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Hyperparathyroidism in Emergency Medicine

  • Author: Philip N Salen, MD; Chief Editor: Erik D Schraga, MD  more...
 
Updated: Oct 27, 2014
 

Background

The parathyroid glands regulate serum calcium and phosphorus levels through the secretion of parathyroid hormone (PTH), which raises serum calcium levels while lowering the serum phosphorus concentration. The regulation of PTH secretion occurs through a negative feedback loop in which calcium-sensing receptors on the membranes of parathyroid cells trigger decreased PTH production as serum calcium concentrations rise.

Primary hyperparathyroidism (PHPT), which accounts for most hyperparathyroidism cases, results from excessive release of PTH and manifests as hypercalcemia.[1] Patients with hypercalcemia who have normal renal function and no malignancy must be suspected of having primary hyperparathyroidism and must be subsequently tested for elevated PTH levels.

Hyperparathyroidism is often incidentally discovered during routine laboratory testing when hypercalcemia is noted. In 80% of patients with hyperparathyroidism, the symptoms of hypercalcemia are mild or are not notable at the time of discovery. Management of these patients is not clear-cut because routine laboratory tests have not been shown to assist in predicting development of overt manifestations of the disease. Conversely, patients with overtly symptomatic hyperparathyroidism (eg, those with urinary tract stones, bone pain, cognitive abnormalities) and those with marked hypercalcemia (calcium levels >10.2 mg/dL) should be referred for consideration for parathyroidectomy.[2]

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Pathophysiology

Primary hyperparathyroidism is one of the most common causes of hypercalcemia and should be considered in any individual with an elevated calcium level.[3] PHPT is usually the result of a single benign adenoma; a minority of patients have hyperplasia in all 4 parathyroid glands. Parathyroid carcinoma accounts for an insignificant minority, less than 0.5%, of hyperparathyroidism cases.

Asymptomatic PHPT manifests with serum calcium concentrations only slightly elevated to within 1 mg/dL above the upper limit of the reference range. Within the setting of asymptomatic PHPT, the parathyroid hormone (PTH) level is typically 1.5-2 times the upper limit of the reference range. Hypophosphatemia and hyperchloremia are typically seen only in patients who are highly symptomatic patients and have advanced hyperparathyroidism.

When hyperparathyroidism manifests with hyperplasia in all 4 glands, familial-genetic syndromes should be contemplated within the differential diagnosis. Syndromes to be consider include type I and type II multiple endocrine neoplasia (MEN) or, less commonly, familial hypocalciuric hypercalcemia and hyperparathyroidism–jaw tumor syndrome. Also, a syndrome of familial isolated hyperparathyroidism has been observed. Radiation therapy to the head and neck increases the risk of development of parathyroid tumors.

Secondary hyperparathyroidism occurs when the parathyroid glands become hyperplastic after long-term hyperstimulation and release of PTH. In secondary hyperparathyroidism, elevated PTH levels do not result in hypercalcemia. Secondary hyperparathyroidism has been attributed to a physiologic response to the hypocalcemia present in those with chronic renal failure (CRF). However, hypocalcemia is not necessary for the development of secondary hyperparathyroidism in this setting. Nearly all patients on maintenance dialysis will develop secondary hyperparathyroidism regardless of the calcium level.[4] Calcium balance becomes an issue of concern because of accelerated vascular calcification seen in patients on dialysis.

Additional risk factors for the development of secondary hyperparathyroidism include phosphorus retention, intrinsic parathyroid gland abnormalities, diminished serum calcitriol levels, and resistance to PTH by skeletal tissue. Rickets and malabsorption syndromes are rarer causes.

With long-term hyperstimulation, the glands function autonomously and produce high levels of PTH even after correction of chronic hypocalcemia. Tertiary hyperparathyroidism refers to hypercalcemia caused by autonomous parathyroid function after long-term hyperstimulation.

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Epidemiology

Frequency

United States

Primary hyperparathyroidism is a common endocrine disease that affects nearly 1 in 500 women and 1 in 2000 men per year, most often in the fifth, sixth, and seventh decades of life.[5]

Mortality/Morbidity

Most patients, who are predominantly middle aged or elderly, present with mild elevations of serum calcium and are not overtly symptomatic. Usually, the rate of progression of hyperparathyroidism is slow, and monitoring these patients and medically managing the disease is usually safe.

All patients with biochemically confirmed, symptomatic PHPT should be referred for surgical parathyroidectomy. In symptomatic patients, there is evidence that after parathyroidectomy, cognitive function improves, bone density improves, fracture rate declines, and the incidence of ureteral colic declines. Furthermore, cardiovascular disease and premature death also appear to decrease after surgery in symptomatic patients.[6] Complication rates and symptom relief are similar in younger and older patients who undergo surgery.[3]

Of note, many "supposedly asymptomatic" patients do not realize that their hyperparathyroid symptoms may be a manifestation of their hyperparathyroidism until after these symptoms diminish or disappear following parathyroidectomy.[7]

Sex

Most individuals with hyperparathyroidism, asymptomatic and symptomatic, are postmenopausal women.[3]

Asymptomatic PHPT is a disease that affects mainly women in their middle years. The disease occurs most commonly within the first decade of the menopause. Women with PHPT outnumber men by approximately 3:1.[8]

Age

Although hyperparathyroidism can manifest at any age, its occurrence rises markedly in persons older than 40 years. Hyperparathyroidism is rare in children.

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Contributor Information and Disclosures
Author

Philip N Salen, MD Clinical Professor, Department of Emergency Medicine, PA Program, DeSales University; Adjunct Clinical Associate Professor, Department of Emergency Medicine, Temple University School of Medicine; Research Director, Emergency Medicine Education, St Luke's Hospital

Philip N Salen, MD is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Jeffrey L Arnold, MD, FACEP Chairman, Department of Emergency Medicine, Santa Clara Valley Medical Center

Jeffrey L Arnold, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine, American College of Physicians

Disclosure: Nothing to disclose.

Chief Editor

Erik D Schraga, MD Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates

Disclosure: Nothing to disclose.

Additional Contributors

Erik D Schraga, MD Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates

Disclosure: Nothing to disclose.

References
  1. Allerheiligen DA, Schoeber J, Houston RE, et al. Hyperparathyroidism. Am Fam Physician. 1998 Apr 15. 57(8):1795-802, 1807-8. [Medline].

  2. Jacobs DS, Kasten BL, DeMott WR, Wolfson WL. Laboratory Test Handbook. Williams & Wilkins. 1990:284-7.

  3. Boonen S, Vanderschueren D, Pelemans W, Bouillon R. Primary hyperthyroidism: diagnosis and management in the older individual. Eur J Endocrinol. 2004 Sept. 151(3):297-304. [Medline].

  4. Brommage D, Gallgano C. The role of cinacalcet in treating secondary hyperparathyroidism. Nephrol Nurs J. 2005 Mar-Apr. 32(2):229-31. [Medline].

  5. Ruda JM, Hollenbeak CS, Stack BC. A systematic review of the diagnosis and treatment of primary hyperparathyroidism from 1995 to 2003. Otolaryngology- Head and Neck Surgery. March 2005. 132:359-372.

  6. Udelsman R, Pasieka JL, Sturgeon C, Young JE, Clark OH. Surgery for asymptomatic primary hyperparathyroidism: proceedings of the third international workshop. J Clin Endocrinol Metab. 2009 Feb. 94(2):366-72. [Medline].

  7. Perrier ND. Asymptomatic hyperparathyroidism: a medical misnomer?. Surgery. 2005 Feb. 137(2):127-31. [Medline].

  8. Silverberg SJ, Walker MD, Bilezikian JP. Asymptomatic primary hyperparathyroidism. 2013;16(1):14–21. J Clin Densitom. 2013. 16:14-21.

  9. Sorensen HA. Surgery for primary hyperparathyroidism. BMJ. 2002 Oct 12. 325(7368):785-6. [Medline].

  10. Udelsman R, Pasieka JL, Sturgeon C, Young JE, Clark OH. Surgery for asymptomatic primary hyperparathyroidism: proceedings of the third international workshop. J Clin Endocrinol Metab. 2009 Feb. 94(2):366-72. [Medline].

  11. Khan A, Grey A, Shoback D. Medical management of asymptomatic primary hyperparathyroidism: proceedings of the third international workshop. J Clin Endocrinol Metab. 2009 Feb. 94(2):373-81. [Medline].

  12. Triponez F, Clark OH, Vanrenthergem Y, Evenepoel P. Surgical treatment of persistent hyperparathyroidism after renal transplantation. Ann Surg. 2008 Jul. 248(1):18-30. [Medline].

  13. Beard CM, Heath H 3rd, O'Fallon WM, et al. Therapeutic radiation and hyperparathyroidism. A case-control study in Rochester, Minn. Arch Intern Med. 1989 Aug. 149(8):1887-90. [Medline].

  14. Tezelman S, Rodriguez JM, Shen W, et al. Primary hyperparathyroidism in patients who have received radiation therapy and in patients who have not received radiation therapy. J Am Coll Surg. 1995 Jan. 180(1):81-7. [Medline].

  15. National Institutes of Health. Consensus conference. Diagnosis and management of asymptomatic primary hyperparathyroidism. Conn Med. 1991 Jun. 55(6):349-54. [Medline].

  16. [Guideline] Bilezikian JP, Khan AA, Potts JT. Guidelines for the management of asymptomatic primary hyperparathyroidism: summary statement from the third international workshop. The Journal of clinical endocrinology and metabolism. 94 (2):335-9. [Medline].

  17. Carter AB, Howanitz PJ. Intraoperative testing for parathyroid hormone: a comprehensive review of the use of the assay and the relevant literature. Arch Pathol Lab Med. 2003 Nov. 127(11):1424-42. [Medline].

  18. Boggs JE, Irvin GL 3rd, Carneiro DM, Molinari AS. The evolution of parathyroidectomy failures. Surgery. 1999 Dec. 126(6):998-1002; discussion 1002-3. [Medline].

  19. Guarda LA. Rapid intraoperative parathyroid hormone testing with surgical pathology correlations: the "chemical frozen section". Am J Clin Pathol. 2004 Nov. 122(5):704-12. [Medline].

  20. Irvin GL, Carneiro DM. Management changes in primary hyperparathyroidism. JAMA. 2000 Aug 23-30. 284(8):934-6. [Medline].

  21. Alexander HR Jr, Chen CC, Shawker T, et al. Role of preoperative localization and intraoperative localization maneuvers including intraoperative PTH assay determination for patients with persistent or recurrent hyperparathyroidism. J Bone Miner Res. 2002 Nov. 17 Suppl 2:N133-40. [Medline].

  22. Sankaran S, Gamble G, Bolland M, Reid IR, Grey A. Skeletal effects of interventions in mild primary hyperparathyroidism: a meta-analysis. J Clin Endocrinol Metab. 2010 Apr. 95(4):1653-62. [Medline].

  23. LeGrand SB, Leskuski D, Zama I. Narrative review: furosemide for hypercalcemia: an unproven yet common practice. Ann Intern Med. 2008 Aug 19. 149(4):259-63. [Medline].

  24. VanderWalde LH, Liu IL, O'Connell TX, Haigh PI. The effect of parathyroidectomy on bone fracture risk in patients with primary hyperparathyroidism. Arch Surg. 2006 Sep. 141(9):885-9; discussion 889-91. [Medline].

  25. Coker LH, Rorie K, Cantley L, et al. Primary hyperparathyroidism, cognition, and health-related quality of life. Ann Surg. 2005 Nov. 242(5):642-50. [Medline]. [Full Text].

  26. Peacock M, Bolognese MA, Borofsky M, Scumpia S, Sterling LR, Cheng S, et al. Cinacalcet treatment of primary hyperparathyroidism: biochemical and bone densitometric outcomes in a five-year study. J Clin Endocrinol Metab. 2009 Dec. 94(12):4860-7. [Medline].

  27. al Zahrani A, Levine MA. Primary hyperparathyroidism. Lancet. 1997 Apr 26. 349(9060):1233-8. [Medline].

  28. Bilezikian JP. Management of acute hypercalcemia. N Engl J Med. 1992 Apr 30. 326(18):1196-203. [Medline].

  29. Bilezikian JP, Silverberg SJ. Clinical practice. Asymptomatic primary hyperparathyroidism. N Engl J Med. 2004 Apr 22. 350(17):1746-51. [Medline].

  30. Potts JT. Diseases of the parathyroid gland and other hyper- and hypocalcemic disorders. Harrison's Principles of Internal Medicine. 14th ed. 1998. 2227-32.

 
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