidectomy is the definitive treatment for primary hyperparathyroidism. When performed by expe- rienced endocrine surgeons, the procedure has success rates of 90 to 95 percent and a low rate of complications. Asymptomatic patients who decline surgery and meet cri- teria for medical management must commit to conscientious long-term monitoring. Any unexplained elevation of the serum calcium level should be evaluated promptly to prevent complications from hypercalcemia. (Am Fam Physician 2004;69:333-9,340. Copyright© 2004 American Academy of Family Physicians.) rimary hyperparathyroidism is the facilitate determination of etiologic factors in most common cause of hypercal- almost all patients with hypercalcemia.1 cemia in the outpatient setting.1 Most persons with this condition Parathyroid Glands are asymptomatic. However, rec- The four parathyroid glands normally are Pognition of primary hyperparathyroidism has located behind the four poles of the thyroid increased dramatically since the introduction gland. The glands secrete parathyroid hor- of multichannel autoanalyzers in the 1970s.2 mone (PTH), which is the primary regulator The disorder can occur in persons of any age of calcium homeostasis.4 The glands tightly but is more common in persons older than regulate the extracellular calcium concentra- 50 years.1 In the United States, its estimated tion within a narrow normal range. incidence in persons older than 65 years is one The parathyroid glands respond within case per 1,000 in men and two to three cases seconds to a low or falling serum calcium per 1,000 in women.1,3 concentration (Figure 1).The chiefcells of Classic primary hyperparathyroidism with these glands can synthesize, process, and store overt complications of osteitis fibrosa cystica, PTH in a regulated manner and can replicate nephrolithiasis, and nephrocalcinosis is rare.1,2 when chronically stimulated. These factors Primary hyperparathyroidism usually is easily allow for short-, intermediate-, and long- distinguishable from malignancy, which is the term adaptability to fluctuations in the serum 4,5 See page 249 for defi- second most common cause of hypercal- calcium level. nitions of strength-of- cemia. Laboratory measurements of the medi- PTH is an 84–amino-acid single-chain pep- evidence levels. ators of calcium metabolism are reliable and tide that mobilizes calcium from the bones by osteoclastic stimulation. It also stimulates the kidneys to reabsorb calcium and convert Most persons with primary hyperparathyroidism are 25-hydroxyvitamin D3 (produced in the liver) to the active form, 1,25-dihydroxyvitamin D asymptomatic. 3 which, in turn, stimulates gastrointestinal absorption of calcium. Low circulating con- Downloaded from the American Family Physician Web site at www.aafp.org/afp. Copyright© 2004 American Academy of Family Physicians. For the private, noncommercial use of one individual user of the Web site. All other rights reserved. Parathyroid glands Serum Ca2+ 1,25-dihydroxyvitamin D3 PTH PTH Bone resorption GI Ca2+ Renal Ca2+ absorption reabsorption Ca2+ Ca2+ Ca2+ Serum Ca2+ ILLUSTRATION BY MARCIA HARTSOCK FIGURE 1. Parathyroid gland action. Low circulating serum calcium (Ca2+) concentrations stimulate the parathyroid glands to secrete parathyroid hormone (PTH), which mobilizes calcium from bones by osteoclastic stimulation. PTH also stimu- lates the kidneys to reabsorb calcium and to convert 25-hydroxyvitamin D3 (produced in the liver) to the active form, 1,25-dihydroxyvitamin D3, which stimulates gastrointestinal calcium absorption. High serum calcium concentrations have a negative feedback effect on PTH secretion. (GI = gastrointestinal) centrations of calcium stimulate PTH secretion, and high postmenopausal women. The incidence of the condition circulating concentrations of calcium depress PTH secre- increases with age, and the average age at diagnosis is tion. PTH is metabolized rapidly in the liver and kidneys; its 55 years. A small percentage of patients presents years circulating half-life is approximately two to five minutes.5 after external neck irradiation. Lithium therapy also can be responsible for overactive parathyroid glands, with the Etiology and Pathogenesis excess activity persisting even after discontinuation of PRIMARY HYPERPARATHYROIDISM the drug.1 Primary hyperparathyroidism is caused by the inappro- In 10 to 20 percent of patients, primary hyperparathy- priate secretion of PTH, which results in hypercalcemia. The roidism is caused by an inherited hyperfunction of multiple condition usually occurs sporadically, although familial parathyroid glands. These patients tend to be diagnosed at forms are well recognized.4 a younger age.1 In 85 percent of patients with primary hyperparathy- Although rare, familial disorders should be considered roidism, the underlying cause is an adenoma in a single in patients diagnosed with primary hyperparathyroidism. parathyroid gland.1 Hypertrophy of all four parathyroid With several of these familial disorders, patients should be glands and multiple adenomas within the parathyroid evaluated for significant associated abnormalities. Famil- glands account for the remainder of cases. Fewer than 0.5 ial forms of primary hyperparathyroidism include multi- percent of cases are caused by parathyroid malignancies.1 ple endocrine neoplasia type I and type II, neonatal severe Most patients with primary hyperparathyroidism are primary hyperparathyroidism, hyperparathyroidism–jaw 334 AMERICAN FAMILY PHYSICIAN www.aafp.org/afp VOLUME 69, NUMBER 2 / JANUARY 15, 2004 Hyperparathyroidism tumor syndrome, familial hypocalciuric hypercalcemia, and familial isolated hyperparathyroidism.6 In 85 percent of patients with primary hyperpara- Approximately 95 percent of patients with multiple thyroidism, the underlying cause is an adenoma endocrine neoplasia type I, or Werner’s syndrome, have in a single parathyroid gland. associated primary hyperparathyroidism.1,6,7 This syn- drome is associated with various tumors, including pan- creatic and pituitary adenomas.6,7 Patients with multiple endocrine neoplasia type II, or Sipple’s syndrome, may longed hypocalcemia (usually secondary to chronic renal develop a milder form of primary hyperparathy- failure) that causes parathyroid gland hyperplasia. roidism.1,6,7 This syndrome is characterized primarily by Autonomous oversecretion of PTH by the parathyroid medullary thyroid carcinoma and pheochromocytoma. glands results in hypercalcemia.4,8 Genetic testing for both syndromes is available in some medical centers.6,7 Clinical Manifestations Neonatal severe primary hyperparathyroidism presents A National Institutes of Health (NIH) consensus panel with severe hypercalcemia during the newborn period.1,6 classified primary hyperparathyroidism into two cate- Hyperparathyroidism–jaw tumor syndrome is a rare con- gories: symptomatic and asymptomatic.9 [Evidence level dition that usually presents in adolescents or young adults C, expert opinion] Manifestations of symptomatic pri- as a solitary adenoma associated with bone lesions in the mary hyperparathyroidism secondary to hypercalcemia jaw and with Wilms’ tumor or renal cysts.6 (which is becoming less common3) include overt bone dis- Familial hypocalciuric hypercalcemia is caused by a sin- ease; kidney stones; and nonspecific gastrointestinal, car- gle mutation in the calcium-sensing receptor, resulting in diovascular, and neuromuscular dysfunction.9 insensitivity to feedback inhibition of PTH secretion. In Asymptomatic primary hyperparathyroidism accounts affected patients, the calcium/creatinine clearance ratio is for 75 to 80 percent of cases.10 Patients in this category have less than 0.01, compared with a calcium/creatinine clear- no signs or symptoms of hypercalcemia. Signs and symp- ance ratio of greater than 0.02 in patients with primary toms that may be present but are not clearly associated hyperparathyroidism. Patients with familial hypocalciuric with primary hyperparathyroidism include hypertension, hypercalcemia are asymptomatic and require no treat- left ventricular hypertrophy, valvular or myocardial calcifi- ment.1,6,8 Familial isolated hyperparathyroidism has no cation, peptic ulcer disease, pancreatitis, gout or pseudo- specific features. It is usually thought to be an expression of gout, normocytic normochromic anemia, weakness, easy occult multiple endocrine neoplasia type I.6 fatigability,
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