Unmasking of normocalcemic primary hyperparathyroidism after sodium-glucose cotransporter-2 inhibitor initiation

Christodoulos Dolapsakis

https://orcid.org/0000-0001-9251-7872

4th Department of Internal Medicine, National and Kapodistrian University of Athens, School of Medicine, Attikon University Hospital, Athens, Greece

Emmanouil Karofylakis

4th Department of Internal Medicine, National and Kapodistrian University of Athens, School of Medicine, Attikon University Hospital, Athens, Greece

Stamatios Chalvatzis

4th Department of Internal Medicine, National and Kapodistrian University of Athens, School of Medicine, Attikon University Hospital, Athens, Greece

Keywords

SGLT2 inhibitors, hypercalcemia, hyperparathyroidism

Abstract

Sodium-glucose cotransporter-2 (SGLT2) inhibitors have complex interactions with bone metabolism, including an increase in parathyroid hormone (PTH) levels. Here we report a case of a SGLT2 inhibitor-induced hypercalcemia due to primary hyperparathyroidism. In the subset of patients with normocalcemic primary hyperparathyroidism, SGLT2 inhibitor initiation can unmask the disorder causing overt hypercalcaemic hyperparathyroidism. Although normocalcemic primary hyperparathyroidism is a rare entity, we propose obtaining a baseline PTH level before starting a SGLT2 inhibitor in patients with calcium levels in the upper limit of normal and normal total 25-hydroxyvitamin D levels, especially if they are under vitamin D supplementation. PTH should be rechecked in order to exclude overt primary hyperparathyroidism.

References

  • Filippatos TD, Tsimihodimos V, Liamis G, Elisaf MS. SGLT2 inhibitors-induced electrolyte abnormalities: an analysis of the associated mechanisms. Diabetes Metab Syndr 2018;12:59-63.
  • Blau JE, Bauman V, Conway EM. Canagliflozin triggers the FGF23/1,25- dihydroxyvitamin D/PTH axis in healthy volunteers in a randomized crossover study. JCI Insight 2018;3:e99123.
  • Ye Y, Zhao C, Liang J, Yang Y, Yu M, Qu Xl. Effect of Sodium-Glucose Co-transporter 2 Inhibitors on Bone Metabolism and Fracture Risk. Front Pharmacol 2019;9:1517.
  • Macfarlane DP, Yu N, Leese GP. Subclinical and asymptomatic parathyroid disease: implications of emerging data. Lancet Diabetes Endocrinol 2013;1:329-40.
  • Rejnmark L, Amstrup AK, Mollercup CL, Heickendorff L, Mosekilde L. Further insights into the pathogenesis of primary hyperparathyroidism: a nested case-control study. J Clin Endocrinol Metab 2013;98:87-96.
  • Masri ED, Jamil Y, Fares JE. Sodium-glucose co-transporter protein 2 inhibitors induced hypercalcemia: a case series and literature review. AACE Clin Case Rep 2021;8:30-33.
  • Awada M, Melhem Z, Khalaf ZM, Hazimeh Y. Masked primary hyperparathyroidism by empagliflozin use. Cureus 2022;14:e24488.
  • Akhanli P, Hepsen S, Ucan B, Saylam G, Cakal E. Hypercalcemic patient diagnosed with primary hyperparathyroidism after dapagliflozin treatment. AACE Clin Case Rep 2020;6:e319- e321.
  • Kaur A, Winters S. Severe hypercalcemia and hypernatremia in a patient treated with canagliflozin. Endocrinol Diabetes Metab Case Rep 2015;2015:150042.
  • Vidas MM, Gurpide BD, Rubio E, Huerta Ana, Perez JP. Dapagliflozin-induced hypercalcemia. Nefrologia 2018;38:336-337.
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Published: 2025-01-29
Issue: 2025: Vol 12 No 2 (view)

How to cite:
1.
Dolapsakis C, Karofylakis E, Chalvatzis S. Unmasking of normocalcemic primary hyperparathyroidism after sodium-glucose cotransporter-2 inhibitor initiation. EJCRIM [Internet]. 2025 Jan. 29 [cited 2025 May 24];12(2). Available from: https://www.ejcrim.com/index.php/EJCRIM/article/view/5169
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