A Patient on Long-Term Proton Pump Inhibitors Develops Sudden Seizures and Encephalopathy: An Unusual Presentation of Hypomagnesaemia

Abstract

Objective. To present an unusual but known cause of hypomagnesaemia induced-hypocalcaemia in a chronic GORD patient with severe symptoms with a review of the current literature. Methods. Analysis of the clinical and laboratory findings of the patient and discussion of the multi-factorial nature of his disease and the underlying mechanisms. Results. Our patient described features of magnesium deficiency such as weakness, muscle twitches, and fits with clinical signs of hypocalcaemia: a carpal pedal spasm and paraesthesia. Preadmission blood results revealed low calcium and magnesium levels. He was admitted to ITU, when he presented with seizures and developed encephalopathy. The total vitamin D level was 52.4 nmol/L (>49.9). His U&Es and LFTs were within the normal range with the exception of potassium. He was on Omeprazole for his GORD. With omission of the PPI 1 day after admission and replacement therapy, his ion levels normalised. Conclusion. Hypomagnesaemia is often undiagnosed and is associated with multiple biochemical abnormalities. Treatment focus should be aimed at stopping the PPI and replacing the magnesium. Over use of PPIs is a problem in practice, with the FDA issuing a warning over long-term use. Continued monitoring and decision making on dose reduction/withdrawal is essential to avoid complications.

Severe Hypomagnesemia with Long-Term Use of a Proton Pump Inhibitor: A Case Report

“…The exact mechanism by which PPIs induce hypomagnesemia is unknown, but evidence from case reports and recent modelling studies have elucidated probable hypotheses. [14][15][16]18 As highlighted in the systematic review by Hess and colleagues, case reports of hypomagnesemia with PPI use consistently show low renal magnesium excretion. 16 These findings suggest reduced intestinal absorption as the source of magnesium loss.…”

“…13 Since this publication, there have been over 30 cases reported in the literature of severe hypomagnesemia in PPI users. [14][15][16] Severe hypomagnesemia can lead to such nonspecific symptoms as weakness, tremors, tetany, and nausea, as well as potentially life-threatening complications including seizures, cardiac arrhythmias, and secondary electrolyte disturbances, such as hypocalcemia and hypokalemia. The risk of these adverse effects may be greater in patients with a history of seizure disorder, with cardiac conduction abnormalities, or who are on medications such as digoxin or diuretics.…”

“…16 Substitution with an H2RA does not cause further magnesium depletion. 13,15,16 Hypomagnesemia has been found to quickly recur, within four days on average, with PPI rechallenge. 13,16 Oral magnesium supplementation, while still on a PPI, has been found to fail to correct or only partially correct hypomagnesemia.…”

Pantoprazole‐induced hypomagnesaemia causing cerebellar syndrome and seizures

“…[4][5][6] PPI are believed to cause hypomagnesaemia by inhibition of the transient receptor potential melastin 6 and 7 channels, thereby impairing gastrointestinal magnesium absorption. There are several previous reports of a subacute cerebellar syndrome occurring in association with hypomagnesaemia.…”

“…The neurological manifestations of PPI-induced hypomagnesaemia in previous cases have been limited to seizures. [4][5][6] PPI are believed to cause hypomagnesaemia by inhibition of the transient receptor potential melastin 6 and 7 channels, thereby impairing gastrointestinal magnesium absorption. 7 The mechanism of cerebellar dysfunction in hypomagnesaemia is unclear.…”