Hyperparathyroidism in Emergency Medicine
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Primary hyperparathyroidism is one of the most common causes of hypercalcemia and should be considered in the differential of any individual presenting with an elevated calcium level. [1] Primary hyperparathyroidism (PHPT), hypersecretion of parathormone (parathyroid hormone: PTH) from the parathyroid glands, results in persistent hypercalcemia and usually hypercalciuria. [2] Rarely, PHPT manifests as a component of genetically transmitted endocrine diseases, specifically multiple endocrine neoplasia syndromes. PHPT causes symptoms in multiple organ systems throughout the body via its impact on calcium homeostasis. The most recognizable symptoms are renal and skeletal complications: nephrolithiasis, nephrocalcinosis, osteitis fibrosa cystica, and osteoporosis. [2] PHPT also manifests more subtly with nonspecific symptoms in other organ systems including: cardiovascular, gastrointestinal, rheumatic, and neuropsychiatric. Untreated PHPT can lead to irreversible changes including skeletal deformations and renal insufficiency.
The parathyroid glands regulate serum calcium and phosphorus levels by the secretion of parathyroid hormone (PTH), which elevates serum calcium levels while depressing serum phosphorus levels. 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. [3] Patients with hypercalcemia who have normal renal function and no malignancy must be suspected of having primary hyperparathyroidism and must be evaluated for hyperparathyroidism.
Hyperparathyroidism is often incidentally discovered during routine laboratory testing when hypercalcemia is noted. For 80% of patients with hyperparathyroidism, the symptoms of hyperparathyroid induced hypercalcemia are mild or are not notable at the time of discovery. Management of asymptomatic PHPT patients is not clear-cut because routine laboratory tests have not been predictive of 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. [4]
PHPT is usually the result of a single benign adenoma; a minority of patients have hyperplasia of all 4 parathyroid glands. Parathyroid carcinoma manifests rarely, less than 0.5%, as a cause of hyperparathyroidism.
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.
Hypercalciuria, more than 300 mg daily of urinary calcium excretion, is observed in a significant subset of PHPT patients (30%). The most frequent complication of symptomatic PHPT is nephrolithiasis, which occurs in about 20% of patients. [5] PHPT also can decrease glomerular filtration rates, inducing chronic kidney disease.
When hyperparathyroidism manifests with hyperplasia in all 4 glands, familial-genetic syndromes should be contemplated as causal within the differential diagnosis. Syndromes to be considered include type I and type II multiple endocrine neoplasia (MEN) or, less commonly, familial hypocalciuric hypercalcemia and hyperparathyroidism–jaw tumor syndrome. 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 an absolute requirement for the development of secondary hyperparathyroidism in CRF. Nearly all patients on maintenance dialysis will develop secondary hyperparathyroidism regardless of their calcium level. [6] Calcium homeostasis becomes an issue of concern because of accelerated vascular calcifications 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 of secondary hyperparathyroidism.
With long-term parathyroid 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.
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 individuals with PHPT, asymptomatic and symptomatic, are postmenopausal women. [1] The incidence of affected women reaches 21 per 1000 in women older than the age of 50. [2] Asymptomatic PHPT is a disease that affects mainly women in their middle years. Women with PHPT outnumber men by approximately 3:1. [7]
Although hyperparathyroidism can manifest at any age, PHPT occurrence rises markedly in persons older than 40 years. The disease manifests most commonly within the first decade after onset of menopause.
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 PHPT 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 parathyroidectomy in symptomatic patients. [8] Complication rates and symptom relief are similar in younger and older patients who undergo surgery. [1]
Of note, many “supposedly asymptomatic” patients do not realize that their hyperparathyroid symptoms are a manifestation of their PHPT until after these symptoms diminish or disappear following parathyroidectomy. [9]
Hyperparathyroidism is a disease of the 4 parathyroid glands that are next to the thyroid gland in the neck. The parathyroid glands release a hormone called parathormone (parathyroid hormone) that is important for maintaining the normal calcium levels in the body. Primary hyperparathyroidism, the most common kind of hyperparathyroidism, occurs when too much parathormone is released from one or more of the parathyroid glands and is most commonly caused when one of the four parathyroid glands grows abnormally large. Secondary hyperparathyroidism occurs when the parathyroid glands respond to a stimulus within the body to release too much parathormone. Hyperparathyroidism causes high levels of calcium in the blood. The most common symptoms of hyperparathyroid induced hypercalcemia are kidney stones, which can cause flank pain, and weak bones, which can break more easily. Other symptoms of hyperparathyroidism are feeling weak, tired, and depressed.
Hyperparathyroidism is diagnosed by checking the blood for high levels of calcium and parathormone.
Many patients with primary hyperparathyroidism have mild forms of the disease, do not have symptoms, and do not need treatment. Some patients with symptoms of weak bones or kidney stones need to have their parathyroid glands surgically removed.
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Philip N Salen, MD Adjunct Clinical Associate Professor, Department of Emergency Medicine, Temple University School of Medicine; Research Director, Emergency Medicine Education, St Luke’s Hospital
Disclosure: Nothing to disclose.
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.
Erik D Schraga, MD Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates
Disclosure: Nothing to disclose.
Erik D Schraga, MD Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates
Disclosure: Nothing to disclose.
Hyperparathyroidism in Emergency Medicine
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