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Information on X-linked hypophosphataemia
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Crysvita.eu
Adult Dosing Factsheet Paediatric Dosing Table TmP/GFR Factsheet Prescribing Information Patient Site
  • What is XLH?
    • Causes of XLH
    • Clinical manifestations
    • Prevalence
    • Hereditary pattern
  • How does CRYSVITA work?
    • FGF23 and XLH
    • CRYSVITA mode of action
    • Phosphate homeostasis
  • Why CRYSVITA?
    • Paediatric Studies
    • Adult Studies
  • Starting CRYSVITA
    • Dosing
    • Administration
    • Monitoring
    • Storage
  • Resources
    • Downloadable materials
    • Webinars
    • Publications of interest
    • Key facts
    • Useful websites
Prescribing Information

CRYSVITA® (burosumab) is the first and only disease-modifying biologic treatment that targets the pathophysiology of XLH¹

  • FGF23 and XLH
  • CRYSVITA mode of action
  • Phosphate homeostasis

CRYSVITA is a fully human monoclonal antibody (IgG1) that binds to and inhibits excess FGF23 activity1

Excess levels of FGF23 in XLH lead to:2

  • Decreased renal phosphate reabsorption, which increases urinary phosphate excretion
  • Decreased active vitamin D (1,25[OH]2D) production, which reduces intestinal phosphate absorption

The effects of the excess FGF23 leads to chronic hypophosphataemia resulting in impaired bone mineralisation, leading to rickets in children with XLH and osteomalacia in adults with XLH.2

how-does-crysvita-work-pg-02
Learn more about the clinical presentation of XLH

CRYSVITA is the first and only disease-modifying biologic treatment that targets the pathophysiology of XLH, thereby restoring phosphate homeostasis1,4

Conventional therapy for XLH

Conventional therapy for XLH is based on oral phosphate and active vitamin D supplementation,3 but is associated with variable improvement in clinical features and may lead to adverse effects, such as hyperparathyroidism and nephrocalcinosis.5 Conventional therapy does not address the excess levels of FGF23 that underlie the pathophysiology of XLH.3

Taking oral phosphate and active vitamin D supplements has been associated with increases in FGF23 levels, which may diminish their therapeutic effect in XLH.3

Conventional therapy is also associated with low compliance and the multiple daily dosing regimen places a significant burden on patients with XLH and their carers.2,6

Conventional therapy may be poorly tolerated, with many patients experiencing gastrointestinal side-effects such as abdominal pain, diarrhoea and nausea.2,6,7 Potential adverse effects of conventional therapy include nephrocalcinosis and hyperparathyroidism.3

CRYSVITA restores phosphate homeostasis and improves bone mineralisation in people with XLH, by inhibiting excess FGF23 activity1,7,8

Based on pre-clinical studies, CRYSVITA helps restore phosphate homeostasis by:1,9

  • Decreasing renal phosphate excretion by increasing expression of sodium phosphate cotransporters (NaPi-2a/NaPi-2c)
  • Increasing intestinal phosphate absorption by increasing 1-α hydroxylase levels and active vitamin D production

CRYSVITA restores phosphate homeostasis in people with XLH

See how CRYSVITA leads to sustained serum phosphate levels and improved outcomes in people with XLH
1. Kyowa Kirin Limited. CRYSVITA (burosumab). Summary of Product Characteristics. 2. Linglart A, et al. Endocr Connect. 2014;3:R13–R30. 3. Beck-Nielsen SS, et al. Orphanet J Rare Dis. 2019;14:58. 4. Portale AA, et al. Calcified Tissue Int. 2019;105:271-84. 5. Imel EA, et al. Br J Clin Pharmacol. 2019;85:1188–98. 6. Imel EA, et al. Lancet. 2019;393:2416–27. 7. Carpenter, TO et al. J Bone Miner Res. 2011;26:1381–88. 8. Insogna KL, et al. J Bone Miner Res. 2019;34:2183–91. 9. Hernando, N and Wagner, C. Compr Physiol. 2018;8:1065–90.
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March 2021 KKI/INT/BUR/0896

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