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Hypomagnesemia, also spelled hypomagnesaemia, is an electrolyte disturbance in which there is a low level of magnesium in the blood.[1] Normal magnesium levels are between 1.46–2.68 mg/dL (0.6-1.1 mmol/L) with levels less than 1.46 mg/dL (0.6 mmol/L) defining hypomagnesemia.[2] Symptoms include tremor, nystagmus, seizures, and cardiac arrest including torsade de pointes.[2]

Specialty Cardiology, endocrinology

Causes include alcoholism, starvation, diarrhea, increased urinary loss, and poor absorption from the intestines.[2] Hypomagnesemia is not necessarily magnesium deficiency. Specific electrocardiogram (ECG) changes may be seen.[2]

For those with severe disease intravenous magnesium sulfate may be used.[2]

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'.


Signs and symptomsEdit

Deficiency of magnesium can cause tiredness, generalized weakness, muscle cramps, abnormal heart rhythms, increased irritability of the nervous system with tremors, paresthesias, palpitations, hypokalemia, hypoparathyroidism which might result in hypocalcemia, chondrocalcinosis, spasticity and tetany, migraines, epileptic seizures, basal ganglia calcifications and in extreme and prolonged cases coma, intellectual disability or death.[3] Other symptoms that have been suggested to be associated with hypomagnesemia are athetosis, jerking, nystagmus, and an extensor plantar reflex, confusion, disorientation, hallucinations, depression, hypertension and fast heart rate.[citation needed]

People being treated on an intensive care unit who have a low magnesium level may have a higher risk of requiring mechanical ventilation, and death.[4]


Magnesium deficiency is not uncommon in hospitalized patients. Elevated levels of magnesium (hypermagnesemia), however, are nearly always caused by a medical treatment. Up to 12 percent of all people admitted to hospital and as high as 60–65% of people in the intensive care unit (ICU) have hypomagnesemia.[5][6] Hypomagnesemia is probably 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:



Genetic causesEdit

Metabolic abnormalitiesEdit


  • 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
  • Fluoride poisoning
  • Massive transfusion (MT) is a lifesaving treatment of hemorrhagic shock, but can be associated with significant complications.[12]


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.[citation needed]

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.[citation needed] 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 {removed ATP and ADP which are not present in serum at significant levels and therefore cannot be significant chelators of magnesium in serum}proteins and citrate. Roughly 33% is bound to proteins, and 5–10% is not bound.[citation needed] 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 reabsorbed.

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.[10] 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 excretion 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.[13]

In this light, hypomagnesemia is frequently the cause of hypokalaemic patients failing to respond to potassium supplementation. Thus, clinicians should ensure that both Magnesium and Potassium is replaced when deficient. 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.[citation needed]


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.[14]


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 inhibits reuptake of potassium, causing a decrease in intracellular potassium. 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. .[citation needed] 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.[15]

Neurological effectsEdit

  • reducing electrical excitation
  • modulating release of acetylcholine
  • antagonizing N-methyl-D-aspartate (NMDA) glutamate receptors, an excitatory neurotransmitter of the central nervous system and thus providing neuroprotection from excitoxicity.


The diagnosis can be made by finding a plasma magnesium concentration of less than 0.6 mmol/L (1.46 mg/dl).[2] 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.[16]


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.[17]

Numerous oral magnesium preparations are available. In two human trials magnesium oxide, one of the most common forms in magnesium dietary supplements because of its high magnesium content per weight, was less bioavailable than magnesium citrate, chloride, lactate or aspartate.[18][19] Magnesium citrate has been reported as more bioavailable than oxide or amino-acid chelate forms.[20]

Intravenous magnesium sulfate (MgSO4) can be given in response to cardiac arrhythmias to correct for hypokalemia, preventing pre-eclampsia, and has been suggested as having a potential use in asthma.[2]

See alsoEdit


  1. ^ "hypomagnesemia" at Dorland's Medical Dictionary
  2. ^ a b c d e f g Soar, J; Perkins, GD; Abbas, G; Alfonzo, A; Barelli, A; Bierens, JJ; Brugger, H; Deakin, CD; Dunning, J; Georgiou, M; Handley, AJ; Lockey, DJ; Paal, P; Sandroni, C; Thies, KC; Zideman, DA; Nolan, JP (October 2010). "European Resuscitation Council Guidelines for Resuscitation 2010 Section 8. Cardiac arrest in special circumstances: Electrolyte abnormalities, poisoning, drowning, accidental hypothermia, hyperthermia, asthma, anaphylaxis, cardiac surgery, trauma, pregnancy, electrocution". Resuscitation. 81 (10): 1400–33. doi:10.1016/j.resuscitation.2010.08.015. PMID 20956045. 
  3. ^ a b c d e Viering, Daan H. H. M.; Baaij, Jeroen H. F. de; Walsh, Stephen B.; Kleta, Robert; Bockenhauer, Detlef (2016-05-27). "Genetic causes of hypomagnesemia, a clinical overview". Pediatric Nephrology: 1–13. doi:10.1007/s00467-016-3416-3. ISSN 0931-041X. 
  4. ^ Upala, Sikarin; Jaruvongvanich, Veeravich; Wijarnpreecha, Karn; Sanguankeo, Anawin (24 March 2016). "Hypomagnesemia and mortality in patients admitted to intensive care unit: a systematic review and meta-analysis". QJM. 109: hcw048. doi:10.1093/qjmed/hcw048. PMID 27016536. 
  5. ^
  6. ^ ZALMAN S. AGUS (1999). "Hypomagnesemia". Journal of the American Society of Nephrology. 10 (7): 1616. 
  7. ^ a b Whang R, Hampton EM, Whang DD (1994). "Magnesium homeostasis and clinical disorders of magnesium deficiency". Ann Pharmacother. 28 (2): 220–6. doi:10.1177/106002809402800213. PMID 8173141. 
  8. ^
  9. ^ Sheen, E; Triadafilopoulos, G (April 2011). "Adverse effects of long-term proton pump inhibitor therapy". Digestive Diseases and Sciences. 56 (4): 931–50. doi:10.1007/s10620-010-1560-3. PMID 21365243. 
  10. ^ a b al-Ghamdi SM, Cameron EC, Sutton RA (1994). "Magnesium deficiency: pathophysiologic and clinical overview". Am. J. Kidney Dis. 24 (5): 737–52. doi:10.1016/s0272-6386(12)80667-6. PMID 7977315. 
  11. ^ 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. doi:10.1271/bbb.59.302. PMID 7766029. 
  12. ^ Sihler, KC; Napolitano, LM (January 2010). "Complications of massive transfusion". Chest. 137 (1): 209–20. doi:10.1378/chest.09-0252. PMID 20051407. 
  13. ^ Huang CL, Kuo E (2007). "Mechanism of Hypokalemia in Magnesium Deficiency". J Am Soc Nephrol. 18 (10): 2649–2652. doi:10.1681/ASN.2007070792. PMID 17804670. 
  14. ^ Agus, Zalman (July 1999). "Hypomagnesemia". Journal of the American Society of Nephrology. 10 (7): 1616–1622. PMID 10405219. 
  15. ^ 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. doi:10.1111/j.1365-2044.1997.176-az0312.x. PMID 9291766. 
  16. ^ Famularo G1, Gasbarrone L, Minisola G. Hypomagnesemia and proton-pump inhibitors. Expert Opin Drug Saf. 2013 Sep;12(5):709-16.
  17. ^ Durlach J, Durlach V, Bac P, Bara M, Guiet-Bara A (1994). "Magnesium and therapeutics". Magnes Res. 7 (3–4): 313–28. PMID 7786695. 
  18. ^ Firoz M, Graber M (2001). "Bioavailability of US commercial magnesium preparations". Magnes Res. 14 (4): 257–62. PMID 11794633. 
  19. ^ 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. doi:10.1080/07315724.1990.10720349. PMID 2407766. 
  20. ^ 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. PMID 14596323. 

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