HypomagnesemiaMANAGEMENT

ENDOCRINE AND METABOLIC PRESENTATIONS · 12 SECTIONS

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615 items

☷ Legend

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Cardiovascular Presentations71▾

Respiratory Presentations52▾

Neurological Presentations83▾

Gastrointestinal Presentations74▾

Genitourinary and Reproductive Presentations48▾

Infectious Disease Presentations148▾

Trauma Presentations89▾

Toxicologic Presentations80▾

Psychiatric Presentations26▾

Musculoskeletal and Rheumatologic Presentations96▾

Dermatology Presentations23▾

Environmental and Exposure Presentations27▾

Hematologic and Oncologic Presentations36▾

Pediatric-Specific Presentations19▾

Endocrine and Metabolic Presentations45▾

Acute Porphyria Adrenal crisis Adrenal Insufficiency (Addisonian Crisis)Dehydration Diabetes Insipidus Diabetic Ketoacidosis (DKA)Euglycemic DKA (SGLT2 inhibitor)Galactosemia GLP-1 receptor agonist complications (retained gastric contents, aspiration risk)Homocystinuria Hypercalcemia Hyperkalemia Hypermagnesemia Hypernatremia Hyperosmolar Hyperglycemic State (HHS)Hypertensive emergency Hypertensive urgency Hypocalcemia Hypoglycemia Hypogonadism (Acute Presentation)Hypokalemia Hypomagnesemia Hyponatremia Hypoparathyroidism (Tetany)Insulin pump failure Maple Syrup Urine Disease (Crisis)Medium-Chain Acyl-CoA Dehydrogenase Deficiency (MCAD)Metabolic Acidosis Metabolic Alkalosis Myasthenia gravis crisis Myxedema coma Pellagra Pheochromocytoma (Crisis)Pituitary Apoplexy Pompe Disease (GSD II)Respiratory Acidosis Respiratory Alkalosis Scurvy SIADH Starvation Ketosis Tarui Disease (GSD VII)Thyroid storm Tyrosinemia Vitamin D Deficiency (Severe-Rickets)Von Gierke Disease (GSD I)

ENT and Maxillofacial Presentations27▾

Ophthalmologic Presentations19▾

Obstetric Presentations23▾

Systemic and Miscellaneous Presentations17▾

01Approach to the Critical Patient/attcp55

Immediate priorities

›Life-threatening presentations requiring urgent action

›Torsades de pointes or ventricular arrhythmia

›IV magnesium sulfate 2 g bolus over 5-15 minutes regardless of serum level

›Continuous cardiac monitoring in resuscitation bay

›Class I recommendation per ACC/AHA/ESC 2006 ventricular arrhythmia guidelines

›Active seizure due to severe hypomagnesemia

›IV magnesium sulfate 2 g over 5-15 minutes

›Benzodiazepine co-administration if seizure does not terminate

›Serum Mg <0.5 mmol/L warrants immediate IV repletion

›Tetany with carpopedal spasm

›IV magnesium sulfate 1-2 g over 15-30 minutes

›Confirm concurrent hypocalcemia and replicate calcium if present

›Hemodynamic instability with arrhythmia

›Synchronized cardioversion if hemodynamically unstable ventricular tachycardia

›Magnesium sulfate adjunct even after cardioversion

Monitoring and targets

›Monitoring bundle for moderate-to-severe hypomagnesemia

›Continuous cardiac telemetry

›QTc interval trending every 4-6 hours

›PVC burden assessment

›AHA 2017 guidelines recommend continuous monitoring for significant electrolyte imbalance

›Neurological status checks

›Deep tendon reflexes every 2-4 hours during IV infusion

›Loss of patellar reflex is first sign of magnesium toxicity

›Respiratory rate monitoring — depression at Mg >3.5 mmol/L

›Urine output monitoring

›Target >25 mL/hour during IV infusion

02History/hx63

Presenting symptoms

›Neuromuscular symptoms

›Muscle cramps and spasms

›Commonly in calves, hands, and feet

›Carpopedal spasm is hallmark of severe deficiency

›Tremor and fasciculations

›Paresthesias

›Perioral numbness common with concurrent hypocalcemia

›Weakness

›Proximal greater than distal pattern

›Tetany

›Indicates severe depletion with Mg <0.5 mmol/L

Cardiac symptoms

›Palpitations

›Irregular heartbeat perception

›Syncope or presyncope associated with arrhythmia

›Chest pain

›Prior arrhythmia history

›Atrial fibrillation episodes

›Documented torsades de pointes

Gastrointestinal history

›GI losses contributing to depletion

›Chronic diarrhea — frequency, chronicity, consistency

›Steatorrhea suggesting malabsorption

›Short bowel syndrome

›Vomiting — duration and severity

›Nasogastric suction history

›Bariatric surgery or bowel resection

›IBD, celiac disease, chronic pancreatitis history

Medication and substance history

›Causative medications

›Proton pump inhibitors

›Duration of use — chronic use >1 year highest risk

›~20% incidence with long-term PPI use

›Mechanism: impaired intestinal TRPM6/7 channel function

›Loop diuretics (furosemide, bumetanide) — renal magnesium wasting

›Thiazide diuretics — chronic renal wasting

›Aminoglycosides — direct tubular toxicity

›Cisplatin — nephrotoxic tubular injury

›Calcineurin inhibitors (tacrolimus, cyclosporine) — 20-40% incidence

›EGFR inhibitors (cetuximab, erlotinib) — 20-40% incidence

›Amphotericin B, foscarnet, pentamidine

›Alcohol use history

›Quantity and duration of use

›Last drink and withdrawal symptoms

›Alcohol impairs both GI absorption and renal reabsorption

Dietary and nutritional history

›Dietary magnesium intake

›Poor intake of leafy greens, nuts, seeds, whole grains

›Malnutrition or restrictive diet

›Food insecurity, homelessness, eating disorder

›Timing and onset

›Acute onset (post-surgical, medication change, alcohol binge)

›Chronic and insidious onset (PPI use, poor intake, chronic diarrhea)

Risk factors

›High-risk populations

›Alcohol use disorder — present in ~30% of patients with hypomagnesemia

›Type 2 diabetes mellitus — prevalence 10-30% due to renal wasting

›ICU admission — incidence >65%

›General hospital admission — incidence 3-10%

›Organ transplant recipients on calcineurin inhibitors

›Cancer patients on cisplatin or EGFR inhibitors

›Elderly with polypharmacy — number of medications inversely correlates with Mg levels

Family history

›Genetic causes of hypomagnesemia

›Gitelman syndrome — hypomagnesemia, hypokalemia, metabolic alkalosis, hypocalciuria

›Bartter syndrome — similar pattern with hypercalciuria

›Familial hypomagnesemia with secondary hypocalcemia (HSH)

›Pathogenic variants identified in ~80% of familial cases

›Primary hypomagnesemia with secondary hypocalcemia

03Physical Exam/exam39

Vital signs

›Hemodynamic and rhythm assessment

›Heart rate — tachycardia associated with arrhythmia or withdrawal

›Blood pressure — hypertension or hypotension

›Pulse regularity — irregular pulse suggesting atrial fibrillation or PVCs

›Respiratory rate — bradypnea raises toxicity concern if on IV Mg

Neuromuscular examination

›Classic signs of neuromuscular irritability

›Trousseau sign

›Carpal spasm with BP cuff inflated above systolic for 3 minutes

›Sensitivity 94%, specificity 99% for hypocalcemia/hypomagnesemia

›Shared with hypocalcemia — check calcium concurrently

›Chvostek sign

›Facial muscle twitch with tapping anterior to tragus

›Lower specificity — present in 10% of normal individuals

›Deep tendon reflexes

›Hyperreflexia in early deficiency

›Loss of patellar reflex indicates magnesium toxicity during IV infusion

›Tremor

›Fine resting and action tremor

›Fasciculations

›Nystagmus

›Indicates severe or rapidly evolving deficiency

Mental status

›Neuropsychiatric findings

›Confusion or altered mental status

›Irritability and agitation

›Lethargy and fatigue

04Differential Diagnosis/ddx46

Electrolyte mimics

›Hypocalcemia (primary)

›Similar neuromuscular symptoms — carpopedal spasm, Trousseau/Chvostek

›Check PTH and 25-hydroxyvitamin D to distinguish

›ICD-10: E83.51

›Co-occurs with hypomagnesemia — Mg must be corrected first

›Hypokalemia (primary)

›Weakness, cramps, arrhythmia, constipation

›Often coexists — refractory hypokalemia is a hallmark clue to underlying Mg depletion

›ICD-10: E87.6

›Hypophosphatemia

›Weakness, rhabdomyolysis, respiratory muscle failure

›Frequently coexists in alcoholism and refeeding syndrome

›ICD-10: E83.39

Genetic tubulopathies

›Gitelman syndrome

›Hypomagnesemia, hypokalemia, metabolic alkalosis, hypocalciuria

›SLC12A3 gene mutation in distal convoluted tubule NCC transporter

›ICD-10: N25.89

›Bartter syndrome

›Similar electrolyte pattern but with hypercalciuria and normal blood pressure

›Several subtypes (Type I-V) based on gene involved

›ICD-10: E26.8

Endocrine disorders

›Thyrotoxicosis

›Tremor, palpitations, weakness — overlapping features

›TSH and free T4 distinguish

›ICD-10: E05.90

05Laboratory Tests/lt55

Serum electrolytes

›Serum magnesium — cornerstone of diagnosis

›Normal range 0.7-1.0 mmol/L

›Mild hypomagnesemia: 0.5-0.7 mmol/L — often asymptomatic

›Severe hypomagnesemia: <0.5 mmol/L — neuromuscular irritability, arrhythmias, seizures

›Serum level underestimates total body depletion — normal level does not exclude deficiency

›ICD-10: E83.42

Basic metabolic panel

›Concurrent electrolytes to assess and replicate

›Serum potassium — hypokalemia coexists in majority of cases

›Refractory hypokalemia despite replacement is a clinical clue

›ROMK channel function requires magnesium

›Serum calcium (total)

›Ionized calcium more accurate than total

›Hypomagnesemia impairs PTH secretion and end-organ PTH response

›Serum phosphorus — frequently low in alcoholism and malnutrition

›Serum creatinine and eGFR

›Renal insufficiency impairs magnesium excretion

›Adjust IV infusion rate in CKD — max 20 g/48 hours

›Serum glucose

›Hyperglycemia and insulin use promote renal Mg wasting

›Serum albumin

›Hypoalbuminemia can affect magnesium measurement interpretation

›Corrected calcium calculation needed

Etiology workup

›Fractional excretion of magnesium (FEMg)

›Formula: FEMg = (urine Mg x plasma Cr) / (0.7 x plasma Mg x urine Cr) x 100

›FEMg >2% in setting of hypomagnesemia indicates renal wasting

06Diagnostic Tests/dt55

Scoring Systems

›Severity classification system for hypomagnesemia

›Mild: serum Mg 0.5-0.7 mmol/L

›Often asymptomatic or nonspecific (fatigue, cramps)

›Oral repletion appropriate

›Severe: serum Mg <0.5 mmol/L

›Neuromuscular irritability, arrhythmias, seizures

›IV repletion required

CIWA-Ar scoring

›Clinical Institute Withdrawal Assessment for Alcohol (CIWA-Ar)

›10-item scale for alcohol withdrawal severity

›Score <8: mild withdrawal — monitor and oral supplementation

›Score 8-15: moderate withdrawal — consider IV magnesium

›Score >15: severe withdrawal — IV magnesium and benzodiazepines

›Hypomagnesemia worsens alcohol withdrawal severity

›Magnesium repletion reduces seizure threshold risk in withdrawal

MRI

›MRI indications in hypomagnesemia

›Not routinely indicated for primary electrolyte disorder

›Reserved for unexplained neurological findings after correction

›MRI brain for new seizure with atypical features

›Rule out structural lesion, posterior reversible encephalopathy syndrome (PRES)

›MRI spine if focal neurological deficits present

›Rule out compressive myelopathy contributing to weakness

›PRES association

›Calcineurin inhibitor use with severe hypomagnesemia may precipitate PRES

›MRI findings: T2/FLAIR hyperintensity in posterior parieto-occipital regions

07Disposition/dispo40

Admission criteria

›Indications for hospital admission

›Symptomatic severe hypomagnesemia (seizures, tetany, arrhythmia)

›IV repletion required in monitored setting

›Serum Mg <0.4 mmol/L regardless of symptoms

›Torsades de pointes or ventricular arrhythmia

›Cardiac monitoring unit or ICU

›Concurrent significant hypokalemia or hypocalcemia

›Multi-electrolyte repletion requires monitoring

›QTc >500 ms on ECG

›Active alcohol withdrawal requiring treatment

›Hemodynamic instability

›Inability to tolerate oral repletion (vomiting, altered mental status)

ICU criteria

›ICU-level care triggers

›Recurrent or refractory torsades de pointes

›Hemodynamic instability requiring vasopressors

›Seizure not controlled with initial Mg and benzodiazepine

›Respiratory depression or airway compromise

›Concurrent severe multi-electrolyte disorder

Discharge criteria

›Safe discharge parameters

›Mild asymptomatic hypomagnesemia with identifiable correctable cause

›Serum Mg >0.6 mmol/L and tolerating oral supplementation

›Stable vital signs and normal ECG

›No cardiac arrhythmia

›Reliable follow-up arranged within 1-2 weeks

›Patient counseled on dietary sources and medication adjustments

08Treatment/t68

Severe and symptomatic IV repletion

›IV magnesium sulfate — acute severe/symptomatic hypomagnesemia

›Standard IV repletion

›2 g magnesium sulfate (16 mEq) in 50-100 mL D5W or NS

›Infuse over 15-60 minutes

›Follow with 4-8 g over 24 hours via continuous infusion

›Torsades de pointes protocol

›2 g magnesium sulfate IV bolus over 5-15 minutes

›Repeat 2 g in 5-10 minutes if torsades persists

›Class I recommendation per ACC/AHA/ESC 2006 guidelines

›Severe deficiency protocol

›Up to 5 g (40 mEq) in 1 L D5W over 3 hours for extreme depletion

›Serum Mg <0.4 mmol/L with symptoms

›Maximum doses

›Maximum 30-40 g/day in normal renal function

›Maximum 20 g/48 hours in renal insufficiency (GFR <30 mL/min)

IV infusion monitoring

›Safety monitoring during IV magnesium

›Deep tendon reflexes every 2 hours

›Loss of patellar reflex — stop infusion (toxicity at ~3.5-5 mmol/L)

›Respiratory rate every 2 hours

›Hold if RR <12/minute

›Respiratory arrest risk at Mg >5 mmol/L

›Urine output — maintain >25 mL/hour

›Serum magnesium every 4-6 hours

›Calcium gluconate 1 g IV at bedside as antidote

Oral repletion — mild to moderate

›Oral magnesium supplementation

›Elemental magnesium 240-1000 mg/day in divided doses

›Divide into 2-4 doses to improve tolerance and absorption

›Titrate to bowel tolerance (diarrhea is dose-limiting)

›Preferred organic salts (better absorbed)

›Magnesium citrate — 150-200 mg elemental per dose

›Magnesium glycinate — 100-200 mg elemental per dose

›Magnesium gluconate — 100-250 mg elemental per dose

›Magnesium lactate — similar bioavailability to glycinate

›Avoid inorganic salts

›Magnesium oxide — least absorbed, highest laxative effect

›Use only if cost is primary concern

›Duration

›Continue supplementation for at least 3-5 days after normalization

›Replenishes intracellular stores which equilibrate slowly

Co-electrolyte replacement

›Concurrent potassium repletion

›Potassium chloride 20-40 mEq PO 2-4 times daily for mild hypokalemia

›Potassium chloride IV 10-20 mEq/hour for serum K <3.0 mmol/L

›Maximum 40 mEq/hour in monitored setting with cardiac telemetry

›Refractory hypokalemia will not correct until Mg is repleted

›Mg required for ROMK channel-mediated K reabsorption in distal nephron

›Calcium repletion if hypocalcemia concurrent

›Calcium gluconate 1-2 g IV over 10-20 minutes for symptomatic hypocalcemia

›Oral calcium 500-1000 mg elemental 3 times daily for mild deficiency

›Calcium correction will remain incomplete until Mg corrected

›Mg required for normal PTH secretion and PTH end-organ response

Adjunctive and refractory treatment

›Amiloride for refractory hypomagnesemia

›Dose: 5-10 mg orally once daily

›Reduces renal magnesium wasting

›Mechanism: closes ENaC in collecting duct, reduces electrochemical gradient for Mg loss

›Useful in diuretic-induced hypomagnesemia and Gitelman syndrome

›Monitor serum potassium and creatinine

›Avoid in CKD (GFR <30 mL/min) — hyperkalemia risk

›Oral inulin supplementation

›For PPI-induced hypomagnesemia — modifies gut microbiome and luminal pH

›10-20 g/day as prebiotic fiber supplement

›Consider as adjunct when PPI cannot be discontinued

›Medication de-escalation

›Switch PPI to H2 receptor antagonist when clinically safe

›Adjust loop diuretic dose or timing if clinically feasible

›Review and discontinue causative agents when possible

›SGLT2 inhibitors

›May raise serum magnesium in type 2 diabetic patients

›Mechanism: altered tubular cotransporter activity

09Special Populations/sp63

Pregnancy

›Hypomagnesemia in pregnancy

›Physiologic magnesium requirements increase in pregnancy

›Recommended daily intake 350-400 mg/day in pregnancy

›Fetal demands increase maternal depletion risk

›Causes in pregnancy

›Hyperemesis gravidarum — GI losses

›Pre-eclampsia treatment with IV Mg sulfate paradoxically depletes stores

›Gestational diabetes — insulin and renal wasting

›Clinical significance in pregnancy

›Hypomagnesemia associated with gestational hypertension

›Pre-term labor risk — Mg tocolysis also depletes serum levels

›Fetal growth restriction association

›Treatment in pregnancy

›Oral supplementation safe — preferred in mild to moderate deficiency

›IV magnesium sulfate safe — same dosing as non-pregnant

›Fetal monitoring during IV infusion

›Neonatal hypermagnesemia possible if large maternal doses near delivery

›Distinguish from pre-eclampsia management

›Pre-eclampsia protocol: 4-6 g loading dose IV then 1-2 g/hour maintenance

›Monitor for maternal toxicity — reflexes, respiratory rate, urine output

Geriatric

›Hypomagnesemia in older adults

›Prevalence considerations

›Polypharmacy independently associated with lower Mg levels

›Number of medications inversely correlates with serum Mg

›Drug use was significantly associated with lower plasma Mg in geriatric outpatients

›Age-related physiologic changes increasing risk

10Background/b64

Epidemiology

›Prevalence and incidence data

›General population prevalence 3-10%

›ICU patient prevalence >65%

›Hospitalized patients — 3-10% incidence on admission, higher during stay

›Alcohol use disorder — present in ~30% of these patients

›Type 2 diabetes mellitus — prevalence 10-30% due to insulin resistance and renal wasting

›Calcineurin inhibitor use — 20-40% incidence in organ transplant recipients

›EGFR inhibitor use — 20-40% incidence in oncology patients

›Mortality and prognostic data

›Hypomagnesemia associated with increased all-cause and cardiovascular mortality

›QTc prolongation from hypomagnesemia increases sudden cardiac death risk

›ICU patients with hypomagnesemia have longer length of stay and higher mortality

›Underdiagnosis problem

›Frequently underdiagnosed because serum Mg not routinely measured

›<1% of total body magnesium resides in plasma

›Most magnesium stored in bone (60%) and intracellular compartments (39%)

Pathophysiology

›Magnesium homeostasis mechanisms

›Total body magnesium — approximately 24 g (1000 mmol) in 70 kg adult

›60% in bone

›39% intracellular (muscle, soft tissue)

›<1% in plasma — serum level is poor proxy for total stores

›Intestinal absorption sites

›Small bowel: passive paracellular absorption throughout

›Distal ileum and cecum: active transcellular absorption via TRPM6/TRPM7 channels

›30-40% of dietary Mg absorbed under normal conditions

›Renal handling

›Filtered load reabsorbed: ~95%

›Proximal tubule: 15-25% reabsorption

›Thick ascending limb of Henle: 65-70% reabsorption (TRPM6-independent, passive)

›Distal convoluted tubule (DCT): fine tuning via TRPM6/EGF/EGFR signaling

›Mechanisms of deficiency

›GI losses: malabsorption, diarrhea, vomiting, fistula, NG suction

›Renal wasting: tubular injury, channel dysfunction (TRPM6 inhibition by PPIs, calcineurin inhibitors)

›Inadequate intake: malnutrition, alcoholism

›Intracellular shift: glucose/insulin administration, correction of acidosis, catecholamines

›Downstream effects of Mg deficiency

›Impaired PTH secretion → hypocalcemia

›Impaired ROMK channel function → hypokalemia

›Reduced Na-K-ATPase activity → cellular dysfunction

›QTc prolongation from altered cardiac ion channel kinetics

Therapeutic Considerations

›Evidence base for magnesium repletion

›IV vs oral repletion

›IV required for severe/symptomatic cases — faster serum normalization

›Oral preferred for mild-moderate — better long-term intracellular repletion

›IV magnesium is rapidly excreted by kidneys — recheck within 1-2 days post-infusion

›Repletion kinetics

›Serum Mg normalizes within hours of IV infusion

›Total body store repletion requires days to weeks

›Continue supplementation 3-5 days after serum normalization

›Torsades de pointes treatment evidence

›IV magnesium effective for torsades even when serum Mg is normal

›Mechanism: direct L-type calcium channel blockade and membrane stabilization

›Class I ACC/AHA/ESC recommendation

›Refractory hypokalemia — evidence

›Potassium replacement futile without concurrent Mg repletion

›Mg required for ROMK channel-dependent K transport in DCT

›PPI-induced hypomagnesemia management

›De-escalation to H2-blocker is most effective intervention

›Oral Mg supplementation alone insufficient if PPI continued in some patients

›Mechanism: PPI inhibits TRPM6/7-mediated active Mg transport in colon

›Drug-specific considerations

›Cisplatin nephrotoxicity — prophylactic Mg supplementation during cycles reduces severity

›Calcineurin inhibitor — amiloride reduces renal wasting effectively

›EGFR inhibitor — oral Mg and amiloride combination

11Patient Discharge Instructions/pdi29

copy discharge instructions

›Discharge instructions for Hypomagnesemia

›What is low magnesium (hypomagnesemia)?

›Magnesium is a mineral needed for heart rhythm, muscle function, and nerve signals

›Low magnesium can cause muscle cramps, tremors, weakness, and heart rhythm problems

›It is common in people who take certain medications or have digestive conditions

›Your medications

›Take magnesium supplements exactly as prescribed

›Take with food to reduce stomach upset

›Magnesium can cause loose stools — this is common; reduce dose if severe diarrhea occurs

›Do not stop your other medications without asking your doctor first

›Diet recommendations

›Foods high in magnesium: dark leafy greens (spinach, kale), nuts (almonds, cashews), seeds, legumes, whole grains, dark chocolate, avocados, bananas

›Avoid excessive alcohol — it causes your kidneys to lose magnesium

›Limit caffeine intake — mild magnesiuric effect

›Activity

›Avoid driving or operating heavy machinery if you feel weak, dizzy, or confused

›Resume normal activity gradually as strength returns

›Follow-up

›Blood test to recheck magnesium in 1-2 weeks

›Bring a list of all medications to your follow-up appointment

›Discuss whether your proton pump inhibitor or water pill can be adjusted

›Return to the emergency department immediately for

›Muscle spasms, twitching, or cramping that is worsening

›Irregular heartbeat, palpitations, or chest pain

›Fainting or near-fainting

›Seizure or loss of consciousness

›Confusion, severe weakness, or inability to walk

12References/r38

Guidelines and key sources

›Primary evidence sources used in this document

›Touyz RM, de Baaij JHF, Hoenderop JGJ. Magnesium Disorders. New England Journal of Medicine. 2024

›NEJM comprehensive review — epidemiology, homeostasis, clinical manifestations, treatment

›URL: https://www.nejm.org/doi/full/10.1056/NEJMra1510603

›al-Ghamdi SM, Cameron EC, Sutton RA. Magnesium Deficiency: Pathophysiologic and Clinical Overview. American Journal of Kidney Diseases. 1994

›Classic review of pathophysiology and clinical manifestations

›PMID: 7977315

›Palmer BF, Clegg DJ. Electrolyte Disturbances in Patients with Chronic Alcohol-Use Disorder. New England Journal of Medicine. 2017

›URL: https://www.nejm.org/doi/full/10.1056/NEJMra1704724

›Zipes DP et al. ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death. JACC. 2006

›PMID: 16949478

›Class I recommendation for IV magnesium in torsades de pointes

›Lameris AL et al. Drug-Induced Alterations in Mg2+ Homoeostasis. Clinical Science. 2012

›PMID: 22409531

›Drug-specific mechanisms of hypomagnesemia

›Gommers LMM, Hoenderop JGJ, de Baaij JHF. Mechanisms of Proton Pump Inhibitor-Induced Hypomagnesemia. Acta Physiologica. 2022

›PMID: 35652564

›Rosner MH, Ha N, Palmer BF, Perazella MA. Acquired Disorders of Hypomagnesemia. Mayo Clinic Proceedings. 2023

›PMID: 36872194

›Sandau KE et al. Update to Practice Standards for Electrocardiographic Monitoring in Hospital Settings. AHA Scientific Statement. Circulation. 2017

›URL: https://www.ahajournals.org/doi/10.1161/CIR.0000000000000527

›Recommends continuous telemetry for significant electrolyte imbalances

›Aslan R et al. Serum Magnesium and Ventricular Repolarization Heterogeneity. Biological Trace Element Research. 2026

›PMID: 41699176

›Magnesium as independent predictor of QTc prolongation

›van Orten-Luiten ACB et al. Drug Use Is Associated With Lower Plasma Magnesium Levels in Geriatric Outpatients. Clinical Nutrition. 2019

›PMID: 30581015

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Reviewed by SymptomDx Medical Team · Last reviewed August 18, 2026

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