Case-Letter| Volume 348, ISSUE 2, P179-180, August 2014

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).
      Table 1Baseline and follow-up laboratory findings
      Laboratory Data December 2012 February 2013 May 2013
      Serum calcium (normal range, 8.5–10.2), mg/dL 10.4 10.3 8.4
      Ionized calcium (normal range, 1–1.35), mmol/L 1.32 1.2
      Serum phosphorus (normal range, 2.2–4.5), mg/dL 6.5 6.7 3.2
      Serum PTH (normal range, 16.5–70), pg/mL
      PTH, parathyroid harmone.
      10 10 100
      Serum bicarbonate (normal range, 22–30), mg/dL 33 27
      25-hydroxyvitamin D (normal range, 35–80), ng/mL 16.7 20
      1,25-hydroxyvitamin D (normal range, 10–75), pg/mL 9 18.6
      Urine calcium to creatinine ratio 0.149 0.01
      Fractional excretion of phosphorus (FePO4) 5.20% 16%
      Tubular reabsorption of phosphorus 94.70% 84.00%
      TmP/GFR (mg/dL)
      TMP/GFR, The ratio of tubular maximum reabsorption rate of phosphate to the glomerular filtration rate.
      7.64 4.102
      FGF-23 level (normal range, 44–215 RU/mL)
      FGF-23, Fibroblast Growth Factor-23.
      Serum albumin, serum magnesium, cortisol, and TSH levels
      TsH, Thyroid stimulating Hormone.
      Normal Limits
      a PTH, parathyroid harmone.
      b TMP/GFR, The ratio of tubular maximum reabsorption rate of phosphate to the glomerular filtration rate.
      c FGF-23, Fibroblast Growth Factor-23.
      d TsH, Thyroid stimulating Hormone.
      To read this article in full you will need to make a payment

      Purchase one-time access:

      Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online access
      One-time access price info
      • For academic or personal research use, select 'Academic and Personal'
      • For corporate R&D use, select 'Corporate R&D Professionals'


      Subscribe to The American Journal of the Medical Sciences
      Already a print subscriber? Claim online access
      Already an online subscriber? Sign in
      Institutional Access: Sign in to ScienceDirect


        • Labossiere R.
        • Hintzke C.
        • Ileana S.
        Hypercalcemia of immobilization.
        J Am Med Dir Assoc. 2009; 10: 284-285
        • Bilancio G.
        • Lombardi C.
        • Pisot R.
        • et al.
        Effects of prolonged immobilization on sequential changes in mineral and bone disease parameters.
        Am J Kidney Dis. 2013; 61: 845-847
        • Cirillo M.
        • Ciacci C.
        • De Santo N.G.
        Age, renal tubular phosphate reabsorption, and serum phosphate levels in adults.
        N Engl J Med. 2008; 359: 864-866
        • Berndt T.
        • Kumar R.
        Novel mechanisms in the regulation of phosphorus homeostasis.
        Physiology (Bethesda). 2009; 24: 17-25
        • Sato Y.
        • Iwamoto J.
        • Honda Y.
        An open-label trial comparing alendronate and alphacalcidol in reducing falls and hip fractures in disabled stroke patients.
        J Stroke Cerebrovasc Dis. 2011; 20: 41-46
        • Gallacher S.J.
        • Ralston S.H.
        • Dryburgh F.J.
        • et al.
        Immobilization-related hypercalcemia—a possible novel mechanism and response to pamidronate.
        Postgrad Med J. 1990; 66: 918-922
        • Tseng C.F.
        • Lu K.C.
        • Wang J.S.
        • et al.
        Bisphosphonate aggravates secondary hyperparathyroidism in hemodialysis patients.
        Fu Jen J of Med. 2004; 2: 301-310