Abstract

Introduction: Proton-pump inhibitors (PPI) are the mainstay therapy for acid-related gastrointestinal entities. Longstanding PPI use is associated with an increased risk of adverse effects; however, clinically significant side effects, such as metabolic derangements, are rare. Here we highlight a case of critical electrolyte derangements secondary to prolonged omeprazole use. Case Description/Methods: A 61-year-old female with a history of hypertension and GERD presented with intermittent numbness for several months involving bilateral upper extremities. Exam showed no focal neurologic deficits with intact sensation and appropriate motor strength. CT head and cervical spine were unremarkable. Initial labs showed significant electrolyte derangements, including hypokalemia 3.3 mmol/L, hypocalcemia 5.7 mg/dL (0.64 mmol/L ionized), and hypomagnesemia 0.5 mg/dL. TSH, PTH, and 25-hydroxyvitamin D levels were intact (Table). EKG showed normal sinus rhythm with QTc prolongation at 542 ms. Despite aggressive intravenous repletion, her electrolytes remained suboptimal. After evaluation by endocrinology, her symptoms were thought to be secondary to PPI-induced hypomagnesemia. The patient had been taking omeprazole for nearly 20 years after evaluation by ENT for vocal cord hoarseness thought to be secondary to GERD. Patient was transitioned from PPI to an H2 blocker. She underwent EGD which showed mild gastritis with biopsies negative for Helicobacter pylori. Fortunately, her symptoms resolved after electrolyte stabilization with potassium 3.9 mmol/L, calcium 8.8 mg/dL, and magnesium 1.8 mg/dL. She was discharged on famotidine with instructions to follow up with gastroenterology. Discussion: Hypomagnesemia has become an increasingly well-recognized, albeit rare side effect of PPI use. The mechanism is thought to involve interference of TRPM6 and TRPM7 located on apical membranes of enterocytes leading to intestinal malabsorption with resulting hypomagnesemia as well as hypocalcemia and hypokalemia. Interestingly, manifestations of hypocalcemia and hypokalemia can be concealed by calcium and potassium-sparing agents, which was likely the case in our patient who was taking candesartan-hydrochlorothiazide combination therapy for hypertension. Our case demonstrates the importance of limiting chronic PPI therapy given the potential for serious consequences. Increased efforts should be aimed at deprescribing PPI therapy. Table 1. - Electrolyte derangements including hypokalemia, hypocalcemia, and hypomagnesemia, which remained suboptimal despite aggressive repletion. Electrolytes finally stabilized after switching from PPI to H2 blocker Day 0 Day 3 Day 5 Day 6 K+ (mmol/L) 3.3 3.2 3.8 3.9 Ca+2 (mg/dL) 5.7 6.6 7.8 9.5 Mg+2 (mg/dL) 0.5 1.6 1.7 1.6

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