Preventing recurrent hypomagnesaemia: oral magnesium glycerophosphate

Evidence review: efficacy

No published clinical trials comparing magnesium glycerophosphate with placebo or active comparator for preventing recurrent hypomagnesaemia after treatment with intravenous magnesium were identified.

Three case reports on the use of oral magnesium glycerophosphate in adults for preventing recurrent hypomagnesaemia after intravenous treatment were identified^{[17],[18],[19]}.

The first patient was a 39-year-old woman who presented with paraesthesia and cramps in the hands and feet for the previous 3 days (Ross et al. 2001). She was also passing increased volumes of fluid secretions into her ileostomy (up to 4–8 litres a day). Fifteen months previously she had extensive resection of the small and large bowel, ileostomy, left nephrectomy, and a hysterectomy as a result of a septic abortion.

She was found to be clinically dehydrated, with low magnesium (0.13 mmol/litre), corrected calcium and albumin, and abnormal renal function. She was rehydrated, given intravenous magnesium at a dose of 60 mmol/day initially, and oral calcium supplements. Her serum calcium normalised and her renal function returned to a stable baseline. Treatment was also given to reduce her ileostomy output.

Oral magnesium glycerophosphate was given in increasing doses to a maximum of 108 mmol/day of magnesium (285 mg, 9 times a day). However, this did not maintain adequate serum magnesium concentrations, and intravenous top ups were needed as a result of repeat symptomatic episodes of hypomagnesaemia.

An alternative magnesium preparation, magnesium oxide was then substituted. When the patient was taking 67.5 mmol of magnesium per day (300 mg magnesium oxide, 9 times a day), her serum magnesium levels stabilised at 0.58 mmol/litre. She remained asymptomatic after discharge from hospital, with serum magnesium levels between 0.58 and 0.62 mmol/litre with continued magnesium oxide supplementation. Her serum magnesium levels fell to 0.42 mmol/litre when she reduced the dose to 200 mg, 4 times a day, but responded quickly after this was returned to the original dose of 300 mg, 9 times a day.

The patient's hypomagnesaemia was attributed to her extensive bowel resection, because the small intestine is thought to be the area of maximum absorption of magnesium. In this case, absorption appeared to be dependent on the preparation used, but the reason for this was not known.

The second patient was a 65-year-old woman with short bowel syndrome as a result of surgery for colorectal cancer and subsequent abscess formation (Arasaradnam and Bolton 2002). She had high ileostomy output and clinical signs of hypomagnesaemia and hypocalcaemia. Oral magnesium glycerophosphate was not sufficient to maintain her serum magnesium level, and frequent intravenous top ups were needed. The magnesium glycerophosphate was switched to oral magnesium oxide but this did not reduce the need for intravenous top ups. Her condition was managed with ongoing magnesium oxide supplementation plus intravenous magnesium top ups through a peripheral line every 3–6 months.

The third patient was a 78-year-old woman hospitalised after an exacerbation of chronic obstructive pulmonary disease, as well as diarrhoea and vomiting (Shabajee et al. 2008). She had been diagnosed 7 years previously with non-erosive duodenitis, diverticular disease and a hiatus hernia after experiencing postprandial pain, early satiety, nausea and weight loss. She was prescribed omeprazole (40 mg/day) and these symptoms improved slightly.

On admission, the patient was found to be hypokalaemic but her condition did not respond to withdrawal of diuretics and administration of intravenous and oral potassium. She developed hallucinations and agitation on day 4, and had muscle excitability. She was found to be hypokalaemic, hypomagnesaemic, hypocalcaemic and hypophosphataemic.

After administration of intravenous magnesium sulfate, calcium gluconate and continued potassium the patient's symptoms resolved. Her magnesium levels were normal while she was receiving intravenous magnesium, but fell once this stopped. After 10 days she was discharged taking oral magnesium glycerophosphate and a phosphate supplement.

On outpatient follow-up, the patient's serum magnesium and calcium were still low, although tests suggested that her kidney conservation of magnesium was normal, and she no longer had diarrhoea and denied using laxatives or alcohol.

The patient's omeprazole was discontinued because of previous case reports of hypomagnesaemic hypoparathyroidism associated with this drug, and ranitidine was prescribed instead. The patient's electrolyte levels subsequently improved dramatically and were maintained even after the magnesium glycerophosphate was stopped.

No studies of oral magnesium glycerophosphate for preventing recurrent hypomagnesaemia after intravenous infusion in children were identified.