Hypercalcemia overview: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
Normal calcium homeostasis is maintained by parathyroid hormone and vitamin D. Normally, [[parathyroid hormone]] increases serum [[calcium]] and [[magnesium]] concentration, and decreases serum [[phosphate]] concentration. Secretion of [[parathyroid hormone]] from [[parathyroid gland]] is stimulated by low serum [[calcium]]. [[Parathyroid gland]]<nowiki/>s have [[calcium]]-sensing receptors responsible for sensing [[extracellular]] ionized [[calcium]]. [[Calcium]] and [[magnesium]] provides a [[negative feedback]]<nowiki/>for [[secretion]] of [[parathyroid hormone]]. Hypercalcemia may result due to increase in [[secretion]] of [[parathyroid hormone]] ([[PTH]]), most common cause. Other mechanism of hyperlcacemia include secretion of [[parathyroid hormone-related protein]] ([[PTHrP]]) by tumor cells, which has similar action as [[parathyroid hormone]], excess intake of [[calcium]] or [[vitamin D]], and production of [[vitamin D]] by [[macrophages]] in granulomatous diseases. | |||
==Causes== | ==Causes== | ||
Hypercalcemia is most commonly caused by [[hyperparathyroidism]] and [[malignancy]]. Other causes of hypercalcemia include [[hyperthyroidism]], [[Hypervitaminosis D|vitamin D toxicity]], increased calcium intake, granulomatous diseases ( such [[sarcoidosis]]), and various renal disorders. | |||
==Differentiating Hypercalcemia from Other Diseases== | ==Differentiating Hypercalcemia from Other Diseases== | ||
Various common causes of hypercalcemia should be differentiated from each other. | |||
==Epidemiology and Demographics== | ==Epidemiology and Demographics== | ||
The prevalence of hypercalcemia in the cancer patient is approximately 3286.23 per 100,000 individuals over the period of 2009 to 2013 in the United States. | |||
==Risk Factors== | ==Risk Factors== | ||
Common risk factors in the development of hypercalcemia include [[postmenopausal]] women, age group 50-60 year, family history of [[hyperparathyroidism]], history of familial syndromes, and [[Renal disease|renal diseases]]. | |||
==Screening== | ==Screening== | ||
There is insufficient evicence to recommend routine screening for hypercalcemia. | |||
==Natural History, Complications, and Prognosis== | ==Natural History, Complications, and Prognosis== | ||
Mild hypercalcemia is usually asymptomatic and goes undetected in a large number of patients. Furthermore, it commonly reflects in routine laboratory exams. Hypercalcemia may complicated various organ systems including [[renal]] (most commonly), [[gastrointestinal]], and [[skelatal]]. Prognosis of hypercalcemia is usually excellent after treatment. | |||
==Diagnosis== | ==Diagnosis== | ||
===Diagnostic | ===Diagnostic Study of Choice=== | ||
Serum calcium levels is the study of choice for the diagnosis of hypercalcemia. However, a panel of tests may be required to reach the underlying cause of hypercalcemia. | |||
===History and Symptoms=== | ===History and Symptoms=== | ||
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American Roentgen Ray Society Images of Hypercalcemia |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
Hypercalcemia (in UK English Hypercalcaemia) is an elevated calcium level in the blood. (Normal range: 9-10.5 mg/dL or 2.2-2.6 mmol/L). It can be an asymptomatic laboratory finding, but because an elevated calcium level is often indicative of other diseases, a diagnosis should be undertaken if it persists. It can be due to excessive skeletal calcium release, increased intestinal calcium absorption, or decreased renal calcium excretion.
- Calcium is the most abundant mineral in the the body
- 99% of the calcium in the body is stored in the bone
- Calcium in the plasma is either ionized or protein-bound and readily available for use
- An increase in total plasma calcium concentration above 10.4 mg/dL signifies hypercalcemia
- Serum concentration is regulated through parathyroid hormone (PTH), vitamin D and calcitonin
Historical Perspective
In 1932, L. I. Pugsley AND Hans Selye, described the histological changes in the bone due to parathyroid hormone action and calcium metabolism in rat experiments. In the same year, Iftakhar Jahan and Robert F. Pitts described effect of parathyroid hormone in decreasing calcium and magnesium excretion.
Classification
There are several ways in which hypercalcemia may be classified. Common Terminology Criteria for Adverse Events (CTCAE) grade classifies hypercalcemia into 4 grades on the basis of corrected serum calcium (CSC). Hypercalcemia may be classified according to severity into 3 groups including mild, moderate, and severe hypercalcemia. Hypercalcemia associated with malignancy may be classified according to mechanism of increased production of calcium.
Pathophysiology
Normal calcium homeostasis is maintained by parathyroid hormone and vitamin D. Normally, parathyroid hormone increases serum calcium and magnesium concentration, and decreases serum phosphate concentration. Secretion of parathyroid hormone from parathyroid gland is stimulated by low serum calcium. Parathyroid glands have calcium-sensing receptors responsible for sensing extracellular ionized calcium. Calcium and magnesium provides a negative feedbackfor secretion of parathyroid hormone. Hypercalcemia may result due to increase in secretion of parathyroid hormone (PTH), most common cause. Other mechanism of hyperlcacemia include secretion of parathyroid hormone-related protein (PTHrP) by tumor cells, which has similar action as parathyroid hormone, excess intake of calcium or vitamin D, and production of vitamin D by macrophages in granulomatous diseases.
Causes
Hypercalcemia is most commonly caused by hyperparathyroidism and malignancy. Other causes of hypercalcemia include hyperthyroidism, vitamin D toxicity, increased calcium intake, granulomatous diseases ( such sarcoidosis), and various renal disorders.
Differentiating Hypercalcemia from Other Diseases
Various common causes of hypercalcemia should be differentiated from each other.
Epidemiology and Demographics
The prevalence of hypercalcemia in the cancer patient is approximately 3286.23 per 100,000 individuals over the period of 2009 to 2013 in the United States.
Risk Factors
Common risk factors in the development of hypercalcemia include postmenopausal women, age group 50-60 year, family history of hyperparathyroidism, history of familial syndromes, and renal diseases.
Screening
There is insufficient evicence to recommend routine screening for hypercalcemia.
Natural History, Complications, and Prognosis
Mild hypercalcemia is usually asymptomatic and goes undetected in a large number of patients. Furthermore, it commonly reflects in routine laboratory exams. Hypercalcemia may complicated various organ systems including renal (most commonly), gastrointestinal, and skelatal. Prognosis of hypercalcemia is usually excellent after treatment.
Diagnosis
Diagnostic Study of Choice
Serum calcium levels is the study of choice for the diagnosis of hypercalcemia. However, a panel of tests may be required to reach the underlying cause of hypercalcemia.