Endocrine Abstracts

Serum magnesium concentration is regulated by the balance between intestinal absorption and renal excretion. Hypomagnesaemia is relatively common, with an estimated prevalence in the general population ranging from 2.5 to 15%. It may result from inadequate magnesium intake, increased gastrointestinal or renal loss, or redistribution from extracellular to intracellular space. Drug-induced hypomagnesaemia, particularly related to proton-pump inhibitor (PPI) therapy, is being increasingly recognised. Although most patients with hypomagnesaemia are asymptomatic, manifestations may include neuromuscular, cardiovascular and metabolic features.

Measurement of total serum magnesium is the method of choice for determining clinical magnesium status. However serum magnesium may not always accurately reflect the intracellular magnesium status and a subject with normal serum magnesium levels may have total body magnesium depletion. Although 30% of serum magnesium is bound to albumin and is therefore inactive, conventionally serum magnesium concentrations are not ‘adjusted’ for albumin concentrations, as there is generally a high correlation between serum total and ionised magnesium concentrations.

Once hypomagnesaemia is confirmed, in many cases the cause can be obtained from the history. If no cause is apparent, the distinction between gastrointestinal and renal losses can be made by measuring 24-h urinary magnesium excretion or fractional excretion of magnesium.

Patients with symptomatic hypomagnesaemia should be treated with intravenous magnesium, reserving oral replacement for asymptomatic patients. Consensus statements suggest administration of 8–12 g of magnesium sulphate in the first 24 h followed by 4–6 g/day for 3 or 4 days to replete body stores. Oral magnesium salts can be used to supplement body magnesium, but they are generally not well absorbed from the gastro-intestinal tract.