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Endocrine Abstracts (2026) 117 P265 | DOI: 10.1530/endoabs.117.P265

SFEBES2026 Poster Presentations Late Breaking (54 abstracts)

Severe hypomagnesaemia and hypocalcaemia with secondary hypoparathyroidism induced by long-term proton pump inhibitor use

Emily O’Boyle , Lanitha Srikugan , Cynthia Mohandas , Arthur Ogunko , Itopa Fidelis Abedo & Muhammad Saad


Dartford and Gravesham Trust, Dartford, United Kingdom


Background: Proton pump inhibitors (PPIs) are widely prescribed for gastroesophageal reflux disease (GORD) but have been associated with hypomagnesaemia. Chronic hypomagnesaemia can lead to hypocalcaemia and secondary hypoparathyroidism, which may present with neuromuscular symptoms. Recognition of this adverse effect is critical to avoid unnecessary investigations and ensure appropriate management.

Clinical Case: A 59-year-old female presented to A&E with a three-year history of intermittent paraesthesia affecting her hands, feet, and mouth. Her past medical history included hypertension, GORD, and previous myocardial infarction. She was prescribed long-term high dose lansoprazole therapy (30mg BD). Initial laboratory investigations revealed severe hypocalcaemia (1.50 mmol/l; normal range: 2.20–2.60) and hypomagnesaemia (0.24 mmol/l; normal range: 0.70–1.00), low vitamin D (26 nmol/l; normal >50) and inappropriately low parathyroid hormone (PTH) (29 ng/l; normal: 12–88), consistent with secondary hypoparathyroidism. Her symptoms resolved with intravenous magnesium and calcium replacement. She was discharged on oral supplementation with follow up in endocrinology clinic. Despite treatment adherence, she re-presented with recurrent symptoms and persistently low magnesium (0.25mmol/l) and calcium (1.80mmol/l), again requiring intravenous replacement. In endocrinology clinic, chronic PPI use was identified as a potential cause and lansoprazole discontinued. She required further intravenous replacement followed by oral magnesium, calcium and high dose vitamin D supplementation. Subsequent blood tests demonstrated normalisation of calcium (2.46mmol/l), magnesium (0.84mmol/l), and PTH (38 pg/mL) within 3 weeks.

Conclusion: This case highlights PPI-induced hypomagnesaemia as an under-recognised cause of secondary hypoparathyroidism and hypocalcaemia. Long-term PPI use should be considered as a potential cause in patients with unexplained neuromuscular symptoms or electrolyte disturbances, particularly when refractory to treatment. Regular monitoring of serum magnesium and calcium levels should be considered in long-term PPI users, particularly those at higher risk, such as older adults and those on concurrent diuretic therapy.

Volume 117

Society for Endocrinology BES 2026

Harrogate, United Kingdom
02 Mar 2026 - 04 Mar 2026

Society for Endocrinology 

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