Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2008) 15 P24

University Hospital of Wales, Cardiff, UK.


A 43-year-old policeman was referred for investigation of recurrent symptomatic hypomagnesaemia. He initially presented with a one week history of dizziness, headaches, and ‘funny turns,’ on a background history of bronchial asthma, reflux oeosphagitis and hypertension. Initial investigations demonstrated hypocalcaemia, hypomagnesaemia and hypophosphataemia. These disturbances were attributed to his thiazide diuretic which was subsequently discontinued; his symptoms improved upon correction of the electrolyte abnormalities. The possibility of malabsorption was also considered but GI investigations including upper GI endoscopy, small bowel studies, and anti-TTG antibodies were normal. He continued to experience headaches, dizzy spells and paraesthesiae in both hands despite discontinuing the diuretic, and was noted to remain significantly hypomagnesaemic requiring oral magnesium replacement supplemented with 3-weekly infusions. His symptoms would worsen in the week prior to infusion and were associated with magnesium levels of 0.3–0.5 mmol/l. His renal function, 24 urinary magnesium excretion and plasma PRA were normal.

This patient had been on high dose omeprazole for reflux oeosphagitis for three years prior to presentation which has been reported to be associated with hypomagnesaemia. As no other cause for his electrolyte disturbance had been identified this treatment was withdrawn. His biochemistry normalised within the following 6 weeks and his symptoms resolved completely within 12 weeks, thus no longer requiring magnesium supplementation.

This case illustrates an association between PPI therapy and hypomagnesaemia which has been described in isolated case reports in the literature. The mechanism is not yet fully understood but may be related to calcium absorption which is enhanced in an acid environment. With increasing use of PPI therapy, patients should be monitored for electrolyte disturbances, particularly in those with concomitant neuromuscular symptoms or cardiac conduction disease.

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