Intermittent use of pantoprazole and famotidine in severe hypomagnesaemia due to omeprazole.

We read with interest the article ‘Hypomagnesaemia due to use of proton pump inhibitorsa review’, by Kuipers et al. We present here a patient with severe hypomagnesaemia due to omeprazole. We emphasise that the intermittent use of pantoprazole and a histamine H2-receptor antagonist may be an appropriate therapeutic alternative for normalising serum magnesium concentrations, without recurrence of gastro-oesophageal symptoms. The patient is a 67-year-old man who presented in April 2010 with paresthesia, numbness and weakness in his limbs. His medical history included hypertension, chronic obstructive airways disease and ischaemic heart disease. In October 2006 and December 2006 he was hospitalised because of tetany, with severe hypocalcaemia and hypomagnesaemia, which was attributed to alcoholism, without further studies. In 2006 he was on omeprazole therapy for gastroprotection. The patient was followed up in the outpatient clinic until July 2007, with serum magnesium at the lower limit of normal range or slightly reduced despite oral magnesium supplements. After that, he was lost to follow-up; he continued treatment with omeprazole until his current hospitalisation. The laboratory findings showed hypocalcaemia (1.55 mmol/l), hypomagnesaemia (0.14 mmol/l) and a level of 25-OH-vitamin D at 27.45 nmol/l (our laboratory range, 29.9 to 134.7). The complete blood count, and serum levels of albumin, glucose, creatinine, alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, gamma glutamyl transpeptidase, sodium, potassium, and phosphorus were normal. He denied alcohol use, and other causes of hypomagnesaemia were absent, including family history of genetic electrolyte disorders, diarrhoea, and use of laxatives, or diuretics. The slightly low level of 25-OH vitamin D coincided with extraction at the beginning of spring. His medications l e t t e r t o t h e e d i t or