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Classification and external resources
Specialty Cardiology, endocrinology
ICD-10 E83.4
ICD-9-CM 275.2
DiseasesDB 6469
MedlinePlus 000315
eMedicine med/3382 emerg/274 ped/1122

Hypomagnesemia (or hypomagnesaemia) is an electrolyte disturbance in which there is an abnormally low level of magnesium in the blood.[1] Normal magnesium levels in humans fall between 1.5 - 2.5 mg/dL. Usually a serum level less than 0.7 mmol/L is used as reference for hypomagnesemia (not hypomagnesia which refers to low magnesium content in food/supplement sources). The prefix hypo- means under (contrast with hyper-, meaning over). The root 'magnes' refers to magnesium. The suffix of the word, -emia, means 'in the blood.'

Hypomagnesemia is not necessarily magnesium deficiency. Hypomagnesemia can be present without magnesium deficiency and vice versa. Note, however, that hypomagnesemia is usually indicative of a systemic magnesium deficit.

Hypomagnesemia may result from a number of conditions including inadequate intake of magnesium, chronic diarrhea, malabsorption, alcoholism, chronic stress, and medications such as diuretic use among others.[2]


  • Signs and symptoms 1
  • Causes 2
    • Drugs 2.1
    • Medications 2.2
    • Metabolic abnormalities 2.3
    • Other 2.4
  • Homeostasis 3
  • Pathophysiology 4
    • Potassium 4.1
    • Calcium 4.2
    • Arrhythmia 4.3
    • Pre-eclampsia 4.4
    • Asthma 4.5
  • Diagnosis 5
  • Treatment 6
  • See also 7
  • References 8
  • External links 9

Signs and symptoms

Deficiency of magnesium causes weakness, muscle cramps, abnormal heart rhythms, increased irritability of the nervous system with tremors, athetosis, jerking, nystagmus, and an extensor plantar reflex. In addition, there may be confusion, disorientation, hallucinations, depression, epileptic fits, hypertension, a fast heart rate, and tetany.


Magnesium deficiency is not uncommon in hospitalized patients. Elevated levels of magnesium (hypermagnesemia), however, are nearly always iatrogenic (caused by a medical treatment). Ten to twenty percent of all hospital patients and 60–65.0625% of patients in the intensive care unit (ICU) have hypomagnesemia. Hypomagnesemia is underdiagnosed, as testing for serum magnesium levels is not routine.

Low levels of magnesium in blood may mean that there is not enough magnesium in the diet, the intestines are not absorbing enough magnesium, or the kidneys are excreting too much magnesium. Deficiencies may be due to the following conditions:



Metabolic abnormalities


  • Acute myocardial infarction: within the first 48 hours after a heart attack, 80% of patients have hypomagnesemia. This could be the result of an intracellular shift because of an increase in catecholamines.
  • Malabsorption
  • Acute pancreatitis
  • Hydrogen fluoride poisoning
  • Massive transfusion (MT) is a lifesaving treatment of hemorrhagic shock, but can be associated with significant complications.[8]


Magnesium is abundant in nature. It can be found in green vegetables, chlorophyll, cocoa derivatives, nuts, wheat, seafood, and meat. It is absorbed primarily in the duodenum of the small intestine. The rectum and sigmoid colon can absorb magnesium. Forty percent of dietary magnesium is absorbed. Hypomagnesemia stimulates and hypermagnesemia inhibits this absorption.

The body contains 21–28 grams of magnesium (0.864–1.152 mol). Of this, 53% is located in bone, 19% in non-muscular tissue, and 1% in extracellular fluid. For this reason, blood levels of magnesium are not an adequate means of establishing the total amount of available magnesium.

In terms of serum magnesium, the majority is bound to chelators, including ATP, ADP, proteins and citrate. Roughly 33% is bound to proteins, and 5–10% is not bound. This "free" magnesium is essential in regulating intracellular magnesium. Normal plasma Mg is 1.7–2.3 mg/dl (0.69–0.94 mmol/l).

The kidneys regulate the serum magnesium. About 2400 mg of magnesium passes through the kidneys daily, of which 5% (120 mg) is excreted through urine. The loop of Henle is the major site for magnesium homeostasis, and 60% is reasorbed.

Magnesium homeostasis comprises three systems: kidney, small intestine, and bone. In the acute phase of magnesium deficiency there is an increase in absorption in the distal small intestine and tubular resorption in the kidneys. When this condition persists, serum magnesium drops and is corrected with magnesium from bone tissue. The level of intracellular magnesium is controlled through the reservoir in bone tissue.


Magnesium is a cofactor in more than 300 enzyme-catalyzed reactions, most importantly reactions forming and using ATP.[7] There is a direct effect on sodium (Na), potassium (K), and calcium (Ca) channels. Magnesium has several effects:


Potassium channel efflux is inhibited by magnesium. Thus hypomagnesemia results in an increased efflux of potassium in kidney, resulting in a hypokalaemia. This condition is believed to occur secondary to the decreased normal physiologic magnesium inhibition of the ROMK channels in the apical tubular membrane.[9]

In this light, hypomagnesemia is frequently the cause hypokalaemic patients failing to respond to potassium supplementation. For example, patients with diabetic ketoacidosis should have their magnesium levels monitored to ensure that the serum loss of potassium, which is driven intracellularly by insulin administration, is not exacerbated by additional urinary losses.


Release of calcium from the sarcoplasmic reticulum is inhibited by magnesium. Thus hypomagnesemia results in an increased intracellular calcium level. This inhibits the release of parathyroid hormone, which can result in hypoparathyroidism and hypocalcemia. Furthermore, it makes skeletal and muscle receptors less sensitive to parathyroid hormone.[10]

  • Through relaxation of bronchial smooth muscle it causes bronchodilation.
  • The neurological effects are:


Magnesium is needed for the adequate function of the Na+/K+-ATPase pumps in cardiac myocytes, the muscles cells of the heart. A lack of magnesium increases potassium loss, causing intracellular potassium loss to increase. This decrease in intracellular potassium results in a tachycardia.


Magnesium has an indirect antithrombotic effect upon platelets and endothelial function. Magnesium increases prostaglandins, decreases thromboxane, and decreases angiotensin II), microvascular leakage and vasospasm through its function similar to calcium channel blockers. . Convulsions are the result of cerebral vasospasm. The vasodilatatory effect of magnesium seems to be the major mechanism.


Magnesium exerts a bronchodilatatory effect, probably by antagonizing calcium-mediated bronchoconstriction.[11]


The diagnosis can be made by finding a plasma magnesium concentration of less than 0.7 mmol/l. Since most magnesium is intracellular, a body deficit can be present with a normal plasma concentration.

The ECG may show a tachycardia with a prolonged QT interval, which has been noted in proton pump inhibitor-associated hypomagnesemia.[12]


Treatment of hypomagnesemia depends on the degree of deficiency and the clinical effects. Oral replacement is appropriate for patients with mild symptoms, while intravenous replacement is recommended for patients with severe clinical effects.[13]

Numerous oral magnesium preparations are available. Magnesium oxide, one of the most common because it has high magnesium content per weight, has been reported to be the least bioavailable.[14][15] Magnesium citrate has been reported as more bioavailable than oxide or amino-acid chelate (glycinate) forms.[16]

Intravenous magnesium sulfate (MgSO4) can be given in response to cardiac arrhythmias, pre-eclampsia, and has been suggested as having a potential use in asthma .

See also


  1. ^ "hypomagnesemia" at Dorland's Medical Dictionary
  2. ^ Romani, Andrea, M.P. (2013). "Chapter 3. Magnesium in Health and Disease". In Astrid Sigel, Helmut Sigel and Roland K. O. Sigel. Interrelations between Essential Metal Ions and Human Diseases. Metal Ions in Life Sciences 13. Springer. pp. 49–79.  
  3. ^ a b Whang R, Hampton EM, Whang DD (1994). "Magnesium homeostasis and clinical disorders of magnesium deficiency". Ann Pharmacother 28 (2): 220–6.  
  4. ^
  5. ^ Sheen, E; Triadafilopoulos, G (April 2011). "Adverse effects of long-term proton pump inhibitor therapy.". Digestive diseases and sciences 56 (4): 931–50.  
  6. ^ Chareonpong-Kawamoto N, Yasumoto K (1995). "Selenium deficiency as a cause of overload of iron and unbalanced distribution of other minerals". Biosci. Biotechnol. Biochem. 59 (2): 302–6.  
  7. ^ a b al-Ghamdi SM, Cameron EC, Sutton RA (1994). "Magnesium deficiency: pathophysiologic and clinical overview". Am. J. Kidney Dis. 24 (5): 737–52.  
  8. ^ Sihler, KC; Napolitano, LM (January 2010). "Complications of massive transfusion.". Chest 137 (1): 209–20.  
  9. ^ Huang, CL, Kuo E (2007). "Mechanism of Hypokalemia in Magnesium Deficiency". J Am Soc Nephrol. 18 (10): 2649–2652.  
  10. ^ Agus, Zalman (July 1999). "Hypomagnesemia". Journal of the American Society of Nephrology 10 (7): 1616–1622.  
  11. ^ Mills R, Leadbeater M, Ravalia A (1997). "Intravenous magnesium sulphate in the management of refractory bronchospasm in a ventilated asthmatic". Anaesthesia 52 (8): 782–5.  
  12. ^ Famularo G1, Gasbarrone L, Minisola G. Hypomagnesemia and proton-pump inhibitors. Expert Opin Drug Saf. 2013 Sep;12(5):709-16.
  13. ^ Durlach J, Durlach V, Bac P, Bara M, Guiet-Bara A (1994). "Magnesium and therapeutics". Magnes Res 7 (3–4): 313–28.  
  14. ^ Firoz M, Graber M (2001). "Bioavailability of US commercial magnesium preparations". Magnes Res 14 (4): 257–62.  
  15. ^ Lindberg JS, Zobitz MM, Poindexter JR, Pak CY (1990). "Magnesium bioavailability from magnesium citrate and magnesium oxide". J Am Coll Nutr 9 (1): 48–55.  
  16. ^ Walker AF, Marakis G, Christie S, Byng M (2003). "Mg citrate found more bioavailable than other Mg preparations in a randomised, double-blind study". Magnes Res 16 (3): 183–91.  
  • Delhumeau , Granry J.C., Monrigal J.P., Costerousse F. (1995). "Indications Du Magnésium En Anesthésie-Réanimation". Annales Francaises D'Anesthésie et De Réanimation 14 (5): 406–416.  
  • Faber MD, Kupin WL, Heilig CW, Narins RG (1994). "Common fluid-electrolyte and acid-base problems in the intensive care unit: selected issues". Semin. Nephrol. 14 (1): 8–22.  
  • A.E. Meinders, Professor of Internal Medicine at Leids Universitair Medisch Centrum, "Magnesium", Bij Intensive Care Patiënten
  • Reinhart RA (1992). "Magnesium deficiency: recognition and treatment in the emergency medicine setting". Am J Emerg Med 10 (1): 78–83.  
  • Reinhart RA, Desbiens NA (1985). "Hypomagnesemia in patients entering the ICU". Crit. Care Med. 13 (6): 506–7.  
  • Ryzen E, Wagers PW, Singer FR, Rude RK (1985). "Magnesium deficiency in a medical ICU population". Crit. Care Med. 13 (1): 19–21.  
  • Ryzen E (1989). "Magnesium homeostasis in critically ill patients". Magnesium 8 (3–4): 201–12.  
  • Hoorn, EJ; van der Hoek, J; de Man, RA; Kuipers, EJ; Bolwerk, C; Zietse, R (Jul 2010). "A case series of proton pump inhibitor-induced hypomagnesemia.". American journal of kidney diseases : the official journal of the National Kidney Foundation 56 (1): 112–6.  

External links

  • Magnesium
  • – Magnesium
  • Dietary Reference Intake
  • Magnesium at Lab Tests Online
  • Magnesium: analyte monograph - the Association for Clinical Biochemistry and Laboratory Medicine.
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