Immobilization-Induced Hyperphosphatemia and Functional Hypoparathyroidism Successfully Treated With Oral Bisphosphonates

Apreviously healthy 46-year-old man with 5-month history of T5-T6 level paraplegia after a motor vehicle accident was admitted to the spinal cord rehabilitation center. The patient was found to have persistent hyperphosphatemia in the range of 6.5 to 6.7 mg/dL during routine laboratory evaluations. His phosphorus (Pi) level was previously normal (3.1 mg/dL) at the time of the motor vehicle accident. Physical examination was remarkable for T5-T6 level paraplegia and left elbow calcification. The patient was also found to have mildly elevated serum calcium (Ca) (10.4 mg/dL), suppressed parathyroid hormone (PTH) (10 pg/mL) and elevated fibroblast growth factor-23 (FGF-23) (263 RU/mL). Additional laboratory data are shown in Table 1. The oral intake consisted of 1 L of "Peptamen" bolus tube feeding containing 667 mg of Pi per liter. The patient was not taking any medications or oral supplements. sevelamer carbonate 2.4 g with meals was initiated to reduce intestinal absorption. No improvement in serum Pi levels was observed with sevelamer carbonate, and it was subsequently discontinued. Because of suppressed PTH levels, PTH-dependent Pi excretion using synthetic PTH was assessed. Fractional excretion of phosphate (FePO4) was measured before and after intravenous administration of 60 mg of teriparatide. Pre- and post-teriparatide FePO4 were 14.01% and 28.22%, respectively, confirming appropriate tubular responsiveness to PTH. Bone-specific markers demonstrated increased bone resorption (N-telopeptide to creatinine ratio was 248 with normal range of 3–51) and bone turnover (bone-specific alkaline phosphatase was 24.7 μg/L with normal range of 0–20.1 μg/L) values that are characteristic for immobilization. The patient was initiated on oral alendronate 70 mg weekly and 3 weeks later, levels of serum Ca and Pi normalized to 8.4 mg/dL and 3.2 mg/dL, respectively. Normalization of Ca and Pi levels led to increased PTH (100 pg/mL), reduction of N-telopeptide to creatinine ratio (112), and normalization of bone-specific alkaline phosphatase (20 μg/L) (Table 1).