How is XLH treated clinically?

• A. Phosphate supplements and active vitamin D analogs; burosumab (anti-FGF23) is newer therapy.
• B. Vitamin D2 supplementation alone.
• C. Calcium carbonate supplementation only.
• D. Bisphosphonates.

Answer: (C)

XLH is a phosphate-wasting disorder driven by excess FGF23, which lowers kidney phosphate reabsorption and suppresses 1,25-dihydroxy vitamin D. Clinically, treatment aims to correct hypophosphatemia to improve bone mineralization. The standard approach combines phosphate supplements with active vitamin D analogs (such as calcitriol) to enhance intestinal phosphate and calcium absorption and support bone mineralization. A newer option targets the root cause by inhibiting FGF23 with burosumab, which increases phosphate reabsorption and raises 1,25(OH)2D, leading to better bone health.

Calcium carbonate alone won’t fix the underlying phosphate wasting, and vitamin D2 is not sufficient on its own to correct the hypophosphatemia. Bisphosphonates don’t address the phosphate handling defect and are not first-line for XLH.