Vonoprazan-associated hypomagnesemia presenting to the emergency department with altered mental status and a suspected seizure.

An older woman without seizure history presented to the emergency department (ED) after an unwitnessed loss of consciousness, with persistent altered mental status. Initial tests showed profound hypomagnesemia (0.6 mg/dL) with low ionized calcium; lactate declined rapidly. Urine showed low magnesium with a fractional excretion of magnesium (FEMg) ≤2.8 %. She had been taking long-term vonoprazan, a potassium-competitive acid blocker (P-CAB). Perfusion MRI with arterial spin labeling (ASL) showed right-hemispheric hyperperfusion, while conventional sequences showed only a chronic cerebellar infarct. These findings resulted in hospital admission with a suspected postictal state. Vonoprazan was discontinued on admission, and magnesium and calcium were repleted. During hospitalization, she improved steadily and returned to baseline within one week. The initial inpatient electroencephalogram showed diffuse low-amplitude slowing without definite epileptiform discharges; by Day 5 the background was more organized. On Day 8, single-photon emission computed tomography (SPECT) showed reduced perfusion in the previously hyperperfused region. QTc peaked at 603 ms and shortened as electrolytes normalized. No antiseizure medication was started, and outpatient labs remained stable on alternative acid suppression. This case suggests that hypomagnesemia associated with a P-CAB, similar to proton pump inhibitor-associated cases, can be a reversible cause of seizure-related ED presentations. Supported by prior case reports and the absence of other culprit drugs or non-drug losses, it underscores early magnesium testing, prompt magnesium and calcium repletion, and medication review with withdrawal of the suspected agent and follow-up monitoring.