As magnesium and other medicinal products may mutually influence each other's absorption, a time interval of 2 to 3 hours should generally be respected if possible.
This specifically applies to:
• Cellulose sodium phosphate; edetate disodium: concurrent use with magnesium supplements may result in binding of magnesium; patients should be advised not to take magnesium supplements within 1 hour of cellulose sodium phosphate or edentate disodium.
• Fluorides and tetracycline: if they must be used, the doses must be separated by 2 to 3 hours or more to prevent their admixture in the gut.
• Aminoquinolines, quinidine and quinidine derivatives, nitrofurantoin, penicillamine, iron, bisphosphonates, eltrombopag, nitroxoline: to avoid impairment of absorption, magnesium preparations should be taken 3 to 4 hours before or after the administration of those drugs.
Magnesium homeostasis influenced by medication Because of increased magnesium losses, a dose adjustment of magnesium may be necessary when taking the following substances:
Diuretics (e.g. thiazide, furosemide) are widely used in the treatment of hypertension, heart failure and kidney diseases. They increase urinary output with hypermagnesuria probably leading to hypomagnesaemia and magnesium depletion.
EGF-receptor antagonist (e.g. cetuximab, erlotinib, panitumumab). Since EGF is a magnesiotropic hormone, treatment with EGF-receptor antagonists can result in severe hypomagnesaemia.
VEGF-blockers Bevacizumab is a humanised IgG1 antibody that binds and inhibits VEGF activity. Hypomagnesaemia is recognised as a very common adverse reaction associated with bevacizumab therapy.
PD-1 inhibitors Nivolumab is a human IgG4 anti-PD-1 monoclonal antibody that works as a checkpoint inhibitor that allows the immune system to kill cancer cells. Treatment with nivolumab can result in dysregulation of magnesium metabolism.
Long-term treatment with proton pump inhibitors (e.g. omeprazole, esomeprazole, lansoprazole and pantoprazole) has been related to severe hypomagnesaemia, probably due to disturbances in absorption.
Aminoglycoside antibiotics (e.g. gentamycin, tobramycin and amikacin) are widely used in the treatment of severe bacterial infections. Studies showed that in 25 % of the patients, hypomagnesaemia occurs due to renal magnesium loss.
Foscarnet is a pyrophosphate analogue that inhibits many viral DNA polymerases.
Hypomagnesaemia is among others a side effect of foscarnet treatment as foscarnet is a potent chelator of divalent cations. Other viral DNA polymerase inhibitors include Pentamidine, Rapamycin and Amphotericin B.
Immunosuppressive agents (e.g. Ciclosporin A and Tacrolimus) increase the loss of magnesium via the kidneys.
Chemotherapy agents (e.g. Cisplatin and Carboplatin) can result in hypomagnesemia - a widely recognised toxic side effect of chemotherapy and occurs due to renal tubular toxicity.
Magnesium homeostasis influenced by medical conditions
Excessive excretion of magnesium into the urine is a cause of magnesium depletion. Osmotic diuresis due to glucosuria can result in magnesium depletion, therefore, those with diabetes mellitus have an increased requirement for magnesium.