THE PERILOUS PROTON PUMP INHIBITOR

Abstract

INTRODUCTION
Proton pump inhibitors (PPIs) are the mainstays of therapy for all gastric acid related diseases. PPIs have been associated with various adverse effects, including hypomagnesemia. The postulated mechanism of PPI-related hypomagnesemia involves inhibition of intestinal magnesium absorption via transient receptor potential melastin (TRPM) 6 and 7 cation channels. PPI-induced hypomagnesaemia (PPIH) has become a well recognized phenomenon since it was first reported in 2006. In this article, we report 2 cases of PPIH referred to endocrine unit for severe hypocalemia related to PPIH.

CASE
Patient 1 was newly diagnosed with pulmonary tuberculosis (PTB). She was started on pantoprazole due to vomiting after taking anti-TB medications. She presented a week later with supraventricular tachycardia. Blood investigations showed multiple electrolyte abnormalities, including hypomagnesaemia, hypocalcaemia, and hypokalemia. Her serum electrolytes failed to return to normal despite multiple corrections given. After pantoprazole was discontinued, the serum levels of magnesium, potassium and calcium started to respond to corrections given and returned to normal. Patient 2 was diagnosed with peptic ulcer disease and started on pantoprazole. 4 months later, she presented with lethargy and bilateral hand numbness. Blood investigations revealed severe hypocalcaemia and hypomagnesaemia. Her magnesium and calcium levels slowly returned to normal after the pantoprazole was discontinued.

CONCLUSION
Known risks of long-term PPIs administration must be considered in clinical practice and judicious use of PPIs is important to avoid potentially fatal complications.