Severe Concurrent Hypocalcemia and Hypophosphatemia Following Ferric Carboxymaltose After Roux-en-Y Gastric Bypass: A Comparative Two-Patient Case Series.
5 affiliations
- 1Biomedical Sciences, Mohammed Bin Rashid University of Medicine and Health Sciences, Dubai, ARE.
- 2Internal Medicine, Tanta University Hospital, Tanta, EGY.
- 3Medicine, St. George's University, St. George's, GRD.
- 4Internal Medicine, Detroit Medical Center/Wayne State University, Detroit, USA.
- 5Endocrinology, Mohammed Bin Rashid University of Medicine and Health Sciences, Dubai, ARE.
Abstract
Ferric carboxymaltose (FCM) can cause hypophosphatemia through fibroblast growth factor 23 (FGF23)-associated renal phosphate wasting. Patients who have undergone Roux-en-Y gastric bypass may be particularly vulnerable because calcium and vitamin D homeostasis may already be impaired. We describe two women with previous Roux-en-Y gastric bypass who developed severe symptomatic concurrent hypocalcemia and hypophosphatemia after FCM. Both had preexisting mineral vulnerability, and the findings are therefore interpreted as a multifactorial interaction rather than evidence that FCM alone caused the hypocalcemia. The first patient, aged 39 years, received FCM 500 mg weekly for five weeks (cumulative dose approximately 2,500 mg) and developed calcium 5.3 mg/dL and phosphate 0.8 mg/dL, with elevated C-terminal FGF23 and inappropriate urinary phosphate excretion during hypophosphatemia. The second patient, aged 37 years, received FCM 500 mg weekly for two doses (cumulative dose 1,000 mg) and presented approximately seven weeks later with calcium 5.9 mg/dL and a subsequent phosphate nadir of 1.3 mg/dL. Her C-terminal FGF23 was measured during early biochemical recovery and remained elevated; urinary phosphate excretion remained measurable during the hypophosphatemic/repletion period, although interpretation was limited by concurrent treatment. Both required prolonged mineral replacement, and the second patient required multiple admissions and repeated IV calcium. These cases suggest that FCM-associated phosphate disturbance may act as an additional metabolic stressor in post-bariatric patients with reduced calcium and vitamin D reserve, producing a severe combined mineral phenotype rather than isolated hypophosphatemia.
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BibTeX
@article{ali2026severe,
title = {{Severe Concurrent Hypocalcemia and Hypophosphatemia Following Ferric Carboxymaltose After Roux-en-Y Gastric Bypass: A Comparative Two-Patient Case Series.}},
author = {Isra Ali and Ahmed Mahgoub and Anaida Singh and Abu-Bekr Mohamed and Ahmed Elhassan},
journal = {Cureus},
year = {2026},
month = oct,
doi = {10.7759/cureus.117621},
url = {https://europepmc.org/article/MED/42999789},
note = {CC BY},
}
RIS
TY - JOUR
TI - Severe Concurrent Hypocalcemia and Hypophosphatemia Following Ferric Carboxymaltose After Roux-en-Y Gastric Bypass: A Comparative Two-Patient Case Series.
AU - Isra Ali
AU - Ahmed Mahgoub
AU - Anaida Singh
AU - Abu-Bekr Mohamed
AU - Ahmed Elhassan
PY - 2026
DA - 2026/10/08
JO - Cureus
DO - 10.7759/cureus.117621
UR - https://europepmc.org/article/MED/42999789
AB - Ferric carboxymaltose (FCM) can cause hypophosphatemia through fibroblast growth factor 23 (FGF23)-associated renal phosphate wasting. Patients who have undergone Roux-en-Y gastric bypass may be particularly vulnerable because calcium and vitamin D homeostasis may already be impaired. We describe two women with previous Roux-en-Y gastric bypass who developed severe symptomatic concurrent hypocalcemia and hypophosphatemia after FCM. Both had preexisting mineral vulnerability, and the findings are therefore interpreted as a multifactorial interaction rather than evidence that FCM alone caused the hypocalcemia. The first patient, aged 39 years, received FCM 500 mg weekly for five weeks (cumulative dose approximately 2,500 mg) and developed calcium 5.3 mg/dL and phosphate 0.8 mg/dL, with elevated C-terminal FGF23 and inappropriate urinary phosphate excretion during hypophosphatemia. The second patient, aged 37 years, received FCM 500 mg weekly for two doses (cumulative dose 1,000 mg) and presented approximately seven weeks later with calcium 5.9 mg/dL and a subsequent phosphate nadir of 1.3 mg/dL. Her C-terminal FGF23 was measured during early biochemical recovery and remained elevated; urinary phosphate excretion remained measurable during the hypophosphatemic/repletion period, although interpretation was limited by concurrent treatment. Both required prolonged mineral replacement, and the second patient required multiple admissions and repeated IV calcium. These cases suggest that FCM-associated phosphate disturbance may act as an additional metabolic stressor in post-bariatric patients with reduced calcium and vitamin D reserve, producing a severe combined mineral phenotype rather than isolated hypophosphatemia.
SN - 2168-8184
ER -