Severe symptomatic hypocalcemia with neuromuscular hyperexcitability associated with long-term pantoprazole use: a case report

Hypocalcemia is a common electrolyte abnormality; however, severe symptomatic hypocalcemia presenting with neuromuscular hyperexcitability and cardiac manifestations is an uncommon clinical condition requiring prompt recognition and management. Long-term proton pump inhibitor (PPI) therapy has been associated with disturbances in mineral metabolism, particularly hypomagnesemia, which may contribute to impaired calcium homeostasis. A 54-year-old woman from a remote rural area was referred to our hospital after developing progressive weakness, paresthesia, and painful involuntary muscle contractions. Neurological examination revealed bilateral carpopedal spasms with positive Trousseau’s and Chvostek’s signs. Electrocardiography demonstrated QTc prolongation. Laboratory evaluation showed severe hypocalcemia with a total calcium level of 5.2 mg/dL and ionized calcium of 0.74 mmol/L, accompanied by mild hypomagnesemia, vitamin D insufficiency, and an inappropriately low parathyroid hormone (PTH) response. The patient had been self-administering pantoprazole 40 mg daily for approximately four years without regular reassessment. Pantoprazole was discontinued because of its potential contribution to impaired calcium and magnesium homeostasis. She was treated with intravenous calcium gluconate under cardiac monitoring, followed by magnesium and vitamin D supplementation and transition to oral calcium therapy. Her clinical symptoms resolved during hospitalization. At the one-month follow-up, she remained asymptomatic, with sustained normalization of serum calcium and magnesium levels and no recurrence of electrolyte imbalance. This case highlights the importance of considering severe symptomatic hypocalcemia in patients receiving long-term pantoprazole therapy, particularly when neuromuscular and cardiac manifestations are present. Although a direct causal relationship cannot be definitively established, the coexistence of prolonged PPI exposure, mild hypomagnesemia, vitamin D insufficiency, and impaired PTH response suggests a multifactorial mechanism. Early recognition, comprehensive evaluation of calcium homeostasis, and appropriate correction of electrolyte abnormalities are essential to prevent serious complications.