SUN-762 Suspected Fibroblast Growth Factor 23 Mediated Hypophosphatemia in a Patient with Multiple Myeloma

Abstract Disclosure: M. Stefanelli: None. M. Ansar: None. F.H. Morgan: None. Introduction: Phosphate levels are regulated by parathyroid hormone (PTH), vitamin D, fibroblast growth factor 23 (FGF 23), and other electrolytes. FGF 23 levels can be elevated in multiple myeloma, which can contribute to dysregulation of phosphate metabolism and lead to tumor induced osteomalacia [1]. CASE PRESENTATION A 68-year-old male with a history of relapsed multiple myeloma presented for elective bispecific T-cell engager (BiTE) therapy with Elranatamab step-up dosing. Prior to admission, the patient was noted to have disease progression on PET/CT with hypermetabolic lytic lesions throughout the skeleton which was treated with palliative radiation. Admission labs were notable for a phosphorus of 1.3 mg/dl, a corrected calcium of 8.4 mg/dl, and magnesium of 1.9 mg/dl. Despite repletion, the patient remained hypophosphatemic. Further work up was significant for an elevated PTH of 265 pg/ml and a vitamin D 25-OH of 9 ng/ml. The patient denied taking calcium, vitamin D supplementation, or other medication that would affect phosphorus levels. Due to the disproportionate degree of hypophosphatemia relative to the vitamin D deficiency and PTH elevation, an FGF 23 level was ordered but unfortunately not drawn. The patient was discharged on 50,000 IU of vitamin D weekly and calcitriol 0.25 mcg with plans to initiate Neutra-Phos 250 mg three times daily​ three days after starting calcitriol. Follow up labs showed phosphorus of 3.7 mg/dl with an initial FGF 23 level of 86 RU/ml though repeat FGF 23 level was elevated to 297 RU/ml with a phosphorus of 3.0 mg/dl. The patient was continued on vitamin D and phosphorus supplementation and will be following up with endocrinology. DISCUSSION This case highlights the different mechanisms that can contribute to hypophosphatemia in patients with multiple myeloma. It is well documented that oncogenic osteomalacia can be associated with mesenchymal tumors, but elevated FGF levels / FGF receptor-signaling can also be seen in myeloma [1]. The hypophosphatemia in this case was likely multifactorial. Vitamin D deficiency and borderline low calcium likely contributed to the elevation in PTH and subsequent hypophosphatemia. However, the severity of hypophosphatemia was greater than would be expected for the patient’s PTH elevation and vitamin D deficiency, causing suspicion for an FGF 23 mediated process contributing to hypophosphatemia. Unfortunately, the FGF23 in this patient is hard to interpret given it was drawn after calcitriol was started which may have stimulated FGF23. Clinicians should be aware of the association between myeloma and elevated FGF 23 levels and how this can impact electrolytes and bone homeostasis. REFERENCES 1.Cancarevic I, Ilyas U, Nassar M. Hypophosphatemia in Patients With Multiple Myeloma. Cureus. 2023;15(6):e40487. Published 2023 Jun 15. Presentation: Sunday, July 13, 2025

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Journal of the Endocrine Society
Published
2025-10-01
DOI
https://doi.org/10.1210/jendso/bvaf149.710
Primary Topic
Parathyroid Disorders and Treatments
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article

SUN-762 Suspected Fibroblast Growth Factor 23 Mediated Hypophosphatemia in a Patient with Multiple Myeloma

Michelle Stefanelli, Farah Morgan, Muhammad Ansar
Journal of the Endocrine Society
Parathyroid Disorders and Treatments
article

SUN-762 Suspected Fibroblast Growth Factor 23 Mediated Hypophosphatemia in a Patient with Multiple Myeloma

Michelle Stefanelli, Farah Morgan, Muhammad Ansar
article en

Abstract

Abstract Disclosure: M. Stefanelli: None. M. Ansar: None. F.H. Morgan: None. Introduction: Phosphate levels are regulated by parathyroid hormone (PTH), vitamin D, fibroblast growth factor 23 (FGF 23), and other electrolytes. FGF 23 levels can be elevated in multiple myeloma, which can contribute to dysregulation of phosphate metabolism and lead to tumor induced osteomalacia [1]. CASE PRESENTATION A 68-year-old male with a history of relapsed multiple myeloma presented for elective bispecific T-cell engager (BiTE) therapy with Elranatamab step-up dosing. Prior to admission, the patient was noted to have disease progression on PET/CT with hypermetabolic lytic lesions throughout the skeleton which was treated with palliative radiation. Admission labs were notable for a phosphorus of 1.3 mg/dl, a corrected calcium of 8.4 mg/dl, and magnesium of 1.9 mg/dl. Despite repletion, the patient remained hypophosphatemic. Further work up was significant for an elevated PTH of 265 pg/ml and a vitamin D 25-OH of 9 ng/ml. The patient denied taking calcium, vitamin D supplementation, or other medication that would affect phosphorus levels. Due to the disproportionate degree of hypophosphatemia relative to the vitamin D deficiency and PTH elevation, an FGF 23 level was ordered but unfortunately not drawn. The patient was discharged on 50,000 IU of vitamin D weekly and calcitriol 0.25 mcg with plans to initiate Neutra-Phos 250 mg three times daily​ three days after starting calcitriol. Follow up labs showed phosphorus of 3.7 mg/dl with an initial FGF 23 level of 86 RU/ml though repeat FGF 23 level was elevated to 297 RU/ml with a phosphorus of 3.0 mg/dl. The patient was continued on vitamin D and phosphorus supplementation and will be following up with endocrinology. DISCUSSION This case highlights the different mechanisms that can contribute to hypophosphatemia in patients with multiple myeloma. It is well documented that oncogenic osteomalacia can be associated with mesenchymal tumors, but elevated FGF levels / FGF receptor-signaling can also be seen in myeloma [1]. The hypophosphatemia in this case was likely multifactorial. Vitamin D deficiency and borderline low calcium likely contributed to the elevation in PTH and subsequent hypophosphatemia. However, the severity of hypophosphatemia was greater than would be expected for the patient’s PTH elevation and vitamin D deficiency, causing suspicion for an FGF 23 mediated process contributing to hypophosphatemia. Unfortunately, the FGF23 in this patient is hard to interpret given it was drawn after calcitriol was started which may have stimulated FGF23. Clinicians should be aware of the association between myeloma and elevated FGF 23 levels and how this can impact electrolytes and bone homeostasis. REFERENCES 1.Cancarevic I, Ilyas U, Nassar M. Hypophosphatemia in Patients With Multiple Myeloma. Cureus. 2023;15(6):e40487. Published 2023 Jun 15. Presentation: Sunday, July 13, 2025

Journal of the Endocrine SocietyVol. 9(Supplement_1)
Cooper University Health Care (US)
Openalex Percentile: Top 66%
Parathyroid Disorders and Treatments
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