Magnesium deficiency: Difference between revisions

Magnesium deficiency
Magnesium deficiency
Other names	Hypomagnesia, hypomagnesemia
	Magnesium
Specialty	Endocrinology
Symptoms	Tremor, poor coordination, nystagmus, seizures
Complications	Seizures, cardiac arrest (torsade de pointes), low potassium
Causes	Alcoholism, starvation, diarrhea, increased urinary loss, poor absorption from the intestines, certain medications
Diagnostic method	Blood levels < 0.6 mmol/L (1.46 mg/dL)
Treatment	Magnesium salts
Frequency	Relatively common (hospitalized people)

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Magnesium deficiency is an electrolyte disturbance in which there is a low level of magnesium in the body.^[3] Symptoms include tremor, poor coordination, muscle spasms, loss of appetite, personality changes, and nystagmus.^[1]^[2] Complications may include seizures or cardiac arrest such as from torsade de pointes.^[1] Those with low magnesium often have low potassium.^[1]

Causes include low dietary intake, alcoholism, diarrhea, increased urinary loss, and poor absorption from the intestines.^[1]^[4]^[5] Some medications may also cause low magnesium, including proton pump inhibitors (PPIs) and furosemide.^[2] The diagnosis is typically based on finding low blood magnesium levels, also called hypomagnesemia.^[6] Normal magnesium levels are between 0.6 and 1.1 mmol/L (1.46–2.68 mg/dL) with levels less than 0.6 mmol/L (1.46 mg/dL) defining hypomagnesemia.^[1] Specific electrocardiogram (ECG) changes may be seen.^[1]

Treatment is with magnesium either by mouth or intravenously.^[2] For those with severe symptoms, intravenous magnesium sulfate may be used.^[1] Associated low potassium or low calcium should also be treated.^[2] The condition is relatively common among people in hospitals.^[2]

Signs and symptoms

Deficiency of magnesium can cause tiredness, generalized weakness, muscle cramps, abnormal heart rhythms, increased irritability of the nervous system with tremors, paresthesias, palpitations, low potassium levels in the blood, hypoparathyroidism which might result in low calcium levels in the blood, chondrocalcinosis, spasticity and tetany, migraines, epileptic seizures,^[7] basal ganglia calcifications^[8] and in extreme and prolonged cases coma, intellectual disability or death.^[9] Magnesium deficiency is strongly associated with and appears to contribute to obesity, insulin resistance, metabolic syndrome, and type 2 diabetes, although the causal mechanism is not fully understood.^[10]^[4]^[5]

Causes

Magnesium deficiency may result from gastrointestinal or kidney causes. Gastrointestinal causes include low dietary intake of magnesium, reduced gastrointestinal absorption or increased gastrointestinal loss due to rapid gastrointestinal transits. Kidney causes involve increased excretion of magnesium. Poor dietary intake of magnesium has become an increasingly important factor: many people consume diets high in refined foods such as white bread and polished rice which have been stripped of magnesium-rich plant fiber.^[11]

Magnesium deficiency is common in hospitalized patients. Up to 12% of all people admitted to hospital, and as high as 60–65% of people in an intensive care unit (ICU), have hypomagnesemia.^[12]

About 57% of the US population does not meet the US RDA for dietary intake of magnesium.^[13] Kidneys are very efficient at maintaining body levels; however, if the diet is deficient, or certain medications such as diuretics or proton pump inhibitors are used,^[14] or in chronic alcoholism,^[15] levels may drop.

Deficiencies may be due to the following conditions:

Medications

Loop and thiazide diuretic use (the most common cause of hypomagnesemia),^[16]
Antibiotics (i.e. aminoglycoside, amphotericin, pentamidine, gentamicin, tobramycin, viomycin) block resorption in the loop of Henle. 30% of patients using these antibiotics have hypomagnesemia,^[17]
Long term, high dosage use of proton-pump inhibitors such as omeprazole,^[18]^[19]
Other drugs:
- Digitalis, displaces magnesium into the cell. Digitalis causes an increased intracellular concentration of sodium, which in turn increases intracellular calcium by passively increasing the action of the sodium-calcium exchanger in the sarcolemma. The increased intracellular calcium gives a positive inotropic effect,^[16]
- Adrenergics, displace magnesium into the cell,
- Cisplatin, stimulates kidney excretion,
- Ciclosporin, stimulates kidney excretion,
- Mycophenolate mofetil.

Genetics

Gitelman-like diseases, which include the syndromes caused by genetic mutations in SLC12A3, CLNCKB,^[20] BSND, KCNJ10, FXYD2, HNF1B or PCBD1. In these diseases, the hypomagnesemia is accompanied by other defects in electrolyte handling such as hypocalciuria and hypokalemia. The genes involved in this group of diseases all encode proteins that are involved in reabsorbing electrolytes (including magnesium) in the distal convoluted tubule of the kidney,^[9]
Hypercalciuric hypomagnesemic syndromes, which encompass the syndromes caused by mutations in CLDN16, CLDN19, CASR or CLCNKB. In these diseases, reabsorption of divalent cations (such as magnesium and calcium) in the thick ascending limb of Henle's loop of the kidney is impaired. This results in loss of magnesium and calcium in the urine,^[9]
Mitochondriopathies, especially mutations in the mitochondrial tRNAs MT-TI or MT-TF.^[21] Mutations in SARS2, or mitochondrial DNA deletions as seen with Kearns-Sayre syndrome, can also cause hypomagnesemia,^[9]
Other genetic causes of hypomagnesemia, such as mutations in TRPM6, CNNM2, EGF, EGFR, KCNA1 or FAM111A. Many of the proteins encoded by these genes play a role in the transcellular absorption of magnesium in the distal convoluted tubule,^[9]

Metabolic abnormalities

Insufficient selenium,^[22] vitamin D or sunlight exposure, or vitamin B6,^[23]
Gastrointestinal causes: the distal digestive tract secretes high levels of magnesium. Therefore, secretory diarrhea can cause hypomagnesemia. Thus, Crohn's disease, ulcerative colitis, Whipple's disease and celiac sprue can all cause hypomagnesemia,
Postobstructive diuresis, diuretic phase of acute tubular necrosis (ATN) and kidney transplant,^[24]

Other

Chronic alcoholism: Alcohol intake leads to enhanced diuresis of electrolytes, possibly due to alcohol induced kidney tubular cell damage.^[25] Hypomagnesemia is also thought to occur due to reduced magnesium intake due to malnutrition and increased gastrointestinal losses.^[25]^[26]^[27]^[28]^[29] Hypomagnesemia is the most common electrolyte abnormality in those with chronic alcoholism.^[25] Chronic hypomagnesemia in those with chronic alcoholism is associated with liver disease and a worse prognosis,^[25]
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.^[30]

Pathophysiology

Magnesium is ubiquitous in the human body as well as being present in all living organisms and the ion is a known co-factor in over known 300 enzymatic reactions including DNA and RNA replication, protein synthesis, acting as an essential co-factor of ATP during its phosphorylation via ATPase. It is also extensively involved in intracellular signaling.^[20]^[25] It is involved in protein synthesis, regulating glucose, lipid and protein metabolism, muscle and nerve functioning, vascular tone (affecting blood vessel contraction, thus helping to regulate blood pressure), bone development, energy production, the maintenance of normal heart rhythm, and the regulation of glucose, among other important roles.^[15]^[25] Physiologically, it acts as a calcium antagonist.^[25] Thus, the effects of low magnesium are widespread. Low magnesium intake over time can increase the risk of illnesses, including high blood pressure and heart disease, diabetes mellitus type 2, osteoporosis, and migraines.^[15]

Magnesium has several effects:

Potassium

Low potassium levels are usually associated with hypomagnesemia. Low magnesium levels act to inhibit the sodium-potassium pump (Na-K-ATPase) which normally pumps sodium to the extracellular space and potassium into the intracellular space, using ATP as energy to pump both cations against their concentration gradient, to maintain relatively high levels of potassium in the intracellular compartment and high levels of sodium in the extracellular space.^[25] Hypomagnesemia also causes activation of the Renal outer medullary potassium channel (ROMK), a potassium channel which causes potassium losses in the urine via the cortical collecting duct in the kidney.^[25] And hypomagnesemia prevents low potassium levels from activating the sodium-chloride cotransporter (NCC) and downregulates NCC levels, which prevents sodium and chloride reabsorption from the kidney tubule.^[25] The inhibition of the sodium-potassium pump results in more potassium remaining in the extracellular space (interstitial fluid and plasma). And this potassium is then lost as blood is filtered in the kidney as ROMK channel activation causes potassium losses in the cortical collecting duct and NCC inhibition causes decreased sodium-chloride reabsorption by kidney tubules, with subsequent increased sodium-chloride (and water) delivery to the distal tubule, and associated diuresis and kaliuresis (kidney potassium loss in the urine).^[25] Overall, the net effect of low magnesium levels in the body is renal potassium losses (in the urine), thus clinically, low potassium levels are often refractory to supplementation without also correcting low magnesium levels.^[25]^[31]

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]}

Calcium

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.^[12]

Arrhythmia

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 tachycardia.^{[citation needed]}

Pre-eclampsia

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.

Asthma

Magnesium exerts a bronchodilatatory effect, probably by antagonizing calcium-mediated bronchoconstriction.^[32]

Neurological effects

Reducing electrical excitation,
Modulating release of acetylcholine,
GABAA receptor agonism,^[33]
Antagonising N-methyl-D-aspartate (NMDA) glutamate receptors, an excitatory neurotransmitter of the central nervous system and thus providing neuroprotection from excitoxicity.

Diabetes mellitus

Magnesium deficiency is frequently observed in people with type 2 diabetes mellitus, with an estimated prevalence ranging between 11 and 48%.^[34] Magnesium deficiency is strongly associated with high glucose and insulin resistance, which indicate that it is common in poorly controlled diabetes.^[35] Patients with type 2 diabetes and a magnesium deficiency have a higher risk of heart failure, atrial fibrillation and microvascular complications.^[36] Oral magnesium supplements has been demonstrated to improve insulin sensitivity and lipid profile.^[37]^[38]^[39] A 2016 meta-analysis not restricted to diabetic subjects found that increasing dietary magnesium intake, while associated with a reduced risk of stroke, heart failure, diabetes, and all-cause mortality, was not clearly associated with lower risk of coronary heart disease (CHD) or total cardiovascular disease (CVD).^[40]

Homeostasis

Magnesium rich foods include cereals, green vegetables (with magnesium being a main component of chlorophyll), beans, and nuts.^[25] It is absorbed primarily in the small intestine via paracellular transport; passing between intestinal cells. Magnesium absorption in the large intestine is mediated by the transporters TRPM6 and TRPM7.^[25]

The body contains about 25 grams of magnesium.^[25] Of the body's magnesium, 50-60% is stored in bone, with the remainder, about 40-50%, being stored in muscle or soft tissue, with about 1% being in the plasma.^[41] Therefore, normal plasma levels of magnesium may sometimes be seen despite a person being in a state of magnesium deficiency and plasma magnesium levels may underestimate the level of deficiency. Plasma magnesium levels may more accurately reflect magnesium stores when consideration is also given to urinary magnesium losses and oral intake of magnesium. ^[25]

Inside cells, 90-95% of magnesium is bound to ligands, including ATP, ADP, citrate, other proteins and nucleic acids.^[25] In the plasma, 30% of magnesium is bound to proteins via free fatty acids, therefore elevated levels of free fatty acids are associated with hypomagnesemia as well as a possible risk of cardiovascular disease.^[25]

The kidneys regulate magnesium levels by reabsorbing magnesium from the tubules. In the proximal tubule (at the beginning of the nephron, the functional unit of the kidney) 20% of magnesium is reabsorbed via paracellular transport with claudin 2 and claudin 12 forming channels to allow for reabsorption.^[25] 70% of magnesium is reabsorbed in the thick ascending limb of the loop of Henle where claudins 16 and 19 form the channels to allow for reabsorption.^[25] In the distal convoluted tubule, 5-10% of magnesium is reabsorbed transcellularly (through the cells) via the transporters TRPM6 and TRPM7. Epidermal growth factor and insulin activate TRPM6 and 7 and increase magnesium levels via increased renal reabsorption.^[25]

Diagnosis

Magnesium deficiency or depletion is a low total body level of magnesium; it is not easy to measure directly.^[42]

Blood magnesium

Typically the diagnosis is based on finding hypomagnesemia, a low blood magnesium level,^[43] which often reflects low body magnesium;^[6] however, magnesium deficiency can be present without hypomagnesemia, and vice versa.^[42] A plasma magnesium concentration of less than 0.6 mmol/L (1.46 mg/dL) is considered to be hypomagnesemia;^[1] severe disease generally has a level of less than 0.5 mmol/L (1.25 mg/dL).^[2]

Electrocardiogram

The electrocardiogram (ECG) change may show a tachycardia with a prolonged QT interval.^[44] Other changes may include prolonged PR interval, ST segment depression, flipped T waves, and long QRS duration.^[1]

Treatments

Treatment of magnesium deficiency depends on the degree of deficiency and the clinical effects. Replacement by mouth is appropriate for people with mild symptoms, while intravenous replacement is recommended for people with severe effects.^[45]

Numerous oral magnesium preparations are available. In two trials of magnesium oxide, one of the most common forms in magnesium dietary supplements because of its high magnesium content per weight, was found to be less bioavailable than magnesium citrate, chloride, lactate or aspartate.^[46]^[47] Amino-acid chelate was also less bioavailable.^[48]

Intravenous magnesium sulfate (MgSO₄) can be given in response to heart arrhythmias to correct for hypokalemia, preventing pre-eclampsia, and has been suggested as having a potential use in asthma.^[1]

Food

Food sources of magnesium include leafy green vegetables, beans, nuts, and seeds.^[49]

Epidemiology

Hypomagnesemia may be seen in 3-10% of the general population.^[25] It is present in an estimated 10-30% of people with diabetes, 10-60% of hospitalized people and greater than 65% of people in the ICU.^[25]^[2] In hospitalized patients, hypomagnesemia is associated with an increased length of stay. And in those in an ICU, it is associated with a higher risk of requiring mechanical ventilation, and death.^[50]^[51] In population based cohort studies, chronic magnesium deficiency was associated with an increased risk of cardiovascular death and overall death.^[25]^[52]

History

Magnesium deficiency in humans was first described in the medical literature in 1934.^[53]

Plants

Magnesium deficiency is a detrimental plant disorder that occurs most often in strongly acidic, light, sandy soils, where magnesium can be easily leached away. Magnesium is an essential macronutrient constituting 0.2-0.4% of plants' dry matter and is necessary for normal plant growth.^[54] Excess potassium, generally due to fertilizers, further aggravates the stress from magnesium deficiency,^[55] as does aluminium toxicity.^[56]

Magnesium has an important role in photosynthesis because it forms the central atom of chlorophyll.^[54] Therefore, without sufficient amounts of magnesium, plants begin to degrade the chlorophyll in the old leaves. This causes the main symptom of magnesium deficiency, interveinal chlorosis, or yellowing between leaf veins, which stay green, giving the leaves a marbled appearance. Due to magnesium's mobile nature, the plant will first break down chlorophyll in older leaves and transport the Mg to younger leaves which have greater photosynthetic needs. Therefore, the first sign of magnesium deficiency is the chlorosis of old leaves which progresses to the young leaves as the deficiency progresses.^[57] Magnesium also acts as an activator for many critical enzymes, including ribulosebisphosphate carboxylase (RuBisCO) and phosphoenolpyruvate carboxylase (PEPC), both essential enzymes in carbon fixation. Thus low amounts of Mg lead to a decrease in photosynthetic and enzymatic activity within the plants. Magnesium is also crucial in stabilizing ribosome structures, hence, a lack of magnesium causes depolymerization of ribosomes leading to premature aging of the plant.^[54] After prolonged magnesium deficiency, necrosis and dropping of older leaves occurs. Plants deficient in magnesium also produce smaller, woodier fruits.

Magnesium deficiency in plants may be confused with zinc or chlorine deficiencies, viruses, or natural aging, since all have similar symptoms. Adding Epsom salts (as a solution of 25 grams per liter or 4 oz per gal) or crushed dolomitic limestone to the soil can rectify magnesium deficiencies. An organic treatment is to apply compost mulch, which can prevent leaching during excessive rainfall and provide plants with sufficient amounts of nutrients, including magnesium.^[58]

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^ "Abridged List Ordered by Nutrient Content in Household Measure Source: USDA National Nutrient Database for Standard Reference Legacy (2018) Nutrients: Magnesium, Mg(mg)" (PDF). United States Department of Agriculture. Retrieved May 20, 2020.
^ Upala S, Jaruvongvanich V, Wijarnpreecha K, Sanguankeo A (July 2016). "Hypomagnesemia and mortality in patients admitted to intensive care unit: a systematic review and meta-analysis". QJM. 109 (7): 453–459. doi:10.1093/qjmed/hcw048. PMID 27016536.
^ Peres IT, Hamacher S, Oliveira FL, Thomé AM, Bozza FA (December 2020). "What factors predict length of stay in the intensive care unit? Systematic review and meta-analysis". Journal of Critical Care. 60: 183–194. doi:10.1016/j.jcrc.2020.08.003. PMID 32841815.
^ Ye L, Zhang C, Duan Q, Shao Y, Zhou J (19 September 2023). "Association of Magnesium Depletion Score With Cardiovascular Disease and Its Association With Longitudinal Mortality in Patients With Cardiovascular Disease". Journal of the American Heart Association. 12 (18): e030077. doi:10.1161/JAHA.123.030077. PMC 10547298. PMID 37681518.
^ Hirschfelder AD, Haury VG (1934). "Clinical Manifestations of High and Low Plasma Magnesium; Dangers of Epsom Salt Purgation in Nephritis". Journal of the American Medical Association. 102 (14): 1138. doi:10.1001/jama.1934.02750140024010.
^ ^a ^b ^c Huner NP, Hopkins W (2008-11-07). "3 & 4". Introduction to Plant Physiology 4th Edition. John Wiley & Sons, Inc. ISBN 978-0-470-24766-2.
^ Ding Y, Chang C, Luo W (2008). "High Potassium Aggravates the Oxidative Stress Induced by Magnesium Deficiency in Rice Leaves". Pedosphere. 18 (3): 316–327. doi:10.1016/S1002-0160(08)60021-1.
^ Merhaut DJ (2006). "Magnesium". In Barker AV, Pilbeam DJ (eds.). Handbook of plant nutrition. Boca Raton: CRC Press. p. 154. ISBN 9780824759049.
^ Hermans C, Vuylsteke F, Coppens F (2010). "Systems Analysis of the responses to long-term magnesium deficiency and restoration in Arabidopsis thaliana". New Phytologist. 187 (1): 132–144. Bibcode:2010NewPh.187..132H. doi:10.1111/j.1469-8137.2010.03257.x. hdl:2066/83962. PMID 20412444.
^ "Problem Solving: Magnesium Deficiency". Gardeners' World Magazine. 6 March 2019.

External links

Magnesium

[EU2010-1] ^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j ^k ^l ^m ⁿ Soar J, Perkins GD, Abbas G, Alfonzo A, Barelli A, Bierens JJ, et al. (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): 1400–1433. doi:10.1016/j.resuscitation.2010.08.015. PMID 20956045.

[Mer2018-2] ^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j "Hypomagnesemia". Merck Manuals Professional Edition. Retrieved 27 October 2018.

[3] "Definition of Magnesium Deficiency". MedicineNet.com. Archived from the original on 31 May 2014. Retrieved 31 May 2014.

[:1-4] Baaij JH, Hoenderop JG, Bindels RJ (January 2015). "Magnesium in man: implications for health and disease". Physiological Reviews. 95 (1): 1–46. CiteSeerX 10.1.1.668.9777. doi:10.1152/physrev.00012.2014. PMID 25540137. S2CID 4999601.

[:2-5] Gommers LM, Hoenderop JG, Bindels RJ, de Baaij JH (January 2016). "Hypomagnesemia in Type 2 Diabetes: A Vicious Circle?". Diabetes. 65 (1): 3–13. doi:10.2337/db15-1028. PMID 26696633.

[Cecil2015-6] Goldman L, Schafer AI (2015). Goldman-Cecil Medicine E-Book. Elsevier Health Sciences. p. 775. ISBN 9780323322850.

[7] Yuen AW, Sander JW (June 2012). "Can magnesium supplementation reduce seizures in people with epilepsy? A hypothesis". Epilepsy Research. 100 (1–2): 152–156. doi:10.1016/j.eplepsyres.2012.02.004. PMID 22406257. S2CID 23147775.

[8] "Basal Ganglia Calcification with Hypomagnesemia". www.japi.org. Archived from the original on 2022-06-30. Retrieved 2021-06-03.

[:0-9] Viering DH, de Baaij JH, Walsh SB, Kleta R, Bockenhauer D (July 2017). "Genetic causes of hypomagnesemia, a clinical overview". Pediatric Nephrology. 32 (7): 1123–1135. doi:10.1007/s00467-016-3416-3. PMC 5440500. PMID 27234911.

[10] Piuri G, Zocchi M, Della Porta M, Ficara V, Manoni M, Zuccotti GV, Pinotti L, Maier JA, Cazzola R (February 2021). "Magnesium in Obesity, Metabolic Syndrome, and Type 2 Diabetes". Nutrients. 13 (2): 320. doi:10.3390/nu13020320. ISSN 2072-6643. PMC 7912442. PMID 33499378.

[11] DiNicolantonio JJ, O'Keefe JH, Wilson W (2018). "Subclinical magnesium deficiency: a principal driver of cardiovascular disease and a public health crisis". Open Heart. 5 (1): e000668. doi:10.1136/openhrt-2017-000668. PMC 5786912. PMID 29387426.

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[fda-14] "FDA Drug Safety Communication: Low magnesium levels can be associated with long-term use of Proton Pump Inhibitor drugs (PPIs)". fda.gov. F.D.A. U.S. Food and Drug Administration. Retrieved 8 November 2014.

[factsheet-15] "Magnesium: Fact Sheet for Health Professionals". nih.gov. National Institutes of Health. Retrieved 8 November 2014.

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[17] Gragossian A, Bashir K, Friede R (2021). "Hypomagnesemia". StatPearls. Treasure Island (FL): StatPearls Publishing. PMID 29763179. Retrieved 2021-06-03.

[18] "Proton Pump Inhibitor drugs (PPIs): Drug Safety Communication - Low Magnesium Levels Can Be Associated With Long-Term Use". www.fda.gov. Archived from the original on 2011-03-04.

[19] Sheen E, Triadafilopoulos G (April 2011). "Adverse effects of long-term proton pump inhibitor therapy". Digestive Diseases and Sciences. 56 (4): 931–950. doi:10.1007/s10620-010-1560-3. PMID 21365243. S2CID 34550326.

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[21] Viering D, Schlingmann KP, Hureaux M, Nijenhuis T, Mallett A, Chan MM, et al. (February 2022). "Gitelman-Like Syndrome Caused by Pathogenic Variants in mtDNA". Journal of the American Society of Nephrology. 33 (2): 305–325. doi:10.1681/ASN.2021050596. PMC 8819995. PMID 34607911.

[22] Chareonpong-Kawamoto N, Yasumoto K (February 1995). "Selenium deficiency as a cause of overload of iron and unbalanced distribution of other minerals". Bioscience, Biotechnology, and Biochemistry. 59 (2): 302–306. doi:10.1271/bbb.59.302. PMID 7766029.

[Johnson_2001_pp._163–170-23] Johnson S (2001). "The multifaceted and widespread pathology of magnesium deficiency". Medical Hypotheses. 56 (2). Elsevier BV: 163–170. doi:10.1054/mehy.2000.1133. ISSN 0306-9877. PMID 11425281.

[Al-Ghamdi_Cameron_Sutton_1994_pp._737–752-24] Al-Ghamdi SM, Cameron EC, Sutton RA (1994). "Magnesium Deficiency: Pathophysiologic and Clinical Overview". American Journal of Kidney Diseases. 24 (5). Elsevier BV: 737–752. doi:10.1016/s0272-6386(12)80667-6. ISSN 0272-6386. PMID 7977315.

[Touyz_2024-25] ^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j ^k ^l ^m ⁿ ^o ^p ^q ^r ^s ^t ^u ^v ^w ^x Touyz RM, de Baaij JH, Hoenderop JG (6 June 2024). "Magnesium Disorders". New England Journal of Medicine. 390 (21): 1998–2009. doi:10.1056/NEJMra1510603. PMID 38838313.

[26] Rivlin RS (October 1994). "Magnesium deficiency and alcohol intake: mechanisms, clinical significance and possible relation to cancer development (a review)". Journal of the American College of Nutrition. 13 (5): 416–423. doi:10.1080/07315724.1994.10718430. PMID 7836619.

[27] Gomella LG, Haist SA, eds. (2007). "Chapter 9. Fluids and Electrolytes". Clinician's Pocket Reference: The Scut Monkey (11th ed.). McGraw Hill. ISBN 978-0-07-145428-5.

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[29] Flink EB (December 1986). "Magnesium deficiency in alcoholism". Alcoholism: Clinical and Experimental Research. 10 (6): 590–594. doi:10.1111/j.1530-0277.1986.tb05150.x. PMID 3544909.

[30] Sihler KC, Napolitano LM (January 2010). "Complications of massive transfusion". Chest. 137 (1): 209–220. doi:10.1378/chest.09-0252. PMID 20051407.

[huang-31] Huang CL, Kuo E (October 2007). "Mechanism of hypokalemia in magnesium deficiency". Journal of the American Society of Nephrology. 18 (10): 2649–2652. doi:10.1681/ASN.2007070792. PMID 17804670.

[asthma-32] Mills R, Leadbeater M, Ravalia A (August 1997). "Intravenous magnesium sulphate in the management of refractory bronchospasm in a ventilated asthmatic". Anaesthesia. 52 (8): 782–785. doi:10.1111/j.1365-2044.1997.176-az0312.x. PMID 9291766.

[33] Maier JA, Locatelli L, Fedele G, Cazzaniga A, Mazur A (January 2023). "Magnesium and the Brain: A Focus on Neuroinflammation and Neurodegeneration". International Journal of Molecular Sciences. 24 (1): 223. doi:10.3390/ijms24010223. ISSN 1422-0067.

[diabetes-34] Pham PC, Pham PM, Pham SV, Miller JM, Pham PT (March 2007). "Hypomagnesemia in patients with type 2 diabetes". Clinical Journal of the American Society of Nephrology. 2 (2): 366–373. doi:10.2215/CJN.02960906. PMID 17699436.

[diabetes2-35] Pham PC, Pham PM, Pham SV, Miller JM, Pham PT (March 2007). "Hypomagnesemia in patients with type 2 diabetes". Clinical Journal of the American Society of Nephrology. 2 (2): 366–373. doi:10.1530/EJE-16-0517. PMID 17699436.

[diabetes-cvd-36] Oost LJ, van der Heijden AA, Vermeulen EA, Bos C, Elders PJ, Slieker RC, et al. (August 2021). "Serum Magnesium Is Inversely Associated With Heart Failure, Atrial Fibrillation, and Microvascular Complications in Type 2 Diabetes". Diabetes Care. 44 (8): 1757–1765. doi:10.2337/dc21-0236. PMID 34385344. S2CID 236991270.

[diabetes3-37] Rodríguez-Morán M, Guerrero-Romero F (April 2003). "Oral magnesium supplementation improves insulin sensitivity and metabolic control in type 2 diabetic subjects: a randomized double-blind controlled trial". Diabetes Care. 26 (4): 1147–1152. doi:10.2337/diacare.26.4.1147. PMID 12663588.

[diabetes4-38] Asbaghi O, Moradi S, Nezamoleslami S, Moosavian SP, Hojjati Kermani MA, Lazaridi AV, Miraghajani M (March 2021). "The Effects of Magnesium Supplementation on Lipid Profile Among Type 2 Diabetes Patients: a Systematic Review and Meta-analysis of Randomized Controlled Trials". Biological Trace Element Research. 199 (3): 861–873. Bibcode:2021BTER..199..861A. doi:10.1007/s12011-020-02209-5. PMID 32468224. S2CID 218978772.

[39] Verma H, Garg R (2 February 2017). "Effect of magnesium supplementation on type 2 diabetes associated cardiovascular risk factors: a systematic review and meta-analysis". Journal of Human Nutrition and Dietetics. 30 (5). Wiley: 621–633. doi:10.1111/jhn.12454. ISSN 0952-3871. PMID 28150351. S2CID 19778171.

[40] Fang X, Wang K, Han D, He X, Wei J, Zhao L, Imam MU, Ping Z, Li Y, Xu Y, Min J, Wang F (2016). "Dietary magnesium intake and the risk of cardiovascular disease, type 2 diabetes, and all-cause mortality: a dose–response meta-analysis of prospective cohort studies". BMC Medicine. 14 (1): 210. doi:10.1186/s12916-016-0742-z. ISSN 1741-7015. PMC 5143460. PMID 27927203.

[Jahnen-Dechent_2012-41] Jahnen-Dechent W, Ketteler M (1 February 2012). "Magnesium basics". Clinical Kidney Journal. 5 (Suppl 1): i3–i14. doi:10.1093/ndtplus/sfr163. PMC 4455825. PMID 26069819.

[Swam2003-42] Swaminathan R (May 2003). "Magnesium metabolism and its disorders". The Clinical Biochemist. Reviews. 24 (2): 47–66. PMC 1855626. PMID 18568054.

[43] Davis CP (29 March 2021). "Hypomagnesemia". Medterms medical dictionary a-z list. MedicineNet. Archived from the original on 31 May 2014. Retrieved 31 May 2014.

[44] Famularo G, Gasbarrone L, Minisola G (September 2013). "Hypomagnesemia and proton-pump inhibitors". Expert Opinion on Drug Safety. 12 (5): 709–716. doi:10.1517/14740338.2013.809062. PMID 23808631. S2CID 2726503.

[therapeutics-45] Durlach J, Durlach V, Bac P, Bara M, Guiet-Bara A (December 1994). "Magnesium and therapeutics". Magnesium Research. 7 (3–4): 313–328. PMID 7786695.

[Firoz2001-46] Firoz M, Graber M (December 2001). "Bioavailability of US commercial magnesium preparations". Magnesium Research. 14 (4): 257–262. PMID 11794633.

[Lindberg1990-47] Lindberg JS, Zobitz MM, Poindexter JR, Pak CY (February 1990). "Magnesium bioavailability from magnesium citrate and magnesium oxide". Journal of the American College of Nutrition. 9 (1): 48–55. doi:10.1080/07315724.1990.10720349. PMID 2407766.

[Walker2003-48] Walker AF, Marakis G, Christie S, Byng M (September 2003). "Mg citrate found more bioavailable than other Mg preparations in a randomised, double-blind study". Magnesium Research. 16 (3): 183–191. PMID 14596323.

[49] "Abridged List Ordered by Nutrient Content in Household Measure Source: USDA National Nutrient Database for Standard Reference Legacy (2018) Nutrients: Magnesium, Mg(mg)" (PDF). United States Department of Agriculture. Retrieved May 20, 2020.

[50] Upala S, Jaruvongvanich V, Wijarnpreecha K, Sanguankeo A (July 2016). "Hypomagnesemia and mortality in patients admitted to intensive care unit: a systematic review and meta-analysis". QJM. 109 (7): 453–459. doi:10.1093/qjmed/hcw048. PMID 27016536.

[Peres_2020-51] Peres IT, Hamacher S, Oliveira FL, Thomé AM, Bozza FA (December 2020). "What factors predict length of stay in the intensive care unit? Systematic review and meta-analysis". Journal of Critical Care. 60: 183–194. doi:10.1016/j.jcrc.2020.08.003. PMID 32841815.

[Ye_2023-52] Ye L, Zhang C, Duan Q, Shao Y, Zhou J (19 September 2023). "Association of Magnesium Depletion Score With Cardiovascular Disease and Its Association With Longitudinal Mortality in Patients With Cardiovascular Disease". Journal of the American Heart Association. 12 (18): e030077. doi:10.1161/JAHA.123.030077. PMC 10547298. PMID 37681518.

[53] Hirschfelder AD, Haury VG (1934). "Clinical Manifestations of High and Low Plasma Magnesium; Dangers of Epsom Salt Purgation in Nephritis". Journal of the American Medical Association. 102 (14): 1138. doi:10.1001/jama.1934.02750140024010.

[HunerHopkins2009-54] Huner NP, Hopkins W (2008-11-07). "3 & 4". Introduction to Plant Physiology 4th Edition. John Wiley & Sons, Inc. ISBN 978-0-470-24766-2.

[Ding,Y.,C.Chang_W.Luoetal.2008-55] Ding Y, Chang C, Luo W (2008). "High Potassium Aggravates the Oxidative Stress Induced by Magnesium Deficiency in Rice Leaves". Pedosphere. 18 (3): 316–327. doi:10.1016/S1002-0160(08)60021-1.

[56] Merhaut DJ (2006). "Magnesium". In Barker AV, Pilbeam DJ (eds.). Handbook of plant nutrition. Boca Raton: CRC Press. p. 154. ISBN 9780824759049.

[Hermans,C.,M.Vuylsteke,F.Coppens_et_al._2010-57] Hermans C, Vuylsteke F, Coppens F (2010). "Systems Analysis of the responses to long-term magnesium deficiency and restoration in Arabidopsis thaliana". New Phytologist. 187 (1): 132–144. Bibcode:2010NewPh.187..132H. doi:10.1111/j.1469-8137.2010.03257.x. hdl:2066/83962. PMID 20412444.

[58] "Problem Solving: Magnesium Deficiency". Gardeners' World Magazine. 6 March 2019.

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@@ Line 26: / Line 26: @@
 }}
 <!-- Definition and symptoms -->
-'''Magnesium deficiency''' is an [[electrolyte disturbance]] in which there is a low level of [[magnesium]] in the body. It can result in multiple symptoms.<ref>{{cite web|title=Definition of Magnesium Deficiency|url=http://www.medterms.com/script/main/art.asp?articlekey=4244|publisher=MedicineNet.com|access-date=31 May 2014|archive-date=31 May 2014|archive-url=https://web.archive.org/web/20140531090430/http://www.medterms.com/script/main/art.asp?articlekey=4244|url-status=dead}}</ref> Symptoms include [[tremor]], poor coordination, muscle spasms, loss of appetite, personality changes, and [[nystagmus]].<ref name=EU2010/><ref name=Mer2018/> Complications may include [[seizures]] or [[cardiac arrest]] such as from [[torsade de pointes]].<ref name=EU2010/> Those with low magnesium often have [[low potassium]].<ref name=EU2010/>
+'''Magnesium deficiency''' is an [[electrolyte disturbance]] in which there is a low level of [[magnesium]] in the body.<ref>{{cite web|title=Definition of Magnesium Deficiency|url=http://www.medterms.com/script/main/art.asp?articlekey=4244|publisher=MedicineNet.com|access-date=31 May 2014|archive-date=31 May 2014|archive-url=https://web.archive.org/web/20140531090430/http://www.medterms.com/script/main/art.asp?articlekey=4244|url-status=dead}}</ref> Symptoms include [[tremor]], poor coordination, [[muscle spasms]], [[loss of appetite]], [[Personality change|personality changes]], and [[nystagmus]].<ref name=EU2010/><ref name=Mer2018/> Complications may include [[seizures]] or [[cardiac arrest]] such as from [[torsade de pointes]].<ref name=EU2010/> Those with low magnesium often have [[low potassium]].<ref name=EU2010/>
 <!-- Cause and diagnosis -->
-Causes include low dietary intake, [[alcoholism]], [[diarrhea]], increased urinary loss, [[malabsorption|poor absorption from the intestines]], and [[diabetes mellitus]].<ref name=EU2010>{{cite journal | vauthors = 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 | display-authors = 6 | title = 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 | journal = Resuscitation | volume = 81 | issue = 10 | pages = 1400–1433 | date = October 2010 | pmid = 20956045 | doi = 10.1016/j.resuscitation.2010.08.015 }}</ref><ref>{{cite journal | vauthors = de Baaij JH, Hoenderop JG, Bindels RJ | title = Magnesium in man: implications for health and disease | journal = Physiological Reviews | volume = 95 | issue = 1 | pages = 1–46 | date = January 2015 | pmid = 25540137 | doi = 10.1152/physrev.00012.2014 | citeseerx = 10.1.1.668.9777 | s2cid = 4999601 }}</ref><ref>{{cite journal | vauthors = Gommers LM, Hoenderop JG, Bindels RJ, de Baaij JH | title = Hypomagnesemia in Type 2 Diabetes: A Vicious Circle? | journal = Diabetes | volume = 65 | issue = 1 | pages = 3–13 | date = January 2016 | pmid = 26696633 | doi = 10.2337/db15-1028 | doi-access = free }}</ref> A number of medications may also cause low magnesium, including [[proton pump inhibitors]] (PPIs) and [[furosemide]].<ref name=Mer2018/> The diagnosis is typically based on finding low blood magnesium levels (hypomagnesemia).<ref name=Cecil2015>{{cite book | vauthors = Goldman L, Schafer AI |title=Goldman-Cecil Medicine E-Book |date=2015 |publisher=Elsevier Health Sciences |isbn=9780323322850 |page=775 |url=https://books.google.com/books?id=40Z9CAAAQBAJ&pg=PA101-IA176 |language=en}}</ref> Normal magnesium levels are between 0.6 and 1.1&nbsp;mmol/L (1.46–2.68&nbsp;mg/dL) with levels less than 0.6&nbsp;mmol/L (1.46&nbsp;mg/dL) defining hypomagnesemia.<ref name=EU2010/> Specific [[electrocardiogram]] (ECG) changes may be seen.<ref name=EU2010/>
+Causes include low dietary intake, [[alcoholism]], [[diarrhea]], increased urinary loss, and [[malabsorption|poor absorption from the intestines.]]<ref name=EU2010>{{cite journal | vauthors = 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 | display-authors = 6 | title = 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 | journal = Resuscitation | volume = 81 | issue = 10 | pages = 1400–1433 | date = October 2010 | pmid = 20956045 | doi = 10.1016/j.resuscitation.2010.08.015 }}</ref><ref name=":1">{{cite journal | vauthors = de Baaij JH, Hoenderop JG, Bindels RJ | title = Magnesium in man: implications for health and disease | journal = Physiological Reviews | volume = 95 | issue = 1 | pages = 1–46 | date = January 2015 | pmid = 25540137 | doi = 10.1152/physrev.00012.2014 | citeseerx = 10.1.1.668.9777 | s2cid = 4999601 }}</ref><ref name=":2">{{cite journal | vauthors = Gommers LM, Hoenderop JG, Bindels RJ, de Baaij JH | title = Hypomagnesemia in Type 2 Diabetes: A Vicious Circle? | journal = Diabetes | volume = 65 | issue = 1 | pages = 3–13 | date = January 2016 | pmid = 26696633 | doi = 10.2337/db15-1028 | doi-access = free }}</ref> Some medications may also cause low magnesium, including [[proton pump inhibitors]] (PPIs) and [[furosemide]].<ref name=Mer2018/> The diagnosis is typically based on finding low blood magnesium levels, also called '''hypomagnesemia'''.<ref name=Cecil2015>{{cite book | vauthors = Goldman L, Schafer AI |title=Goldman-Cecil Medicine E-Book |date=2015 |publisher=Elsevier Health Sciences |isbn=9780323322850 |page=775 |url=https://books.google.com/books?id=40Z9CAAAQBAJ&pg=PA101-IA176 |language=en}}</ref> Normal magnesium levels are between 0.6 and 1.1&nbsp;mmol/L (1.46–2.68&nbsp;mg/dL) with levels less than 0.6&nbsp;mmol/L (1.46&nbsp;mg/dL) defining hypomagnesemia.<ref name=EU2010/> Specific [[electrocardiogram]] (ECG) changes may be seen.<ref name=EU2010/>
 <!-- Treatment and epidemiology -->
@@ Line 36: / Line 36: @@
 ==Signs and symptoms==
-Deficiency of magnesium can cause tiredness, generalized weakness, [[Cramp|muscle cramps]], [[cardiac arrhythmia|abnormal heart rhythms]], increased irritability of the [[nervous system]] with [[tremor]]s, [[paresthesia]]s, [[palpitations]], [[hypokalemia|low potassium levels in the blood]], [[hypoparathyroidism]] which might result in [[Hypocalcaemia|low calcium levels in the blood]], [[chondrocalcinosis]], [[spasticity]] and [[tetany]], [[migraine]]s,<ref>{{Cite web|date=2021-04-26|title=Finding the Best Magnesium Supplements for Migraine|url=https://www.migraineagain.com/magnesium-supplements-for-migraine-management/|access-date=2021-06-03|website=Migraine Again|language=en-US}}</ref> [[epileptic seizure]]s,<ref>{{cite journal | vauthors = Yuen AW, Sander JW | title = Can magnesium supplementation reduce seizures in people with epilepsy? A hypothesis | journal = Epilepsy Research | volume = 100 | issue = 1–2 | pages = 152–156 | date = June 2012 | pmid = 22406257 | doi = 10.1016/j.eplepsyres.2012.02.004 | s2cid = 23147775 }}</ref> [[Primary familial brain calcification|basal ganglia calcifications]]<ref>{{Cite web|title=Basal Ganglia Calcification with Hypomagnesemia|url=https://www.japi.org/t284a4c4/basal-ganglia-calcification-with-hypomagnesemia#:~:text=2%20Thus%20magnesium%20deficiency%20causes,nephrocalcinosis%20and%20basal%20ganglia%20calcification.|access-date=2021-06-03|website=www.japi.org|archive-date=2022-06-30|archive-url=https://web.archive.org/web/20220630001649/https://www.japi.org/t284a4c4/basal-ganglia-calcification-with-hypomagnesemia#:~:text=2%20Thus%20magnesium%20deficiency%20causes,nephrocalcinosis%20and%20basal%20ganglia%20calcification.|url-status=dead}}</ref> and in extreme and prolonged cases [[coma]], [[intellectual disability]] or death.<ref name=":0">{{cite journal | vauthors = Viering DH, de Baaij JH, Walsh SB, Kleta R, Bockenhauer D | title = Genetic causes of hypomagnesemia, a clinical overview | journal = Pediatric Nephrology | volume = 32 | issue = 7 | pages = 1123–1135 | date = July 2017 | pmid = 27234911 | pmc = 5440500 | doi = 10.1007/s00467-016-3416-3 }}</ref> Magnesium plays an important role in carbohydrate metabolism and its deficiency may worsen [[insulin resistance]], a condition that often precedes diabetes, or may be a consequence of insulin resistance.<ref name="pmid2255809">{{cite journal | vauthors = Kobrin SM, Goldfarb S | title = Magnesium deficiency | journal = Seminars in Nephrology | volume = 10 | issue = 6 | pages = 525–535 | date = November 1990 | pmid = 2255809 }}</ref>
+Deficiency of magnesium can cause [[tiredness]], generalized weakness, [[Cramp|muscle cramps]], [[cardiac arrhythmia|abnormal heart rhythms]], increased irritability of the [[nervous system]] with [[tremor]]s, [[paresthesia]]s, [[palpitations]], [[hypokalemia|low potassium levels in the blood]], [[hypoparathyroidism]] which might result in [[Hypocalcaemia|low calcium levels in the blood]], [[chondrocalcinosis]], [[spasticity]] and [[tetany]], [[migraine]]s, [[epileptic seizure]]s,<ref>{{cite journal | vauthors = Yuen AW, Sander JW | title = Can magnesium supplementation reduce seizures in people with epilepsy? A hypothesis | journal = Epilepsy Research | volume = 100 | issue = 1–2 | pages = 152–156 | date = June 2012 | pmid = 22406257 | doi = 10.1016/j.eplepsyres.2012.02.004 | s2cid = 23147775 }}</ref> [[Primary familial brain calcification|basal ganglia calcifications]]<ref>{{Cite web|title=Basal Ganglia Calcification with Hypomagnesemia|url=https://www.japi.org/t284a4c4/basal-ganglia-calcification-with-hypomagnesemia#:~:text=2%20Thus%20magnesium%20deficiency%20causes,nephrocalcinosis%20and%20basal%20ganglia%20calcification.|access-date=2021-06-03|website=www.japi.org|archive-date=2022-06-30|archive-url=https://web.archive.org/web/20220630001649/https://www.japi.org/t284a4c4/basal-ganglia-calcification-with-hypomagnesemia#:~:text=2%20Thus%20magnesium%20deficiency%20causes,nephrocalcinosis%20and%20basal%20ganglia%20calcification.|url-status=dead}}</ref> and in extreme and prolonged cases [[coma]], [[intellectual disability]] or death.<ref name=":0">{{cite journal | vauthors = Viering DH, de Baaij JH, Walsh SB, Kleta R, Bockenhauer D | title = Genetic causes of hypomagnesemia, a clinical overview | journal = Pediatric Nephrology | volume = 32 | issue = 7 | pages = 1123–1135 | date = July 2017 | pmid = 27234911 | pmc = 5440500 | doi = 10.1007/s00467-016-3416-3 }}</ref> Magnesium deficiency is strongly associated with and appears to contribute to [[obesity]], [[insulin resistance]], [[metabolic syndrome]], and [[type 2 diabetes]], although the causal mechanism is not fully understood.<ref>{{Cite journal |last1=Piuri |first1=Gabriele |last2=Zocchi |first2=Monica |last3=Della Porta |first3=Matteo |last4=Ficara |first4=Valentina |last5=Manoni |first5=Michele |last6=Zuccotti |first6=Gian Vincenzo |last7=Pinotti |first7=Luciano |last8=Maier |first8=Jeanette A. |last9=Cazzola |first9=Roberta |date=February 2021 |title=Magnesium in Obesity, Metabolic Syndrome, and Type 2 Diabetes |journal=Nutrients |language=en |volume=13 |issue=2 |pages=320 |doi=10.3390/nu13020320 |doi-access=free |pmid=33499378 |pmc=7912442 |issn=2072-6643}}</ref><ref name=":1" /><ref name=":2" />
 ==Causes==
-Magnesium deficiency may result from gastrointestinal or kidney causes. Gastrointestinal causes include low dietary intake of magnesium, reduced gastrointestinal absorption or increased gastrointestinal loss due to rapid gastrointestinal transits. Kidney causes involve increased excretion of magnesium. Poor dietary intake of magnesium has become an increasingly important factor &ndash; many people consume diets high in refined foods such as white bread and polished rice which have been stripped of magnesium-rich plant fiber.<ref>{{cite journal | vauthors = DiNicolantonio JJ, O'Keefe JH, Wilson W | title = Subclinical magnesium deficiency: a principal driver of cardiovascular disease and a public health crisis | journal = Open Heart | volume = 5 | issue = 1 | pages = e000668 | date = 2018 | pmid = 29387426 | pmc = 5786912 | doi = 10.1136/openhrt-2017-000668 }}</ref>
+Magnesium deficiency may result from gastrointestinal or kidney causes. Gastrointestinal causes include low dietary intake of magnesium, reduced gastrointestinal absorption or increased gastrointestinal loss due to rapid [[Gastrointestinal transit|gastrointestinal transits]]. Kidney causes involve increased excretion of magnesium. Poor dietary intake of magnesium has become an increasingly important factor: many people consume diets high in [[Refined food|refined foods]] such as [[white bread]] and [[polished rice]] which have been stripped of magnesium-rich [[plant fiber]].<ref>{{cite journal | vauthors = DiNicolantonio JJ, O'Keefe JH, Wilson W | title = Subclinical magnesium deficiency: a principal driver of cardiovascular disease and a public health crisis | journal = Open Heart | volume = 5 | issue = 1 | pages = e000668 | date = 2018 | pmid = 29387426 | pmc = 5786912 | doi = 10.1136/openhrt-2017-000668 }}</ref>
-Magnesium deficiency is not uncommon in hospitalized patients. Up to 12% of all people admitted to [[hospital]], and as high as 60–65% of people in an intensive care unit, have hypomagnesemia.<ref name="pmid10405219">{{cite journal | vauthors = Agus ZS | title = Hypomagnesemia | journal = Journal of the American Society of Nephrology | volume = 10 | issue = 7 | pages = 1616–1622 | date = July 1999 | pmid = 10405219 | doi = 10.1681/ASN.V1071616 | doi-access = free }}</ref>
+Magnesium deficiency is common in hospitalized patients. Up to 12% of all people admitted to [[hospital]], and as high as 60–65% of people in an [[intensive care unit]] (ICU), have hypomagnesemia.<ref name="pmid10405219">{{cite journal | vauthors = Agus ZS | title = Hypomagnesemia | journal = Journal of the American Society of Nephrology | volume = 10 | issue = 7 | pages = 1616–1622 | date = July 1999 | pmid = 10405219 | doi = 10.1681/ASN.V1071616 | doi-access = free }}</ref>
-About 57% of the US population does not meet the US [[Dietary Reference Intake|RDA]] for dietary intake of magnesium.<ref>{{cite web |url=http://www.ars.usda.gov/Services/docs.htm?docid=15672 |title=Nutrient Intakes Percent of population 2 years old and over with adequate intakes based on average requirement |access-date=2012-02-11 |date=2009-07-29 |work=Community Nutrition Mapping Project}}</ref> The kidneys are very efficient at maintaining body levels; however, if the diet is deficient, or certain medications such as diuretics or proton pump inhibitors are used,<ref name=fda>{{cite web|title=FDA Drug Safety Communication: Low magnesium levels can be associated with long-term use of Proton Pump Inhibitor drugs (PPIs)|url=https://www.fda.gov/drugs/drugsafety/ucm245011.htm|website=fda.gov|publisher=F.D.A. U.S. Food and Drug Administration|access-date=8 November 2014}}</ref> or in chronic alcoholism,<ref name=factsheet/> levels may drop.
+About 57% of the US population does not meet the US [[Dietary Reference Intake|RDA]] for dietary intake of magnesium.<ref>{{cite web |url=http://www.ars.usda.gov/Services/docs.htm?docid=15672 |title=Nutrient Intakes Percent of population 2 years old and over with adequate intakes based on average requirement |access-date=2012-02-11 |date=2009-07-29 |work=Community Nutrition Mapping Project}}</ref> Kidneys are very efficient at maintaining body levels; however, if the diet is deficient, or certain medications such as [[Diuretic|diuretics]] or proton pump inhibitors are used,<ref name=fda>{{cite web|title=FDA Drug Safety Communication: Low magnesium levels can be associated with long-term use of Proton Pump Inhibitor drugs (PPIs)|url=https://www.fda.gov/drugs/drugsafety/ucm245011.htm|website=fda.gov|publisher=F.D.A. U.S. Food and Drug Administration|access-date=8 November 2014}}</ref> or in chronic [[alcoholism]],<ref name=factsheet/> levels may drop.
 Deficiencies may be due to the following conditions:
 ===Medications===
-* [[Loop diuretic|Loop]] and [[thiazide diuretic]] use (the most common cause of hypomagnesemia)<ref name="homeo">{{cite journal | vauthors = Whang R, Hampton EM, Whang DD | title = Magnesium homeostasis and clinical disorders of magnesium deficiency | journal = The Annals of Pharmacotherapy | volume = 28 | issue = 2 | pages = 220–226 | date = February 1994 | pmid = 8173141 | doi = 10.1177/106002809402800213 | s2cid = 23442909 }}</ref>
+* [[Loop diuretic|Loop]] and [[thiazide diuretic]] use (the most common cause of hypomagnesemia),<ref name="homeo">{{cite journal | vauthors = Whang R, Hampton EM, Whang DD | title = Magnesium homeostasis and clinical disorders of magnesium deficiency | journal = The Annals of Pharmacotherapy | volume = 28 | issue = 2 | pages = 220–226 | date = February 1994 | pmid = 8173141 | doi = 10.1177/106002809402800213 | s2cid = 23442909 }}</ref>
-* Antibiotics (i.e. [[aminoglycoside]], [[amphotericin]], [[pentamidine]], [[gentamicin]], [[tobramycin]], [[viomycin]]) block resorption in the loop of Henle. 30% of patients using these antibiotics have hypomagnesemia.<ref>{{cite book | vauthors = Gragossian A, Bashir K, Friede R | chapter = Hypomagnesemia|date=2021| chapter-url= http://www.ncbi.nlm.nih.gov/books/NBK500003/ | title = StatPearls|place=Treasure Island (FL)|publisher=StatPearls Publishing|pmid=29763179|access-date=2021-06-03 }}</ref>
+* Antibiotics (i.e. [[aminoglycoside]], [[amphotericin]], [[pentamidine]], [[gentamicin]], [[tobramycin]], [[viomycin]]) block resorption in the [[loop of Henle]]. 30% of patients using these antibiotics have hypomagnesemia,<ref>{{cite book | vauthors = Gragossian A, Bashir K, Friede R | chapter = Hypomagnesemia|date=2021| chapter-url= http://www.ncbi.nlm.nih.gov/books/NBK500003/ | title = StatPearls|place=Treasure Island (FL)|publisher=StatPearls Publishing|pmid=29763179|access-date=2021-06-03 }}</ref>
-* Long term, high dosage use of proton-pump inhibitors such as [[omeprazole]]<ref>{{cite web |url=https://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm245275.htm |title=Proton Pump Inhibitor drugs (PPIs): Drug Safety Communication - Low Magnesium Levels Can Be Associated With Long-Term Use |website=www.fda.gov |url-status=dead |archive-url=https://web.archive.org/web/20110304093609/http://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm245275.htm |archive-date=2011-03-04}}</ref><ref>{{cite journal | vauthors = Sheen E, Triadafilopoulos G | title = Adverse effects of long-term proton pump inhibitor therapy | journal = Digestive Diseases and Sciences | volume = 56 | issue = 4 | pages = 931–950 | date = April 2011 | pmid = 21365243 | doi = 10.1007/s10620-010-1560-3 | s2cid = 34550326 }}</ref>
+* Long term, high dosage use of proton-pump inhibitors such as [[omeprazole]],<ref>{{cite web |url=https://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm245275.htm |title=Proton Pump Inhibitor drugs (PPIs): Drug Safety Communication - Low Magnesium Levels Can Be Associated With Long-Term Use |website=www.fda.gov |url-status=dead |archive-url=https://web.archive.org/web/20110304093609/http://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm245275.htm |archive-date=2011-03-04}}</ref><ref>{{cite journal | vauthors = Sheen E, Triadafilopoulos G | title = Adverse effects of long-term proton pump inhibitor therapy | journal = Digestive Diseases and Sciences | volume = 56 | issue = 4 | pages = 931–950 | date = April 2011 | pmid = 21365243 | doi = 10.1007/s10620-010-1560-3 | s2cid = 34550326 }}</ref>
-* Other drugs
+* Other drugs:
-** [[Digitalis]], displaces magnesium into the cell. Digitalis causes an increased intracellular concentration of sodium, which in turn increases intracellular calcium by passively increasing the action of the sodium-calcium exchanger in the [[sarcolemma]]. The increased intracellular calcium gives a positive [[inotropic]] effect.<ref name="homeo" />
+** [[Digitalis]], displaces magnesium into the cell. Digitalis causes an increased intracellular concentration of sodium, which in turn increases intracellular calcium by passively increasing the action of the sodium-calcium exchanger in the [[sarcolemma]]. The increased intracellular calcium gives a positive [[inotropic]] effect,<ref name="homeo" />
-** [[Adrenergics]], displace magnesium into the cell
+** [[Adrenergics]], displace magnesium into the cell,
-** [[Cisplatin]], stimulates kidney excretion
+** [[Cisplatin]], stimulates kidney excretion,
-** [[Ciclosporin]], stimulates kidney excretion
+** [[Ciclosporin]], stimulates kidney excretion,
-** [[Mycophenolate mofetil]]
+** [[Mycophenolate mofetil]].
 === Genetics ===
-* [[Gitelman syndrome|Gitelman]]-like diseases, which include the syndromes caused by [[genetic mutations]] in ''[[Sodium-chloride symporter|SLC12A3]]'', ''[[CLCNKB|CLNCKB]]'',<ref name="cameron" /> ''[[BSND]]'', ''[[KCNJ10]]'', ''[[FXYD2]]'', ''[[HNF1B]]'' or ''[[PCBD1]]''. In these diseases, the hypomagnesemia is accompanied by other defects in electrolyte handling such as hypocalciuria and [[hypokalemia]]. The genes involved in this group of diseases all encode proteins that are involved in reabsorbing electrolytes (including magnesium) in the [[distal convoluted tubule]] of the kidney.<ref name=":0" />
+* [[Gitelman syndrome|Gitelman]]-like diseases, which include the syndromes caused by [[genetic mutations]] in ''[[Sodium-chloride symporter|SLC12A3]]'', ''[[CLCNKB|CLNCKB]]'',<ref name="cameron" /> ''[[BSND]]'', ''[[KCNJ10]]'', ''[[FXYD2]]'', ''[[HNF1B]]'' or ''[[PCBD1]]''. In these diseases, the hypomagnesemia is accompanied by other defects in electrolyte handling such as [[hypocalciuria]] and [[hypokalemia]]. The genes involved in this group of diseases all encode proteins that are involved in reabsorbing electrolytes (including magnesium) in the [[distal convoluted tubule]] of the kidney,<ref name=":0" />
-* [[Hypercalciuria|Hypercalciuric]] hypomagnesemic syndromes, which encompass the syndromes caused by mutations in ''[[CLDN16]]'', ''[[CLDN19]]'', ''[[Calcium-sensing receptor|CASR]]'' or ''[[CLCNKB]]''. In these diseases, reabsorption of [[Cations, divalent|divalent cations]] (such as magnesium and calcium) in the [[Thick ascending limb of loop of Henle|thick ascending limb of Henle's loop]] of the kidney is impaired. This results in loss of magnesium and calcium in the urine.<ref name=":0" />
+* [[Hypercalciuria|Hypercalciuric]] hypomagnesemic syndromes, which encompass the syndromes caused by mutations in ''[[CLDN16]]'', ''[[CLDN19]]'', ''[[Calcium-sensing receptor|CASR]]'' or ''[[CLCNKB]]''. In these diseases, reabsorption of [[Cations, divalent|divalent cations]] (such as magnesium and calcium) in the [[Thick ascending limb of loop of Henle|thick ascending limb of Henle's loop]] of the kidney is impaired. This results in loss of magnesium and calcium in the urine,<ref name=":0" />
-* [[Mitochondrial disease|Mitochondriopathies]], especially mutations in the mitochondrial tRNAs ''[[MT-TI]]'' or ''[[MT-TF]].''<ref>{{cite journal | vauthors = Viering D, Schlingmann KP, Hureaux M, Nijenhuis T, Mallett A, Chan MM, van Beek A, van Eerde AM, Coulibaly JM, Vallet M, Decramer S, Pelletier S, Klaus G, Kömhoff M, Beetz R, Patel C, Shenoy M, Steenbergen EJ, Anderson G, Bongers EM, Bergmann C, Panneman D, Rodenburg RJ, Kleta R, Houillier P, Konrad M, Vargas-Poussou R, Knoers NV, Bockenhauer D, de Baaij JH | display-authors = 6 | title = Gitelman-Like Syndrome Caused by Pathogenic Variants in mtDNA | journal = Journal of the American Society of Nephrology | volume = 33 | issue = 2 | pages = 305–325 | date = February 2022 | pmid = 34607911 | pmc = 8819995 | doi = 10.1681/ASN.2021050596 }}</ref> Mutations in ''[[SARS2]],'' or mitochondrial DNA deletions as seen with [[Kearns–Sayre syndrome|Kearns-Sayre syndrome]], can also cause hypomagnesemia.<ref name=":0" />
+* [[Mitochondrial disease|Mitochondriopathies]], especially mutations in the mitochondrial tRNAs ''[[MT-TI]]'' or ''[[MT-TF]].''<ref>{{cite journal | vauthors = Viering D, Schlingmann KP, Hureaux M, Nijenhuis T, Mallett A, Chan MM, van Beek A, van Eerde AM, Coulibaly JM, Vallet M, Decramer S, Pelletier S, Klaus G, Kömhoff M, Beetz R, Patel C, Shenoy M, Steenbergen EJ, Anderson G, Bongers EM, Bergmann C, Panneman D, Rodenburg RJ, Kleta R, Houillier P, Konrad M, Vargas-Poussou R, Knoers NV, Bockenhauer D, de Baaij JH | display-authors = 6 | title = Gitelman-Like Syndrome Caused by Pathogenic Variants in mtDNA | journal = Journal of the American Society of Nephrology | volume = 33 | issue = 2 | pages = 305–325 | date = February 2022 | pmid = 34607911 | pmc = 8819995 | doi = 10.1681/ASN.2021050596 }}</ref> Mutations in ''[[SARS2]],'' or mitochondrial DNA deletions as seen with [[Kearns–Sayre syndrome|Kearns-Sayre syndrome]], can also cause hypomagnesemia,<ref name=":0" />
-* Other genetic causes of hypomagnesemia, such as mutations in ''[[TRPM6]]'', ''[[CNNM2]]'', ''[[EGF (gene)|EGF]]'', ''[[EGFR (gene)|EGFR]]'', ''[[Kv1.1|KCNA1]]'' or ''[[FAM111A]]''. Many of the proteins encoded by these genes play a role in the [[Transcellular transport|transcellular]] absorption of magnesium in the distal convoluted tubule.<ref name=":0" />
+* Other genetic causes of hypomagnesemia, such as mutations in ''[[TRPM6]]'', ''[[CNNM2]]'', ''[[EGF (gene)|EGF]]'', ''[[EGFR (gene)|EGFR]]'', ''[[Kv1.1|KCNA1]]'' or ''[[FAM111A]]''. Many of the proteins encoded by these genes play a role in the [[Transcellular transport|transcellular]] absorption of magnesium in the distal convoluted tubule,<ref name=":0" />
 ===Metabolic abnormalities===
-* Insufficient [[selenium]],<ref>{{cite journal | vauthors = Chareonpong-Kawamoto N, Yasumoto K | title = Selenium deficiency as a cause of overload of iron and unbalanced distribution of other minerals | journal = Bioscience, Biotechnology, and Biochemistry | volume = 59 | issue = 2 | pages = 302–306 | date = February 1995 | pmid = 7766029 | doi = 10.1271/bbb.59.302 }}</ref> vitamin D or sunlight exposure, or [[vitamin B6]].<ref name="Johnson 2001 pp. 163–170">{{cite journal | last=Johnson | first=S. | title=The multifaceted and widespread pathology of magnesium deficiency | journal=Medical Hypotheses | publisher=Elsevier BV | volume=56 | issue=2 | year=2001 | issn=0306-9877 | doi=10.1054/mehy.2000.1133 | pages=163–170| pmid=11425281 }}</ref>
+* Insufficient [[selenium]],<ref>{{cite journal | vauthors = Chareonpong-Kawamoto N, Yasumoto K | title = Selenium deficiency as a cause of overload of iron and unbalanced distribution of other minerals | journal = Bioscience, Biotechnology, and Biochemistry | volume = 59 | issue = 2 | pages = 302–306 | date = February 1995 | pmid = 7766029 | doi = 10.1271/bbb.59.302 }}</ref> vitamin D or sunlight exposure, or [[vitamin B6]],<ref name="Johnson 2001 pp. 163–170">{{cite journal | last=Johnson | first=S. | title=The multifaceted and widespread pathology of magnesium deficiency | journal=Medical Hypotheses | publisher=Elsevier BV | volume=56 | issue=2 | year=2001 | issn=0306-9877 | doi=10.1054/mehy.2000.1133 | pages=163–170| pmid=11425281 }}</ref>
-* Gastrointestinal causes: the distal digestive tract secretes high levels of magnesium. Therefore, secretory diarrhea can cause hypomagnesemia. Thus, [[Crohn's disease]], [[ulcerative colitis]], [[Whipple's disease]] and [[coeliac disease|celiac sprue]] can all cause hypomagnesemia.
+* Gastrointestinal causes: the distal digestive tract secretes high levels of magnesium. Therefore, secretory diarrhea can cause hypomagnesemia. Thus, [[Crohn's disease]], [[ulcerative colitis]], [[Whipple's disease]] and [[coeliac disease|celiac sprue]] can all cause hypomagnesemia,
-* Postobstructive diuresis, diuretic phase of [[acute tubular necrosis]] (ATN) and [[kidney transplant]].<ref name="Al-Ghamdi Cameron Sutton 1994 pp. 737–752">{{cite journal | last1=Al-Ghamdi | first1=Saeed M.G. | last2=Cameron | first2=Eugene C. | last3=Sutton | first3=Roger A.L. | title=Magnesium Deficiency: Pathophysiologic and Clinical Overview | journal=American Journal of Kidney Diseases | publisher=Elsevier BV | volume=24 | issue=5 | year=1994 | issn=0272-6386 | doi=10.1016/s0272-6386(12)80667-6 | pages=737–752| pmid=7977315 }}</ref>
+* Postobstructive diuresis, diuretic phase of [[acute tubular necrosis]] (ATN) and [[kidney transplant]],<ref name="Al-Ghamdi Cameron Sutton 1994 pp. 737–752">{{cite journal | last1=Al-Ghamdi | first1=Saeed M.G. | last2=Cameron | first2=Eugene C. | last3=Sutton | first3=Roger A.L. | title=Magnesium Deficiency: Pathophysiologic and Clinical Overview | journal=American Journal of Kidney Diseases | publisher=Elsevier BV | volume=24 | issue=5 | year=1994 | issn=0272-6386 | doi=10.1016/s0272-6386(12)80667-6 | pages=737–752| pmid=7977315 }}</ref>
 ===Other===
-* [[Chronic alcoholism]]: Alcohol intake leads to enhanced diuresis of electrolytes, possibly due to alcohol induced kidney tubular cell damage.<ref name="Touyz 2024" /> Hypomagnesemia is also thought to occur due to reduced magnesium intake due to malnutrition and increased gastrointestinal losses.<ref name="Touyz 2024" /><ref>{{cite journal | vauthors = Rivlin RS | title = Magnesium deficiency and alcohol intake: mechanisms, clinical significance and possible relation to cancer development (a review) | journal = Journal of the American College of Nutrition | volume = 13 | issue = 5 | pages = 416–423 | date = October 1994 | pmid = 7836619 | doi = 10.1080/07315724.1994.10718430 }}</ref><ref>{{cite book | chapter = Chapter 9. Fluids and Electrolytes | veditors = Gomella LG, Haist SA | date = 2007 | title = Clinician's Pocket Reference: The Scut Monkey | edition = 11th | publisher = McGraw Hill | chapter-url = https://accessmedicine.mhmedical.com/content.aspx?bookid=365&sectionid=43074918 | isbn = 978-0-07-145428-5 }}</ref><ref>{{cite book | vauthors = Desai S, Seidler M | date = 2017 | chapter = Metabolic & Endocrine Emergencies | veditors = Stone C, Humphries RL | title = Current Diagnosis & Treatment: Emergency Medicine | edition = 8th | publisher = McGraw Hill | chapter-url = https://accessmedicine.mhmedical.com/content.aspx?bookid=2172&sectionid=165068628 | isbn = 978-0-07-184061-3 }}</ref><ref>{{cite journal | vauthors = Flink EB | title = Magnesium deficiency in alcoholism | journal = Alcoholism: Clinical and Experimental Research | volume = 10 | issue = 6 | pages = 590–594 | date = December 1986 | pmid = 3544909 | doi = 10.1111/j.1530-0277.1986.tb05150.x }}</ref> Hypomagnesemia is the most common electrolyte abnormality in those with chronic alcoholism.<ref name="Touyz 2024" /> Chronic hypomagnesemia in those with chronic alcoholism is associated with liver disease and a worse prognosis.<ref name="Touyz 2024" />
+* [[Chronic alcoholism]]: Alcohol intake leads to enhanced diuresis of electrolytes, possibly due to alcohol induced kidney tubular cell damage.<ref name="Touyz 2024" /> Hypomagnesemia is also thought to occur due to reduced magnesium intake due to malnutrition and increased gastrointestinal losses.<ref name="Touyz 2024" /><ref>{{cite journal | vauthors = Rivlin RS | title = Magnesium deficiency and alcohol intake: mechanisms, clinical significance and possible relation to cancer development (a review) | journal = Journal of the American College of Nutrition | volume = 13 | issue = 5 | pages = 416–423 | date = October 1994 | pmid = 7836619 | doi = 10.1080/07315724.1994.10718430 }}</ref><ref>{{cite book | chapter = Chapter 9. Fluids and Electrolytes | veditors = Gomella LG, Haist SA | date = 2007 | title = Clinician's Pocket Reference: The Scut Monkey | edition = 11th | publisher = McGraw Hill | chapter-url = https://accessmedicine.mhmedical.com/content.aspx?bookid=365&sectionid=43074918 | isbn = 978-0-07-145428-5 }}</ref><ref>{{cite book | vauthors = Desai S, Seidler M | date = 2017 | chapter = Metabolic & Endocrine Emergencies | veditors = Stone C, Humphries RL | title = Current Diagnosis & Treatment: Emergency Medicine | edition = 8th | publisher = McGraw Hill | chapter-url = https://accessmedicine.mhmedical.com/content.aspx?bookid=2172&sectionid=165068628 | isbn = 978-0-07-184061-3 }}</ref><ref>{{cite journal | vauthors = Flink EB | title = Magnesium deficiency in alcoholism | journal = Alcoholism: Clinical and Experimental Research | volume = 10 | issue = 6 | pages = 590–594 | date = December 1986 | pmid = 3544909 | doi = 10.1111/j.1530-0277.1986.tb05150.x }}</ref> Hypomagnesemia is the most common electrolyte abnormality in those with chronic alcoholism.<ref name="Touyz 2024" /> Chronic hypomagnesemia in those with chronic alcoholism is associated with [[liver disease]] and a worse prognosis,<ref name="Touyz 2024" />
-* [[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 [[catecholamine]]s.
+* [[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 [[catecholamine]]s,
-* [[Malabsorption]]
+* [[Malabsorption]],
-* [[Acute pancreatitis]]
+* [[Acute pancreatitis]],
-* [[Fluoride toxicity|Fluoride poisoning]]
+* [[Fluoride toxicity|Fluoride poisoning]],
 * Massive transfusion (MT) is a lifesaving treatment of [[Hypovolemia|hemorrhagic shock]], but can be associated with significant complications.<ref>{{cite journal | vauthors = Sihler KC, Napolitano LM | title = Complications of massive transfusion | journal = Chest | volume = 137 | issue = 1 | pages = 209–220 | date = January 2010 | pmid = 20051407 | doi = 10.1378/chest.09-0252 }}</ref>
 ==Pathophysiology==
-Magnesium is ubiquitous in the human body as well as being present in all living organisms and the ion is a known co-factor in over known 300 enzymatic reactions including DNA and RNA replication, protein synthesis, acting as an essential co-factor of [[adenosine triphosphate|ATP]] during its phosphorylation via [[ATPase]]. It is also extensively involved in intracellular signaling.<ref name="cameron">{{cite journal | vauthors = al-Ghamdi SM, Cameron EC, Sutton RA | title = Magnesium deficiency: pathophysiologic and clinical overview | journal = American Journal of Kidney Diseases | volume = 24 | issue = 5 | pages = 737–752 | date = November 1994 | pmid = 7977315 | doi = 10.1016/s0272-6386(12)80667-6 }}</ref><ref name="Touyz 2024" /> It is involved in [[protein synthesis]], regulating gucose, lipid and protein metabolism, muscle and nerve functioning, vascular tone (affecting blood vessel contraction, thus helping to regulate blood pressure), bone development, energy production, the maintenance of normal heart rhythm, and the regulation of [[glucose]], among other important roles.<ref name=factsheet>{{cite web|title=Magnesium: Fact Sheet for Health Professionals|url=http://ods.od.nih.gov/factsheets/Magnesium-HealthProfessional/#en3|website=nih.gov|publisher=National Institutes of Health|access-date=8 November 2014}}</ref><ref name="Touyz 2024" /> Physiologically, it acts as a calcium antagonist.<ref name="Touyz 2024" /> Thus, the effects of low magnesium are widespread. Low magnesium intake over time can increase the risk of illnesses, including [[hypertension|high blood pressure]] and [[cardiovascular disease|heart disease]], [[diabetes mellitus type 2]], [[osteoporosis]], and [[migraine]]s.<ref name=factsheet/>
+Magnesium is ubiquitous in the human body as well as being present in all living organisms and the ion is a known co-factor in over known 300 enzymatic reactions including DNA and RNA replication, protein synthesis, acting as an essential co-factor of [[adenosine triphosphate|ATP]] during its phosphorylation via [[ATPase]]. It is also extensively involved in intracellular signaling.<ref name="cameron">{{cite journal | vauthors = al-Ghamdi SM, Cameron EC, Sutton RA | title = Magnesium deficiency: pathophysiologic and clinical overview | journal = American Journal of Kidney Diseases | volume = 24 | issue = 5 | pages = 737–752 | date = November 1994 | pmid = 7977315 | doi = 10.1016/s0272-6386(12)80667-6 }}</ref><ref name="Touyz 2024" /> It is involved in [[protein synthesis]], regulating glucose, lipid and protein metabolism, muscle and nerve functioning, vascular tone (affecting blood vessel contraction, thus helping to regulate blood pressure), bone development, energy production, the maintenance of normal heart rhythm, and the regulation of [[glucose]], among other important roles.<ref name=factsheet>{{cite web|title=Magnesium: Fact Sheet for Health Professionals|url=http://ods.od.nih.gov/factsheets/Magnesium-HealthProfessional/#en3|website=nih.gov|publisher=National Institutes of Health|access-date=8 November 2014}}</ref><ref name="Touyz 2024" /> Physiologically, it acts as a calcium antagonist.<ref name="Touyz 2024" /> Thus, the effects of low magnesium are widespread. Low magnesium intake over time can increase the risk of illnesses, including [[hypertension|high blood pressure]] and [[cardiovascular disease|heart disease]], [[diabetes mellitus type 2]], [[osteoporosis]], and [[migraine]]s.<ref name=factsheet/>
 Magnesium has several effects:
 ===Potassium===
-[[Potassium in biology|Potassium]] channel efflux is inhibited by magnesium. Thus hypomagnesemia results in an increased excretion of potassium in the kidney, resulting in [[hypokalemia]] (low potassium). This condition is believed to occur secondary to the decreased normal physiologic magnesium inhibition of the [[ROMK]] channels in the apical tubular membrane.<ref name="huang">{{cite journal | vauthors = Huang CL, Kuo E | title = Mechanism of hypokalemia in magnesium deficiency | journal = Journal of the American Society of Nephrology | volume = 18 | issue = 10 | pages = 2649–2652 | date = October 2007 | pmid = 17804670 | doi = 10.1681/ASN.2007070792 | doi-access = free }}</ref>
+Low [[Potassium in biology|potassium]] levels are usually associated with hypomagnesemia. Low magnesium levels act to inhibit the [[sodium-potassium pump]] (Na-K-ATPase) which normally pumps sodium to the extracellular space and potassium into the intracellular space, using ATP as energy to pump both cations against their concentration gradient, to maintain relatively high levels of potassium in the intracellular compartment and high levels of sodium in the extracellular space.<ref name="Touyz 2024" /> Hypomagnesemia also causes activation of the [[ROMK|Renal outer medullary potassium channel]] (ROMK), a potassium channel which causes potassium losses in the urine via the [[cortical collecting duct]] in the kidney.<ref name="Touyz 2024" /> And hypomagnesemia prevents low potassium levels from activating the [[sodium chloride symporter|sodium-chloride cotransporter]] (NCC) and downregulates NCC levels, which prevents sodium and chloride reabsorption from the kidney tubule.<ref name="Touyz 2024" /> The inhibition of the sodium-potassium pump results in more potassium remaining in the extracellular space ([[interstitial fluid]] and [[blood plasma|plasma]]). And this potassium is then lost as blood is filtered in the kidney as ROMK channel activation causes potassium losses in the cortical collecting duct and NCC inhibition causes decreased sodium-chloride reabsorption by kidney tubules, with subsequent increased sodium-chloride (and water) delivery to the distal tubule, and associated [[diuresis]] and [[kaliuresis]] (kidney potassium loss in the urine).<ref name="Touyz 2024" /> Overall, the net effect of low magnesium levels in the body is renal potassium losses (in the urine), thus clinically, low potassium levels are often refractory to supplementation without also correcting low magnesium levels.<ref name="Touyz 2024" /><ref name="huang">{{cite journal | vauthors = Huang CL, Kuo E | title = Mechanism of hypokalemia in magnesium deficiency | journal = Journal of the American Society of Nephrology | volume = 18 | issue = 10 | pages = 2649–2652 | date = October 2007 | pmid = 17804670 | doi = 10.1681/ASN.2007070792 | doi-access = free }}</ref>
-In this light, hypomagnesemia is frequently the cause of hypokalemic 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|date=June 2013}}
+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|date=June 2013}}
 ===Calcium===
@@ Line 90: / Line 91: @@
 ===Arrhythmia===
-Magnesium is needed for the adequate function of the [[Na+/K+-ATPase|Na<sup>+</sup>/K<sup>+</sup>-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 is needed for the adequate function of the [[Na+/K+-ATPase|Na<sup>+</sup>/K<sup>+</sup>-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 [[tachycardia]].{{Citation needed|date=July 2024}}
 ===Pre-eclampsia===
-Magnesium has an indirect antithrombotic effect upon platelets and endothelial function. Magnesium increases [[prostaglandin]]s, decreases [[thromboxane]], and decreases [[angiotensin II]], microvascular leakage, and vasospasm through its function similar to [[calcium channel blocker]]s.{{citation needed|date=June 2013}} Convulsions are the result of cerebral vasospasm. The vasodilatatory effect of magnesium seems to be the major mechanism.
+Magnesium has an indirect [[antithrombotic]] effect upon platelets and endothelial function. Magnesium increases [[prostaglandin]]s, decreases [[thromboxane]], and decreases [[angiotensin II]], microvascular leakage, and vasospasm through its function similar to [[calcium channel blocker]]s.{{citation needed|date=June 2013}} Convulsions are the result of cerebral vasospasm. The vasodilatatory effect of magnesium seems to be the major mechanism.
 ===Asthma===
-Magnesium exerts a bronchodilatatory effect, probably by antagonizing calcium-mediated bronchoconstriction.<ref name="asthma">{{cite journal | vauthors = Mills R, Leadbeater M, Ravalia A | title = Intravenous magnesium sulphate in the management of refractory bronchospasm in a ventilated asthmatic | journal = Anaesthesia | volume = 52 | issue = 8 | pages = 782–785 | date = August 1997 | pmid = 9291766 | doi = 10.1111/j.1365-2044.1997.176-az0312.x | doi-access = free }}</ref>
+Magnesium exerts a [[Bronchodilator|bronchodilatatory]] effect, probably by antagonizing calcium-mediated [[bronchoconstriction]].<ref name="asthma">{{cite journal | vauthors = Mills R, Leadbeater M, Ravalia A | title = Intravenous magnesium sulphate in the management of refractory bronchospasm in a ventilated asthmatic | journal = Anaesthesia | volume = 52 | issue = 8 | pages = 782–785 | date = August 1997 | pmid = 9291766 | doi = 10.1111/j.1365-2044.1997.176-az0312.x | doi-access = free }}</ref>
 === Neurological effects ===
-*reducing electrical excitation
+*Reducing electrical excitation,
-*modulating release of [[acetylcholine]]
+*Modulating release of [[acetylcholine]],
+*[[GABAA receptor]] agonism,<ref>{{Cite journal |last1=Maier |first1=Jeanette A. M. |last2=Locatelli |first2=Laura |last3=Fedele |first3=Giorgia |last4=Cazzaniga |first4=Alessandra |last5=Mazur |first5=André |date=January 2023 |title=Magnesium and the Brain: A Focus on Neuroinflammation and Neurodegeneration |journal=International Journal of Molecular Sciences |language=en |volume=24 |issue=1 |pages=223 |doi=10.3390/ijms24010223 |doi-access=free |issn=1422-0067}}</ref>
-*antagonising ''N''-methyl-<small>D</small>-aspartate ([[NMDA]]) [[glutamate]] receptors, an excitatory [[neurotransmitter]] of the central nervous system and thus providing neuroprotection from excitoxicity.
+*Antagonising ''N''-methyl-<small>D</small>-aspartate ([[NMDA]]) [[glutamate]] receptors, an excitatory [[neurotransmitter]] of the central nervous system and thus providing neuroprotection from excitoxicity.
 === Diabetes mellitus ===
+Magnesium deficiency is frequently observed in people with type 2 diabetes mellitus, with an estimated prevalence ranging between 11 and 48%.<ref name="diabetes">{{cite journal | vauthors = Pham PC, Pham PM, Pham SV, Miller JM, Pham PT | title = Hypomagnesemia in patients with type 2 diabetes | journal = Clinical Journal of the American Society of Nephrology | volume = 2 | issue = 2 | pages = 366–373 | date = March 2007 | pmid = 17699436 | doi = 10.2215/CJN.02960906 | doi-access = free }}</ref> Magnesium deficiency is strongly associated with high glucose and [[insulin resistance]], which indicate that it is common in poorly controlled diabetes.<ref name="diabetes2">{{cite journal | vauthors = Pham PC, Pham PM, Pham SV, Miller JM, Pham PT | title = Hypomagnesemia in patients with type 2 diabetes | journal = Clinical Journal of the American Society of Nephrology | volume = 2 | issue = 2 | pages = 366–373 | date = March 2007 | pmid = 17699436 | doi = 10.1530/EJE-16-0517 | doi-access = free }}</ref> Patients with type 2 diabetes and a magnesium deficiency have a higher risk of heart failure, atrial fibrillation and microvascular complications.<ref name="diabetes-cvd">{{cite journal | vauthors = Oost LJ, van der Heijden AA, Vermeulen EA, Bos C, Elders PJ, Slieker RC, Kurstjens S, van Berkel M, Hoenderop JG, Tack CJ, Beulens JW, de Baaij JH | display-authors = 6 | title = Serum Magnesium Is Inversely Associated With Heart Failure, Atrial Fibrillation, and Microvascular Complications in Type 2 Diabetes | journal = Diabetes Care | volume = 44 | issue = 8 | pages = 1757–1765 | date = August 2021 | pmid = 34385344 | doi = 10.2337/dc21-0236 | s2cid = 236991270 | doi-access = free }}</ref> Oral magnesium supplements has been demonstrated to improve insulin sensitivity and lipid profile.<ref name="diabetes3">{{cite journal | vauthors = Rodríguez-Morán M, Guerrero-Romero F | title = Oral magnesium supplementation improves insulin sensitivity and metabolic control in type 2 diabetic subjects: a randomized double-blind controlled trial | journal = Diabetes Care | volume = 26 | issue = 4 | pages = 1147–1152 | date = April 2003 | pmid = 12663588 | doi = 10.2337/diacare.26.4.1147 | doi-access = free }}</ref><ref name="diabetes4">{{cite journal | vauthors = Asbaghi O, Moradi S, Nezamoleslami S, Moosavian SP, Hojjati Kermani MA, Lazaridi AV, Miraghajani M | title = The Effects of Magnesium Supplementation on Lipid Profile Among Type 2 Diabetes Patients: a Systematic Review and Meta-analysis of Randomized Controlled Trials | journal = Biological Trace Element Research | volume = 199 | issue = 3 | pages = 861–873 | date = March 2021 | pmid = 32468224 | doi = 10.1007/s12011-020-02209-5 | bibcode = 2021BTER..199..861A | s2cid = 218978772 }}</ref><ref>{{cite journal | last1=Verma | first1=H. | last2=Garg | first2=R. | title=Effect of magnesium supplementation on type 2 diabetes associated cardiovascular risk factors: a systematic review and meta-analysis | journal=Journal of Human Nutrition and Dietetics | publisher=Wiley | volume=30 | issue=5 | date=2 February 2017 | issn=0952-3871 | doi=10.1111/jhn.12454 | pages=621–633| pmid=28150351 | s2cid=19778171 }}</ref> A 2016 meta-analysis not restricted to diabetic subjects found that increasing dietary magnesium intake, while associated with a reduced risk of stroke, heart failure, diabetes, and all-cause mortality, was not clearly<!--"no clear association was found between magnesium intake and the risk of coronary heart disease or total cardiovascular disease, which may have been due – at least in part – to the relatively limited number of studies included in our analysis"--> associated with lower risk of coronary heart disease (CHD) or total cardiovascular disease (CVD).<ref>{{cite journal | last1=Fang | first1=Xuexian | last2=Wang | first2=Kai | last3=Han | first3=Dan | last4=He | first4=Xuyan | last5=Wei | first5=Jiayu | last6=Zhao | first6=Lu | last7=Imam | first7=Mustapha Umar | last8=Ping | first8=Zhiguang | last9=Li | first9=Yusheng | last10=Xu | first10=Yuming | last11=Min | first11=Junxia | last12=Wang | first12=Fudi | title=Dietary magnesium intake and the risk of cardiovascular disease, type 2 diabetes, and all-cause mortality: a dose–response meta-analysis of prospective cohort studies | journal=BMC Medicine| volume=14 | issue=1 | year=2016 | page=210 | issn=1741-7015 | doi=10.1186/s12916-016-0742-z| pmid=27927203 | pmc=5143460 |doi-access=free}}</ref>
-Magnesium deficiency is frequently observed in people with type 2 diabetes mellitus, with an estimated prevalence ranging between 11.0 and 47.7%.<ref name="diabetes">{{cite journal | vauthors = Pham PC, Pham PM, Pham SV, Miller JM, Pham PT | title = Hypomagnesemia in patients with type 2 diabetes | journal = Clinical Journal of the American Society of Nephrology | volume = 2 | issue = 2 | pages = 366–373 | date = March 2007 | pmid = 17699436 | doi = 10.2215/CJN.02960906 | doi-access = free }}</ref>
-Magnesium deficiency is strongly associated with high glucose and insulin resistance, which indicate that it is common in poorly controlled diabetes.<ref name="diabetes2">{{cite journal | vauthors = Pham PC, Pham PM, Pham SV, Miller JM, Pham PT | title = Hypomagnesemia in patients with type 2 diabetes | journal = Clinical Journal of the American Society of Nephrology | volume = 2 | issue = 2 | pages = 366–373 | date = March 2007 | pmid = 17699436 | doi = 10.1530/EJE-16-0517 | doi-access = free }}</ref> Patients with type 2 diabetes and a magnesium deficiency have a higher risk of heart failure, atrial fibrillation and microvascular complications.<ref name="diabetes-cvd">{{cite journal | vauthors = Oost LJ, van der Heijden AA, Vermeulen EA, Bos C, Elders PJ, Slieker RC, Kurstjens S, van Berkel M, Hoenderop JG, Tack CJ, Beulens JW, de Baaij JH | display-authors = 6 | title = Serum Magnesium Is Inversely Associated With Heart Failure, Atrial Fibrillation, and Microvascular Complications in Type 2 Diabetes | journal = Diabetes Care | volume = 44 | issue = 8 | pages = 1757–1765 | date = August 2021 | pmid = 34385344 | doi = 10.2337/dc21-0236 | s2cid = 236991270 | doi-access = free }}</ref> Oral magnesium supplements has been demonstrated to improve insulin sensitivity and lipid profile.<ref name="diabetes3">{{cite journal | vauthors = Rodríguez-Morán M, Guerrero-Romero F | title = Oral magnesium supplementation improves insulin sensitivity and metabolic control in type 2 diabetic subjects: a randomized double-blind controlled trial | journal = Diabetes Care | volume = 26 | issue = 4 | pages = 1147–1152 | date = April 2003 | pmid = 12663588 | doi = 10.2337/diacare.26.4.1147 | doi-access = free }}</ref><ref name="diabetes4">{{cite journal | vauthors = Asbaghi O, Moradi S, Nezamoleslami S, Moosavian SP, Hojjati Kermani MA, Lazaridi AV, Miraghajani M | title = The Effects of Magnesium Supplementation on Lipid Profile Among Type 2 Diabetes Patients: a Systematic Review and Meta-analysis of Randomized Controlled Trials | journal = Biological Trace Element Research | volume = 199 | issue = 3 | pages = 861–873 | date = March 2021 | pmid = 32468224 | doi = 10.1007/s12011-020-02209-5 | s2cid = 218978772 }}</ref><ref>{{cite journal | last1=Verma | first1=H. | last2=Garg | first2=R. | title=Effect of magnesium supplementation on type 2 diabetes associated cardiovascular risk factors: a systematic review and meta-analysis | journal=Journal of Human Nutrition and Dietetics | publisher=Wiley | volume=30 | issue=5 | date=2 February 2017 | issn=0952-3871 | doi=10.1111/jhn.12454 | pages=621–633| pmid=28150351 | s2cid=19778171 }}</ref> A 2016 meta-analysis not restricted to diabetic subjects found that increasing dietary magnesium intake, while associated with a reduced risk of stroke, heart failure, diabetes, and all-cause mortality, was not clearly<!--"no clear association was found between magnesium intake and the risk of coronary heart disease or total cardiovascular disease, which may have been due – at least in part – to the relatively limited number of studies included in our analysis"--> associated with lower risk of coronary heart disease (CHD) or total cardiovascular disease (CVD).<ref>{{cite journal | last1=Fang | first1=Xuexian | last2=Wang | first2=Kai | last3=Han | first3=Dan | last4=He | first4=Xuyan | last5=Wei | first5=Jiayu | last6=Zhao | first6=Lu | last7=Imam | first7=Mustapha Umar | last8=Ping | first8=Zhiguang | last9=Li | first9=Yusheng | last10=Xu | first10=Yuming | last11=Min | first11=Junxia | last12=Wang | first12=Fudi | title=Dietary magnesium intake and the risk of cardiovascular disease, type 2 diabetes, and all-cause mortality: a dose–response meta-analysis of prospective cohort studies | journal=BMC Medicine| volume=14 | issue=1 | year=2016 | page=210 | issn=1741-7015 | doi=10.1186/s12916-016-0742-z| pmid=27927203 | pmc=5143460 |doi-access=free}}</ref>
-A 2021 study on blood from 4,400 diabetic patients over 6 to 11 years reported that "People with higher levels of magnesium in the blood were found to have a significantly lower risk of cardiovascular disease", and also of diabetic foot and diabetic retinopathy. The researchers, however, stated that "we have [not] demonstrated that magnesium supplements work. Further research is needed."<ref>{{cite web | title=Magnesium deficiency increases the risk of cardiovascular disease in diabetic patients|first=Pauline|last=Dekhuijzen| publisher=Radboud university medical center| date=21 June 2021 | url=https://www.radboudumc.nl/en/news-items/2021/magnesium-deficiency-increases-the-risk-of-cardiovascular-disease-in-diabetic-patients}}</ref>
 ===Homeostasis===
-Magnesium rich foods include [[cereals]], green vegetables (with magnesium being a main component of [[chlorophyll]]), [[beans]], and [[Nut (fruit)|nuts]].<ref name="Touyz 2024">{{cite journal |last1=Touyz |first1=Rhian M. |last2=de Baaij |first2=Jeroen H.F. |last3=Hoenderop |first3=Joost G.J. |title=Magnesium Disorders |journal=New England Journal of Medicine |date=6 June 2024 |volume=390 |issue=21 |pages=1998–2009 |doi=10.1056/NEJMra1510603}}</ref> It is absorbed primarily in the [[small intestine]] via [[paracellular]] transport; passing between intestinal cells. Magnesium absorption in the [[large intestine]] is mediated by the transporters TRPM6 and [[TRPM7]].<ref name="Touyz 2024" />
+Magnesium rich foods include [[cereals]], green vegetables (with magnesium being a main component of [[chlorophyll]]), [[beans]], and [[Nut (fruit)|nuts]].<ref name="Touyz 2024">{{cite journal |last1=Touyz |first1=Rhian M. |last2=de Baaij |first2=Jeroen H.F. |last3=Hoenderop |first3=Joost G.J. |title=Magnesium Disorders |journal=New England Journal of Medicine |date=6 June 2024 |volume=390 |issue=21 |pages=1998–2009 |doi=10.1056/NEJMra1510603|pmid=38838313 }}</ref> It is absorbed primarily in the [[small intestine]] via [[paracellular]] transport; passing between intestinal cells. Magnesium absorption in the [[large intestine]] is mediated by the transporters TRPM6 and [[TRPM7]].<ref name="Touyz 2024" />
-The body contains about 25 grams of magnesium.<ref name="Touyz 2024" /> Of the body's magnesium, 50-60% is stored in [[bone]], with the remainder, about 40-50%, being stored in muscle or soft tissue, with about 1% being in the plasma.<ref name="Jahnen-Dechent 2012">{{cite journal |last1=Jahnen-Dechent |first1=W. |last2=Ketteler |first2=M. |title=Magnesium basics |journal=Clinical Kidney Journal |date=1 February 2012 |volume=5 |issue=Suppl 1 |pages=i3–i14 |doi=10.1093/ndtplus/sfr163}}</ref> Therefore, normal plasma levels of magnesium may sometimes be seen despite a person being in a state of magnesium deficiency and plasma magnesium levels may underestimate the level of deficiency. Plasma magnesium levels may more accurately reflect magnesium stores when consideration is also given to urinary magnesium losses and oral intake of magnesium. <ref name="Touyz 2024" />
+The body contains about 25 grams of magnesium.<ref name="Touyz 2024" /> Of the body's magnesium, 50-60% is stored in [[bone]], with the remainder, about 40-50%, being stored in muscle or soft tissue, with about 1% being in the plasma.<ref name="Jahnen-Dechent 2012">{{cite journal |last1=Jahnen-Dechent |first1=W. |last2=Ketteler |first2=M. |title=Magnesium basics |journal=Clinical Kidney Journal |date=1 February 2012 |volume=5 |issue=Suppl 1 |pages=i3–i14 |doi=10.1093/ndtplus/sfr163|pmid=26069819 |pmc=4455825 }}</ref> Therefore, normal plasma levels of magnesium may sometimes be seen despite a person being in a state of magnesium deficiency and plasma magnesium levels may underestimate the level of deficiency. Plasma magnesium levels may more accurately reflect magnesium stores when consideration is also given to urinary magnesium losses and oral intake of magnesium. <ref name="Touyz 2024" />
-Inside cells, 90-95% of magnesium is bound to ligands, including [[Adenosine triphosphate|ATP]], [[adenosine diphosphate|ADP]], [[citrate]], other proteins and [[nucleic acids]].<ref name="Touyz 2024" /> In the plasma, 30% of magnesium is bound to free fatty acids, therefore elevated levels of free fatty acids are associated with hypomagnesemia as well as a possible risk of cardiovascular disease.<ref name="Touyz 2024" />
+Inside cells, 90-95% of magnesium is bound to ligands, including [[Adenosine triphosphate|ATP]], [[adenosine diphosphate|ADP]], [[citrate]], other proteins and [[nucleic acids]].<ref name="Touyz 2024" /> In the plasma, 30% of magnesium is bound to proteins via free fatty acids, therefore elevated levels of free fatty acids are associated with hypomagnesemia as well as a possible risk of cardiovascular disease.<ref name="Touyz 2024" />
-The kidneys regulate magnesium levels by reabsorbing magnesium from the tubules. In the [[proximal tubule]] (at the beginning of the [[nephron]], the functional unit of the kidney) 20% of magnesium is reabsorbed via paracellular transport with [[claudin]] 2 and claudin 12 forming channels to allow for reabsorption.<ref name="Touyz 2024" /> 70% of magnesium is reabsorbed in the thick ascending limb of the [[loop of Henle]] where claudins 16 and 19 form the channels to allow for reabsorption.<ref name="Touyz 2024" /> In the [[distal convoluted tubule]], 5-10% of magnesium is reabsorbed [[transcellular transport|transcellularly]] (through the cells) via the transporters TRPM6 and TRPM7. [[Epidermal growth factor]] and [[insulin]] activate TRPM6 and 7 and increase magneisum levels via increased renal reabsorption.<ref name="Touyz 2024" />
+The kidneys regulate magnesium levels by reabsorbing magnesium from the tubules. In the [[proximal tubule]] (at the beginning of the [[nephron]], the functional unit of the kidney) 20% of magnesium is reabsorbed via paracellular transport with [[claudin]] 2 and claudin 12 forming channels to allow for reabsorption.<ref name="Touyz 2024" /> 70% of magnesium is reabsorbed in the thick ascending limb of the [[loop of Henle]] where claudins 16 and 19 form the channels to allow for reabsorption.<ref name="Touyz 2024" /> In the [[distal convoluted tubule]], 5-10% of magnesium is reabsorbed [[transcellular transport|transcellularly]] (through the cells) via the transporters TRPM6 and TRPM7. [[Epidermal growth factor]] and [[insulin]] activate TRPM6 and 7 and increase magnesium levels via increased renal reabsorption.<ref name="Touyz 2024" />
 ==Diagnosis==
+Magnesium deficiency or depletion is a low total body level of magnesium; it is not easy to measure directly.<ref name=Swam2003/>
-Magnesium deficiency or depletion is a low {{Em|total body}} level of magnesium; it is not easy to measure directly.<ref name=Swam2003/> Typically the diagnosis is based on finding hypomagnesemia, a low {{Em|blood}} magnesium level,<ref>{{cite encyclopedia|title=Hypomagnesemia|url=http://www.medterms.com/script/main/art.asp?articlekey=3858|dictionary=Medterms medical dictionary a-z list|publisher=MedicineNet|first=Charles Patrick|last=Davis|date=29 March 2021|access-date=31 May 2014|archive-date=31 May 2014|archive-url=https://web.archive.org/web/20140531090431/http://www.medterms.com/script/main/art.asp?articlekey=3858|url-status=dead}}</ref> which often reflects low body magnesium;<ref name=Cecil2015/> however, magnesium deficiency can be present without hypomagnesemia, and vice versa.<ref name=Swam2003>{{cite journal | vauthors = Swaminathan R | title = Magnesium metabolism and its disorders | journal = The Clinical Biochemist. Reviews | volume = 24 | issue = 2 | pages = 47–66 | date = May 2003 | pmid = 18568054 | pmc = 1855626 }}</ref> A [[Blood plasma|plasma]] magnesium concentration of less than 0.6&nbsp;mmol/L (1.46&nbsp;mg/dL) is considered to be hypomagnesemia;<ref name=EU2010/> severe disease generally has a level of less than 0.50&nbsp;mmol/L (1.25&nbsp;mg/dL).<ref name=Mer2018/>
+=== Blood magnesium ===
+Typically the diagnosis is based on finding hypomagnesemia, a low blood magnesium level,<ref>{{cite encyclopedia|title=Hypomagnesemia|url=http://www.medterms.com/script/main/art.asp?articlekey=3858|dictionary=Medterms medical dictionary a-z list|publisher=MedicineNet|first=Charles Patrick|last=Davis|date=29 March 2021|access-date=31 May 2014|archive-date=31 May 2014|archive-url=https://web.archive.org/web/20140531090431/http://www.medterms.com/script/main/art.asp?articlekey=3858|url-status=dead}}</ref> which often reflects low body magnesium;<ref name="Cecil2015" /> however, magnesium deficiency can be present without hypomagnesemia, and vice versa.<ref name="Swam2003">{{cite journal | vauthors = Swaminathan R | title = Magnesium metabolism and its disorders | journal = The Clinical Biochemist. Reviews | volume = 24 | issue = 2 | pages = 47–66 | date = May 2003 | pmid = 18568054 | pmc = 1855626 }}</ref> A [[Blood plasma|plasma]] magnesium concentration of less than 0.6&nbsp;mmol/L (1.46&nbsp;mg/dL) is considered to be hypomagnesemia;<ref name="EU2010" /> severe disease generally has a level of less than 0.5&nbsp;mmol/L (1.25&nbsp;mg/dL).<ref name="Mer2018" />
 ===Electrocardiogram===
@@ Line 138: / Line 140: @@
 ==Epidemiology==
-The condition is relatively common among people in hospital (especially those in the [[intensive care unit]] (ICU)) and those with diabetes.<ref name=Mer2018/> Hypomagnesemia may be seen in 3-10% of the general population.<ref name="Touyz 2024" /> It is present in an estimated 10-30% of people with diabetes, 10-60% of hospitalized people and greater than 65% of people in the ICU.<ref name="Touyz 2024" /> In hospitalized patients, hypomagnesemia is associated with an increased length of stay. And in those in an ICU, it is associated with a higher risk of requiring [[mechanical ventilation]], and death.<ref>{{cite journal | vauthors = Upala S, Jaruvongvanich V, Wijarnpreecha K, Sanguankeo A | title = Hypomagnesemia and mortality in patients admitted to intensive care unit: a systematic review and meta-analysis | journal = QJM | volume = 109 | issue = 7 | pages = 453–459 | date = July 2016 | pmid = 27016536 | doi = 10.1093/qjmed/hcw048 | doi-access =  }}</ref><ref name="Peres 2020">{{cite journal |last1=Peres |first1=Igor Tona |last2=Hamacher |first2=Silvio |last3=Oliveira |first3=Fernando Luiz Cyrino |last4=Thomé |first4=Antônio Márcio Tavares |last5=Bozza |first5=Fernando Augusto |title=What factors predict length of stay in the intensive care unit? Systematic review and meta-analysis |journal=Journal of Critical Care |date=December 2020 |volume=60 |pages=183–194 |doi=10.1016/j.jcrc.2020.08.003}}</ref> In population based [[cohort studies]], chronic magnesium deficiency was associated with an increased risk of cardiovascular death and overall death.<ref name="Touyz 2024" /><ref name="Ye 2023">{{cite journal |last1=Ye |first1=Liu |last2=Zhang |first2=Cheng |last3=Duan |first3=Qin |last4=Shao |first4=Yue |last5=Zhou |first5=Jianzhong |title=Association of Magnesium Depletion Score With Cardiovascular Disease and Its Association With Longitudinal Mortality in Patients With Cardiovascular Disease |journal=Journal of the American Heart Association |date=19 September 2023 |volume=12 |issue=18 |doi=10.1161/JAHA.123.030077}}</ref>
+Hypomagnesemia may be seen in 3-10% of the general population.<ref name="Touyz 2024" /> It is present in an estimated 10-30% of people with diabetes, 10-60% of hospitalized people and greater than 65% of people in the ICU.<ref name="Touyz 2024" /><ref name="Mer2018" /> In hospitalized patients, hypomagnesemia is associated with an increased length of stay. And in those in an ICU, it is associated with a higher risk of requiring [[mechanical ventilation]], and death.<ref>{{cite journal | vauthors = Upala S, Jaruvongvanich V, Wijarnpreecha K, Sanguankeo A | title = Hypomagnesemia and mortality in patients admitted to intensive care unit: a systematic review and meta-analysis | journal = QJM | volume = 109 | issue = 7 | pages = 453–459 | date = July 2016 | pmid = 27016536 | doi = 10.1093/qjmed/hcw048 | doi-access =  }}</ref><ref name="Peres 2020">{{cite journal |last1=Peres |first1=Igor Tona |last2=Hamacher |first2=Silvio |last3=Oliveira |first3=Fernando Luiz Cyrino |last4=Thomé |first4=Antônio Márcio Tavares |last5=Bozza |first5=Fernando Augusto |title=What factors predict length of stay in the intensive care unit? Systematic review and meta-analysis |journal=Journal of Critical Care |date=December 2020 |volume=60 |pages=183–194 |doi=10.1016/j.jcrc.2020.08.003|pmid=32841815 }}</ref> In population based [[cohort studies]], chronic magnesium deficiency was associated with an increased risk of cardiovascular death and overall death.<ref name="Touyz 2024" /><ref name="Ye 2023">{{cite journal |last1=Ye |first1=Liu |last2=Zhang |first2=Cheng |last3=Duan |first3=Qin |last4=Shao |first4=Yue |last5=Zhou |first5=Jianzhong |title=Association of Magnesium Depletion Score With Cardiovascular Disease and Its Association With Longitudinal Mortality in Patients With Cardiovascular Disease |journal=Journal of the American Heart Association |date=19 September 2023 |volume=12 |issue=18 |pages=e030077 |doi=10.1161/JAHA.123.030077|pmid=37681518 |pmc=10547298 }}</ref>
 ==History==
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 Magnesium deficiency is a detrimental plant disorder that occurs most often in strongly acidic, light, sandy soils, where magnesium can be easily leached away. Magnesium is an essential macronutrient constituting 0.2-0.4% of plants' dry matter and is necessary for normal plant growth.<ref name="HunerHopkins2009">{{cite book| vauthors = Huner NP, Hopkins W |title=Introduction to Plant Physiology 4th Edition|publisher=John Wiley & Sons, Inc.|isbn=978-0-470-24766-2|chapter= 3 & 4|date=2008-11-07}}</ref> Excess potassium, generally due to fertilizers, further aggravates the stress from magnesium deficiency,<ref name="Ding,Y.,C.Chang W.Luoetal.2008">{{cite journal| vauthors = Ding Y, Chang C, Luo W |title=High Potassium Aggravates the Oxidative Stress Induced by Magnesium Deficiency in Rice Leaves|journal=Pedosphere|year=2008 |volume=18|issue=3|pages=316–327 |doi=10.1016/S1002-0160(08)60021-1}}</ref> as does [[Soil pH#Acid soils|aluminium toxicity]].<ref>{{cite book| vauthors = Merhaut DJ | veditors = Barker AV, Pilbeam DJ |title=Handbook of plant nutrition|date=2006|publisher=CRC Press|location=Boca Raton|isbn=9780824759049|page=154|ref=Merhaut 2006|chapter=Magnesium}}</ref>
-Magnesium has an important role in [[photosynthesis]] because it forms the central atom of [[chlorophyll]].<ref name="HunerHopkins2009"/> Therefore, without sufficient amounts of magnesium, plants begin to degrade the chlorophyll in the old leaves. This causes the main symptom of magnesium deficiency, interveinal [[chlorosis]], or yellowing between leaf veins, which stay green, giving the leaves a marbled appearance. Due to magnesium's mobile nature, the plant will first break down chlorophyll in older leaves and transport the Mg to younger leaves which have greater photosynthetic needs. Therefore, the first sign of magnesium deficiency is the chlorosis of old leaves which progresses to the young leaves as the deficiency progresses.<ref name="Hermans,C.,M.Vuylsteke,F.Coppens et al. 2010">{{cite journal| vauthors = Hermans C, Vuylsteke F, Coppens F |title=Systems Analysis of the responses to long-term magnesium deficiency and restoration in ''Arabidopsis thaliana'' |journal=New Phytologist|year=2010 |volume=187|issue=1 |pages=132–144 |pmid=20412444 |doi=10.1111/j.1469-8137.2010.03257.x |hdl=2066/83962 |hdl-access=free }}</ref> Magnesium also acts as an activator for many critical enzymes, including ribulosebisphosphate carboxylase ([[RuBisCO]]) and [[phosphoenolpyruvate carboxylase]] (PEPC), both essential enzymes in [[carbon fixation]]. Thus low amounts of Mg lead to a decrease in photosynthetic and enzymatic activity within the plants. Magnesium is also crucial in stabilizing [[ribosome]] structures, hence, a lack of magnesium causes [[depolymerization]] of ribosomes leading to premature aging of the plant.<ref name="HunerHopkins2009"/> After prolonged magnesium deficiency, [[necrosis]] and dropping of older leaves occurs. Plants deficient in magnesium also produce smaller, woodier fruits.
+Magnesium has an important role in [[photosynthesis]] because it forms the central atom of [[chlorophyll]].<ref name="HunerHopkins2009"/> Therefore, without sufficient amounts of magnesium, plants begin to degrade the chlorophyll in the old leaves. This causes the main symptom of magnesium deficiency, interveinal [[chlorosis]], or yellowing between leaf veins, which stay green, giving the leaves a marbled appearance. Due to magnesium's mobile nature, the plant will first break down chlorophyll in older leaves and transport the Mg to younger leaves which have greater photosynthetic needs. Therefore, the first sign of magnesium deficiency is the chlorosis of old leaves which progresses to the young leaves as the deficiency progresses.<ref name="Hermans,C.,M.Vuylsteke,F.Coppens et al. 2010">{{cite journal| vauthors = Hermans C, Vuylsteke F, Coppens F |title=Systems Analysis of the responses to long-term magnesium deficiency and restoration in ''Arabidopsis thaliana'' |journal=New Phytologist|year=2010 |volume=187|issue=1 |pages=132–144 |pmid=20412444 |doi=10.1111/j.1469-8137.2010.03257.x |bibcode=2010NewPh.187..132H |hdl=2066/83962 |hdl-access=free }}</ref> Magnesium also acts as an activator for many critical enzymes, including ribulosebisphosphate carboxylase ([[RuBisCO]]) and [[phosphoenolpyruvate carboxylase]] (PEPC), both essential enzymes in [[carbon fixation]]. Thus low amounts of Mg lead to a decrease in photosynthetic and enzymatic activity within the plants. Magnesium is also crucial in stabilizing [[ribosome]] structures, hence, a lack of magnesium causes [[depolymerization]] of ribosomes leading to premature aging of the plant.<ref name="HunerHopkins2009"/> After prolonged magnesium deficiency, [[necrosis]] and dropping of older leaves occurs. Plants deficient in magnesium also produce smaller, woodier fruits.
 Magnesium deficiency in plants may be confused with [[Zinc deficiency (plant disorder)|zinc]] or [[chlorine]] deficiencies, viruses, or natural aging, since all have similar symptoms. Adding [[Epsom salts]] (as a solution of 25 grams per liter or 4 oz per gal) or crushed dolomitic limestone to the soil can rectify magnesium deficiencies. An [[Organic matter|organic]] treatment is to apply [[compost]] [[mulch]], which can prevent leaching during excessive rainfall and provide plants with sufficient amounts of nutrients, including magnesium.<ref>{{cite magazine| title=Problem Solving: Magnesium Deficiency | magazine=Gardeners' World Magazine | date=6 March 2019 | url=https://www.gardenersworld.com/how-to/solve-problems/magnesium-deficiency/}}</ref>

v t e Electrolyte imbalances
Calcium	High Low Symptoms and signs Chvostek sign Trousseau sign Milk-alkali syndrome Disorders of calcium metabolism Hypercalcemia of malignancy Calcinosis (Calciphylaxis, Calcinosis cutis) Calcification (Metastatic calcification, Dystrophic calcification) Familial hypocalciuric hypercalcemia
Chloride	High Low
Magnesium	High Low
Phosphate	High Low
Potassium	High Hyperkalemic periodic paralysis equine Low Hypokalemic periodic paralysis Hypokalemic sensory overstimulation
Sodium	High Salt poisoning Low Hypotonic Isotonic Cerebral salt-wasting syndrome

Classification	D ICD-10: E83.4 ICD-9-CM: 275.2 DiseasesDB: 6469
External resources	MedlinePlus: 000315 eMedicine: med/3382 emerg/274 ped/1122