Proton Pump Inhibitors and Severe Hypomagnesaemia

Tim Cundy; Jonathan Mackay


Curr Opin Gastroenterol. 2011;27(2):180-185. 

In This Article


Hypomagnesaemia may arise through inadequate absorption (or intake), by excessive urinary losses or by redistribution of magnesium from extracellular to intracellular sites. Hypomagnesaemia in adults is usually an acquired condition, but there are a number of rare genetic disorders causing defective renal magnesium handling.[6]

Symptoms attributable to hypomagnesaemia do not occur until plasma concentrations are lower than 0.5 mmol/l. The symptoms include anorexia, nausea, tremor, apathy, depression, agitation and confusion. Severely hypomagnesaemic patients usually have coexistent hypokalaemia and a cellular potassium deficit. The effects of hypomagnesaemia on the excitability of nerve and muscle cells appear not to be direct, but mediated by inhibition of the Mg-dependent Na+-K+-ATPase in cell membranes. Potassium is lost from cells into the extracellular fluid and then the urine because magnesium deficiency impairs the renal conservation of potassium. Hypocalcaemia develops with prolonged, severe hypomagnesaemia, principally because of impaired PTH secretion. With the development of hypocalcaemia, neuromuscular signs such as muscle weakness, tremor, tetany, delirium, convulsions and ultimately coma may occur. In severe hypomagnesaemia, the neuromuscular effects are thus mainly secondary to alterations in potassium and calcium metabolism.