Several types of antibiotics are associated with hypomagnesemia primarily because they cause renal loss of Mg (Table 2). These include aminoglycosides, amphotericin B, pentamidine, and foscarnet.
Antibiotics: Taking magnesium supplements may reduce the absorption of quinolone antibiotics, tetracycline antibiotics, and nitrofurantoin (Macrodandin). Magnesium should be taken 1 hour before or 2 hours after taking these medications.
Even when people are very conscientious about their diets, they may be taking medications that can undermine healthy magnesium levels. Diuretics like furosemide (Lasix), bumetanide, chlorthalidone and hydrochlorothiazide often deplete magnesium along with potassium.
These studies have shown that hypomagnesemia facilitates digitalis toxicity which can be promptly terminated with magnesium sulfate.
Symptoms of magnesium toxicity, which usually develop after serum concentrations exceed 1.74–2.61 mmol/L, can include hypotension, nausea, vomiting, facial flushing, retention of urine, ileus, depression, and lethargy before progressing to muscle weakness, difficulty breathing, extreme hypotension, irregular heartbeat, ...
Magnesium toxicity is commonly caused by the overuse of magnesium-containing medication or under-excretion of magnesium by the kidneys.
Conclusions. Thiazide diuretic use is associated with lower serum magnesium levels and an increased risk of hypomagnesaemia.
Cellular Mg2+ depletion occurs in up to 50% of patients receiving thiazide diuretics and can be present despite normal serum Mg2+ concentrations. Hypomagnesemia occurs more frequently in the elderly, and in those receiving high-dose loop diuretic therapy for extended periods of time (such as heart failure patients).
Hypercalciuric hypomagnesemias: Mutations affect the reabsorption of magnesium and calcium ions in the thick ascending limb of Henle (TAL), leading to hypercalciuric hypomagnesemia that ultimately results in nephrocalcinosis or chronic kidney disease.
Statins: Cholesterol-lowering medications, such as Lipitor, are intended to lower levels of low-density lipoprotein cholesterol and triglycerides. These prescription drugs bind to fats that are necessary for mineral absorption, reducing the body's capacity to use magnesium.
Although the mechanism by which omeprazole induces hypomagnesaemia is unclear it has been postulated that it may be due to reduced absorption of magnesium through an active transport mechanism.
In a Drug Safety Communication, the FDA says that it has determined that long-term use of proton pump inhibitors (PPIs), like Nexium and Prilosec, may cause low serum magnesium levels; a condition known as hypomagnesemia.
Magnesium does not react with water to any significant extent. This is in contrast with calcium, immediately below magnesium in the periodic table, which does react slowly with cold water.
High doses of magnesium from supplements or medications can cause nausea, abdominal cramping and diarrhea. In addition, the magnesium in supplements can interact with some types of antibiotics and other medicines.
Magnesium also increases the effectiveness of all antihypertensive drug classes. It remains to be conclusively proven that cardiovascular disease such as coronary heart disease, ischemic stroke, and cardiac arrhythmias can be prevented or treated with magnesium intake.
Hypomagnesemia is often associated with hypokalemia (due to urinary potassium wasting) and hypocalcemia (due both to lower parathyroid hormone secretion and end-organ resistance to its effect).
Hypomagnesemia in congestive heart failure(CHF)
In experimental models without organic cardiac disease hypomagnesemia caused signs of cardiac failure which was improved after Mg administration8, 9.
Hypomagnesemia can be linked to many factors, causing disturbances in energy metabolism, ion channel exchanges, action potential alteration and myocardial cell instability, all mostly leading to ventricular arrhythmia.
Loop diuretics (including furosemide, bumetanide, and ethacrynic acid), produce large increases in magnesium excretion through the inhibition of the electrical gradient necessary for magnesium reabsorption in the TAL.
Proton-pump Inhibitor-induced Severe Hypomagnesemia and Hypocalcemia are Clinically Masked by Thiazide Diuretic - PMC. The .
Treatment for hypomagnesemia depends on how mild or severe it is and the underlying cause. If the hypomagnesemia is mild, your healthcare provider will likely recommend magnesium tablets taken by mouth. If the hypomagnesemia is severe, you'll likely be in a hospital and receive fluids and magnesium through an IV.
Calcium gluconate: the antidote for magnesium toxicity is calcium gluconate 1 g IV over 3 minutes. Repeat doses may be necessary. Calcium chloride can also be used in lieu of calcium gluconate. The suggested dose for calcium chloride for magnesium toxicity is 500 mg of 10% calcium chloride IV given over 5-10 minutes.
If you're getting too much magnesium, the first symptoms that you'll notice are nausea, diarrhea, and cramping. Magnesium toxicity is diagnosed when the concentration of magnesium in your blood reaches 1.74–2.61 millimoles per liter (mmol/L).
The patient should be assessed for signs of toxicity (e.g., visual changes, somnolence, flushing, muscle paralysis, loss of patellar reflexes) or pulmonary edema. If these signs are observed, a physician must be notified.