DOI: https://doi.org/10.36347/sjmcr.2025.v13i09.006

Pages: 1976-1980

Background: Proton pump inhibitors (PPIs) can precipitate clinically significant hypomagnesemia via impaired intestinal magnesium absorption, often with secondary hypo-K and hypo-Ca; the effect is class-wide and may be overlooked in complex patients. Case: A 70-year-old woman on chronic hemodialysis for hypertensive and diabetic nephropathy, with GERD (on omeprazole) and depression, was admitted for vomiting due to a gastrointestinal infection complicated by hyponatremia. During hospitalization (antibiotics given; omeprazole continued), she developed progressive neuromuscular symptoms (cramps, weakness, tremor). Laboratory testing revealed hypomagnesemia with concurrent electrolyte derangements consistent with magnesium deficiency. Management and outcome: Omeprazole was discontinued and intravenous magnesium replacement was initiated, followed by oral supplementation with correction of associated electrolytes. Symptoms improved in parallel with rising serum magnesium. The presentation was attributed to multifactorial magnesium depletion (dialysis, gastrointestinal losses, and PPI-related intestinal malabsorption). In accordance with prior reports, withdrawal of the PPI is central to management; H₂-receptor antagonists are viable alternatives, and recurrence can follow PPI rechallenge. Conclusion: In dialysis patients with gastrointestinal losses, new neuromuscular symptoms should prompt evaluation for hypomagnesemia—particularly with ongoing PPI therapy. Early recognition, PPI cessation, targeted magnesium repletion, and monitoring can rapidly reverse symptoms and prevent complications.