SUN-771 Severe Hypocalcemia as a Result of Hypomagnesemia and Hypoparathyroidism Induced by Proton-Pump Inhibitor Use

Abstract Disclosure: I. Attarwala: None. M.D. Wilson: None. 75-year-old male with history of metastatic prostate cancer, multiple myeloma in remission, and atrial fibrillation presented to the emergency room with vomiting, diarrhea, and progressive weakness for two months; he endorsed perioral paraesthesia in the last two weeks. He was found to have severe hypocalcemia, corrected calcium of 6.9 mg/dL. Other pertinent labs included severe hypomagnesemia (0.4 mg/dL), inappropriately normal parathyroid hormone (PTH) (20.1 pg/mL), and normal vitamin D (34 ng/mL). EKG showed mildly prolonged QTc interval (465 milliseconds). In addition to aggressive repletion of magnesium, he was treated with IV calcium gluconate, followed by oral calcium carbonate. Calcitriol capsules were simultaneously administered to further increase calcium levels. Review of the patient’s home medications revealed long-term proton-pump inhibitor (PPI) use, which was discontinued. With resolution of vomiting/diarrhea and improvement in hypomagnesemia, hypocalcemia resolved, and PTH levels began to rise appropriately. Severe hypomagnesemia is a recognized cause of hypoparathyroidism. While mild deficiencies in magnesium stimulate PTH secretion, severe deficiencies inhibit secretion, known as paradoxical block. This leads to clinically significant hypocalcemia as PTH’s primary role is calcium regulation. Common causes of hypomagnesemia include malnutrition, gastrointestinal losses (diarrhea, vomiting), and medications like PPIs, diuretics, and antibiotics. The patient’s use of omeprazole caused hypomagnesemia which induced hypoparathyroidism. This led to severe hypocalcemia, precipitating paresthesias, vomiting and diarrhea. These gastrointestinal losses further worsened the hypomagnesemia, creating a vicious cycle of electrolyte deficiencies. Cessation of PPI therapy and control of GI disturbances stabilized calcium and magnesium levels. PPI-induced hypomagnesemia and hypoparathyroidism, although rare, has been reported as an adverse effect of this drug class. This case emphasizes the importance of medication reconciliation when evaluating causes of electrolyte abnormalities. Furthermore, it highlights hypomagnesemia as a less common cause of hypocalcemia, and the urgency in aggressive magnesium repletion prior to or in conjunction with calcium repletion. Presentation: Sunday, July 13, 2025

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Journal
Journal of the Endocrine Society
Published
2025-10-01
DOI
https://doi.org/10.1210/jendso/bvaf149.719
Primary Topic
Thyroid and Parathyroid Surgery
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article
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article

SUN-771 Severe Hypocalcemia as a Result of Hypomagnesemia and Hypoparathyroidism Induced by Proton-Pump Inhibitor Use

Insiya Y. Attarwala, Mark Wilson
Journal of the Endocrine Society
Thyroid and Parathyroid Surgery
article

SUN-771 Severe Hypocalcemia as a Result of Hypomagnesemia and Hypoparathyroidism Induced by Proton-Pump Inhibitor Use

Insiya Y. Attarwala, Mark Wilson
article en

Abstract

Abstract Disclosure: I. Attarwala: None. M.D. Wilson: None. 75-year-old male with history of metastatic prostate cancer, multiple myeloma in remission, and atrial fibrillation presented to the emergency room with vomiting, diarrhea, and progressive weakness for two months; he endorsed perioral paraesthesia in the last two weeks. He was found to have severe hypocalcemia, corrected calcium of 6.9 mg/dL. Other pertinent labs included severe hypomagnesemia (0.4 mg/dL), inappropriately normal parathyroid hormone (PTH) (20.1 pg/mL), and normal vitamin D (34 ng/mL). EKG showed mildly prolonged QTc interval (465 milliseconds). In addition to aggressive repletion of magnesium, he was treated with IV calcium gluconate, followed by oral calcium carbonate. Calcitriol capsules were simultaneously administered to further increase calcium levels. Review of the patient’s home medications revealed long-term proton-pump inhibitor (PPI) use, which was discontinued. With resolution of vomiting/diarrhea and improvement in hypomagnesemia, hypocalcemia resolved, and PTH levels began to rise appropriately. Severe hypomagnesemia is a recognized cause of hypoparathyroidism. While mild deficiencies in magnesium stimulate PTH secretion, severe deficiencies inhibit secretion, known as paradoxical block. This leads to clinically significant hypocalcemia as PTH’s primary role is calcium regulation. Common causes of hypomagnesemia include malnutrition, gastrointestinal losses (diarrhea, vomiting), and medications like PPIs, diuretics, and antibiotics. The patient’s use of omeprazole caused hypomagnesemia which induced hypoparathyroidism. This led to severe hypocalcemia, precipitating paresthesias, vomiting and diarrhea. These gastrointestinal losses further worsened the hypomagnesemia, creating a vicious cycle of electrolyte deficiencies. Cessation of PPI therapy and control of GI disturbances stabilized calcium and magnesium levels. PPI-induced hypomagnesemia and hypoparathyroidism, although rare, has been reported as an adverse effect of this drug class. This case emphasizes the importance of medication reconciliation when evaluating causes of electrolyte abnormalities. Furthermore, it highlights hypomagnesemia as a less common cause of hypocalcemia, and the urgency in aggressive magnesium repletion prior to or in conjunction with calcium repletion. Presentation: Sunday, July 13, 2025

Journal of the Endocrine SocietyVol. 9(Supplement_1)
Cottage Health (US)
Openalex Percentile: Top 52%
Thyroid and Parathyroid Surgery
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