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Classification and external resources
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Hypercalcaemia (British English) or hypercalcemia (American English) is an elevated calcium (Ca2+) level in the blood.[1] (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 workup should be undertaken if it persists. It can be due to excessive skeletal calcium release, increased intestinal calcium absorption, or decreased renal calcium excretion.

Signs and symptoms[edit]

The neuromuscular symptoms of hypercalcemia are caused by a negative bathmotropic effect due to the increased interaction of calcium with sodium channels. Since calcium blocks sodium channels and inhibits depolarization of nerve and muscle fibers, increased calcium raises the threshold for depolarization.[2] There is a general mnemonic for remembering the effects of hypercalcaemia: "Stones, Bones, Groans, Thrones and Psychiatric Overtones"

Other symptoms can include fatigue, anorexia, and pancreatitis.[citation needed]

Abnormal heart rhythms can result, and ECG findings of a short QT interval[3] and a widened T wave suggest hypercalcaemia. Significant hypercalcaemia can cause ECG changes mimicking an acute myocardial infarction.[4] Hypercalcaemia has also been known to cause an ECG finding mimicking hypothermia, known as an Osborn wave.[5]

Hypercalcaemia can increase gastrin production, leading to increased acidity so peptic ulcers may also occur.

Symptoms are more common at high calcium blood values (12.0 mg/dL or 3 mmol/l). Severe hypercalcaemia (above 15–16 mg/dL or 3.75–4 mmol/l) is considered a medical emergency: at these levels, coma and cardiac arrest can result. Hypercalcaemia causes the opposite[clarify] - the high levels of calcium ions decrease neuronal excitability, which leads to hypotonicity of smooth and striated muscle. This explains the fatigue, muscle weakness, low tone and sluggish reflexes in muscle groups. In the gut this causes constipation. The sluggish nerves also explain drowsiness, confusion, hallucinations, stupor and / or coma.


Primary hyperparathyroidism and malignancy account for about 90% of cases of hypercalcaemia.[6][7]

Abnormal parathyroid gland function[edit]


Micrograph of ovarian small cell carcinoma of the hypercalcemic type. H&E stain.

Vitamin-D metabolic disorders[edit]

Disorders related to high bone-turnover rates[edit]

Renal failure[edit]


The goal of therapy is to treat the hypercalcaemia first and subsequently effort is directed to treat the underlying cause.

Initial therapy: fluids and diuretics[edit]

Additional therapy: bisphosphonates and calcitonin[edit]

Other therapies[edit]

Hypercalcaemic crisis [edit]

A hypercalcaemic crisis is an emergency situation with a severe hypercalcaemia, generally above approximately 14 mg/dL (or 3.5 mmol/l).[14]

The main symptoms of a hypercalcaemic crisis are oliguria or anuria, as well as somnolence or coma.[15] After recognition, primary hyperparathyroidism should be proved or excluded.[15]

In extreme cases of primary hyperparathyroidism, removal of the parathyroid gland after surgical neck exploration is the only way to avoid death.[15] The diagnostic program should be performed within hours, in parallel with measures to lower serum calcium.[15] Treatment of choice for acutely lowering calcium is extensive hydration and calcitonin, as well as bisphosphonates (which have effect on calcium levels after one or two days).[16]

See also[edit]


  1. ^ "hypercalcemia" at Dorland's Medical Dictionary
  2. ^ Armstrong, C.M., Cota, Gabriel.; Cota (1999). "Calcium block of Na+ channels and its effect on closing rate". Proceedings of the National Academy of Sciences of the United States of America 96 (7): 4154–4157. Bibcode:1999PNAS...96.4154A. doi:10.1073/pnas.96.7.4154. PMC 22436. 
  3. ^ http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/endocrinology/hypercalcemia/
  4. ^ Wesson, L.; Suresh, V.; Parry, R. (2009). "Severe hypercalcaemia mimicking acute myocardial infarction". Clinical medicine (London, England) 9 (2): 186–187. doi:10.7861/clinmedicine.9-2-186. PMID 19435131.  edit
  5. ^ Serafi S, Vliek C, Taremi M (2011) "Osborn waves in a hypothermic patient" The Journal of Community Hospital Internal Medicine Perspectives http://www.jchimp.net/index.php/jchimp/article/view/10742/html
  6. ^ Table 20-4 in: Mitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson. Robbins Basic Pathology. Philadelphia: Saunders. ISBN 1-4160-2973-7.  8th edition.
  7. ^ Tierney, Lawrence M.; McPhee, Stephen J.; Papadakis, Maxine A. (2006). Current Medical Diagnosis and Treatment 2007 (Current Medical Diagnosis and Treatment). McGraw-Hill Professional. p. 901. ISBN 0-07-147247-9. 
  8. ^ Online 'Mendelian Inheritance in Man' (OMIM) 146200
  9. ^ Online 'Mendelian Inheritance in Man' (OMIM) 145980
  10. ^ Online 'Mendelian Inheritance in Man' (OMIM) 145981
  11. ^ Online 'Mendelian Inheritance in Man' (OMIM) 600740
  12. ^ Non-Small Cell Lung Cancer at medscape. Author: Winston W Tan.Chief Editor: Jules E Harris. Updated: Mar 30, 2011
  13. ^ Online 'Mendelian Inheritance in Man' (OMIM) 143880
  14. ^ Hypercalcemia in Emergency Medicine at Medscape. Author: Robin R Hemphill. Chief Editor: Erik D Schraga. Retrieved April 2011
  15. ^ a b c d Ziegler R (February 2001). "Hypercalcemic crisis". J. Am. Soc. Nephrol. 12 Suppl 17: S3–9. PMID 11251025. 
  16. ^ Page 394 in: Roenn, Jamie H. Von; Ann Berger; Shuster, John W. (2007). Principles and practice of palliative care and supportive oncology. Hagerstwon, MD: Lippincott Williams & Wilkins. ISBN 0-7817-9595-8. 
  17. ^ Dauber, Andrew; Nguyen Thutrang T, Sochett Etienne, Cole David E C, Horst Ronald, Abrams Steven A, Carpenter Thomas O, Hirschhorn Joel N (Nov 2011). "Genetic Defect in CYP24A1, the Vitamin D 24-Hydroxylase Gene, in a Patient with Severe Infantile Hypercalcemia". The Journal of Clinical Endocrinology and Metabolism (in ENG) 97 (2): E268–74. doi:10.1210/jc.2011-1972. PMC 3275367. PMID 22112808.