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Abstract: SA-PO315

A Case of Fibroblast Growth Factor 23-Induced Hypophosphatemia in Waldenström Macroglobulinemia

Session Information

Category: Bone and Mineral Metabolism

  • 502 Bone and Mineral Metabolism: Clinical

Authors

  • Kadota, Nozomi, St.Luke's International Hospital, Tokyo, Japan
  • Fujimaru, Takuya, St.Luke's International Hospital, Tokyo, Japan
  • Aizawa, Chiharu, St.Luke's International Hospital, Tokyo, Japan
  • Konishi, Kasumi, St.Luke's International Hospital, Tokyo, Japan
  • Ito, Yugo, St.Luke's International Hospital, Tokyo, Japan
  • Taki, Fumika, St.Luke's International Hospital, Tokyo, Japan
  • Nagahama, Masahiko, St.Luke's International Hospital, Tokyo, Japan
  • Nakayama, Masaaki, St.Luke's International Hospital, Tokyo, Japan
Introduction

Fanconi syndrome and fibroblast growth factor 23 (FGF23)-induced hypophosphatemia are the main causes of hypophosphatemia due to renal phosphorus excretion in cancer patients. FGF23 induced hypophosphatemia is often associated with benign mesenchymal tumors of the mixed connective tissue type. As far as we know, this is the first case of FGF23 induced hypophosphatemia associated with Waldenström macroglobulinemia (WM).

Case Description

The patient was diagnosed with WM at the age of 74 years due to a lumbar compression fracture. Because he had severe neuropathy, he received rituximab as symptomatic WM. After treatment, clinical symptoms disappeared, and serum IgM decreased from 5800 mg/dl to 1800 mg/dl. Four years later, his serum IgM increased (3000 mg/dL) and serum phosphorus decreased (1.5–2.0 mg/dL). Six months later, he was referred to our nephrology department due to hypophosphatemia (serum phosphorus 0.8 mg/dL). He already received alphacalcidol 0.5 μg/day and alendronate 35 mg weekly. His serum IgM was 3263 mg/dL, serum creatinine was 0.98 mg/dl, corrected calcium was 9.6 mg/dl, parathyroid hormone was 39 pg/ml, 1.25-(OH)2 vitamin D was 11 pg/ml (normal range 20-60 pg/ml), and urine glucose was negative. The phosphate excretion rate was 44% and serum FGF23 was 91 pg/ml (normal range <30 pg/ml). The whole-body bone scintigraphy revealed bone destruction in the tenth thoracic vertebra. Contrast-enhanced CT showed multiple enlarged lymph nodes. He was diagnosed as FGF23-related hypophosphatemia due to WM. Sodium phosphate monobasic and tirabrutinib was initiated. Three months after treatment, serum IgM decreased to 423 mg/dl, and serum phosphate increased to 3.7 mg/dl.

Discussion

From the previous report, there are only three types of hematological malignancy that cause FGF23-related hypophosphatemia: diffuse large B-cell lymphoma, natural killer T-cell lymphoma and acute leukemia. We should also consider WM induce FGF23-related hypophosphatemia.