An 81-year-old man presented with light-headedness and paraesthesiae in his arms and legs. Past medical history included ischaemic heart disease, gastro-oesophageal reflux disease, chronic kidney disease, hypertension and loose stools, for many years. There was no previous history of peptic ulcer disease and a recent endoscopy was normal. He was taking aspirin 100 mg daily, perindopril 10 mg daily, amlodipine 10 mg daily, rosuvastatin 20 mg daily, omeprazole 20 mg daily and furosemide (frusemide) 40 mg daily. Examination was unremarkable, except for an unsteady gait.
Investigations revealed a normal full blood count, creatinine 142 micromol/L (normal range 64–108), estimated glomerular filtration rate 40 mL/minute (>60), potassium 3.5 mmol/L (3.5–5.2), sodium 142 mmol/L (135–145) and corrected calcium 1.10 (2.10–2.60). The presence of profound hypocalcaemia prompted the measurement of magnesium and parathyroid hormone. The results were magnesium 0.19 mmol/L (0.70–1.10), phosphate 1.87 mmol/L (0.75–1.50) and parathyroid hormone 3.7 pmol/L (1.0–7.0).
The proton pump inhibitor was considered to be the primary cause of the hypomagnesaemia, but the long history of loose stools, concomitant furosemide and chronic kidney disease could have contributed.
Omeprazole was therefore ceased and electrolytes successfully replaced, but due to ongoing reflux symptoms he was prescribed ranitidine. All other drugs were continued. One week later serum magnesium and calcium were normal.
The patient was readmitted nine days after discharge with a large bleeding duodenal ulcer requiring urgent endoscopy and subsequent embolisation. A proton pump inhibitor (pantoprazole) was restarted but the patient’s magnesium dropped again. Magnesium concentrations were maintained initially with intravenous supplementation, but dropped to 0.51 mmol/L when this supplementation was ceased, despite oral magnesium sulfate 1 g three times a day. They subsequently stayed around this level with oral supplementation.
Patients with suggestive symptoms, hypocalcaemia or ‘idiopathic’ hypoparathyroidism should be asked about their drug history. Consider measuring magnesium in those on proton pump inhibitors particularly if there are other predisposing factors for reduced magnesium concentrations.
Conflict of interest: none declared
- Janett S, Camozzi P, Peeters GG, Lava SA, Simonetti GD, Goeggel Simonetti B, et al. Hypomagnesemia induced by long-term treatment with proton-pump inhibitors. Gastroenterol Res Pract 2015;2015:951768.
- Zipursky J, Macdonald EM, Hollands S, Gomes T, Mamdani MM, Paterson JM, et al. Proton pump inhibitors and hospitalization with hypomagnesemia: a population-based case-control study. PLoS Med 2014;11:e1001736.
- Hoorn EJ, van der Hoek J, de Man RA, Kuipers EJ, Bolwerk C, Zietse R. A case series of proton pump inhibitor-induced hypomagnesemia. Am J Kidney Dis 2010;56:112-6. http://dx.doi.org/j.ajkd.2009.11.019
- Toh JW, Ong E, Wilson R. Hypomagnesaemia associated with long-term use of proton pump inhibitors. Gastroenterol Rep (Oxf) 2015;3:243-53.