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Case report uncovers mineral imbalance in an older woman after acid suppression, suggesting careful therapy evaluation is needed.
Potent gastric acid suppression can disrupt mineral homeostasis. An older woman receiving alfacalcidol developed weakness accompanied by profound hypophosphatemia with hypocalcemia and secondary hyperparathyroidism after initiation of the potassium-competitive acid blocker vonoprazan. Laboratory findings showed an elevated intact parathyroid hormone level and renal phosphate wasting, whereas her serum magnesium level was 2.7 mg/dL (reference range, 1.7–2.6 mg/dL) and her intact fibroblast growth factor 23 was 41.7 pg/mL (reference range, 19.9–52.9 pg/mL). The patient's weakness and calcium–phosphate abnormalities resolved with mineral repletion and switching from vonoprazan to a proton-pump inhibitor. This case highlights that strong acid suppression may precipitate significant calcium–phosphate derangements despite active vitamin D therapy. Early evaluation of mineral metabolism and reassessment of acid-suppressive therapy are especially important in patients with unexplained weakness.
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Hamada et al. (2026) studied this question.
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