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Hyperparathyroidism in Emergency Medicine

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


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]



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.




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]


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]


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]


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

Contributor Information and Disclosures

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.

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