February 2026 Research Update

Bone age is often delayed in XLH

This month, one pediatric XLH study added a clearer picture of growth timing: many children had a delayed bone age, and the delay tended to be larger in boys than in girls. [1] This matters because bone age is one of the tools used to estimate how much growth time may be left. [1]

In the same group, two common adult-height prediction methods produced estimates that were generally close to the final or near-final adult height that was actually reached. [1] The pattern was not identical by sex: one method tended to overestimate adult height in girls, while the other modestly overestimated in boys. [1]

The study also reported that a larger bone age delay went along with lower blood phosphorus levels and higher alkaline phosphatase (a blood marker that can rise with active rickets-related bone turnover). [1] In plain terms, children with more biochemical signs of active phosphate-related bone problems tended to have a bigger lag in skeletal maturity. [1]

What this may mean for families

This evidence may matter now because it helps set expectations about growth assessments in XLH: delayed bone age appears common, especially in boys, and predicted adult height can be reasonably close to eventual height in this dataset. [1] It does not establish a single best prediction method for everyone, but it suggests that bone age-based estimates may be a useful part of understanding growth patterns in XLH. [1]

What remains uncertain is how well these results apply across different care settings and treatment histories, since the report was from one center and final height data were limited (especially for boys). [1] Even with those limits, the study helps clarify that skeletal maturity may lag behind chronological age in XLH, which can affect how families interpret growth charts and timing of growth changes. [1]

A single reported pregnancy course

This month included one detailed pregnancy case that mainly adds a real-world example of how XLH management can look when a person stops burosumab (an anti-FGF23 medicine) to pursue pregnancy. [2] The reported course was a term delivery with a healthy newborn, and no maternal or fetal complications were described. [2]

During pregnancy, the patient switched from burosumab to phosphate supplements and calcitriol (active vitamin D), with frequent lab monitoring. [2] Blood phosphate was maintained within or near the normal range during pregnancy, although after delivery phosphate remained below normal despite ongoing management. [2]

One notable issue during late pregnancy was increased urine calcium along with low blood calcium, which led to added calcium supplementation. [2] In plain language, this case highlights that maintaining phosphate is only one part of the picture, and calcium balance can also shift during pregnancy in someone with XLH. [2]

What this adds (and what it cannot answer)

This mainly matters as early, individual-level evidence: it shows one example of pregnancy and delivery in XLH after stopping burosumab and using conventional supplements with close monitoring. [2] It does not tell us which approach is safest or best, because a single case cannot predict what will happen for others. [2]

What became clearer from this report is the range of lab changes that may need attention during pregnancy, including urine calcium and blood calcium, not just phosphate. [2] What remains uncertain is how often these patterns occur, and how outcomes compare across different XLH treatments during pregnancy, because broader studies were not included this month. [2]

Better localization by combining tests

One adult study this month focused on a different condition that can look similar to XLH in labs: late-onset FGF23-related osteomalacia caused by an FGF23-producing tumor. [3] The main pattern was that combining imaging with a blood-sampling localization procedure found more tumors than imaging alone, at least in the patients whose tumors were confirmed by tissue testing. [3]

In this report, a second expert review of FDG-PET imaging improved how often tumors were correctly localized compared with the first read. [3] Adding systemic FGF23 venous sampling (measuring FGF23 levels from different veins to look for a source) further increased localization, reaching the highest sensitivity when paired with the second FDG-PET review. [3]

Minor side effects were reported from venous sampling, and no major adverse events were described. [3] The paper also noted that imaging often showed tracer uptake in places that were not tumors, which helps explain why extra steps may be needed when scans are unclear. [3]

How this relates to XLH

This evidence may matter later or mainly as background knowledge for families because it addresses tumor-induced FGF23 excess, not inherited XLH. [3] It helps clarify that when doctors suspect an acquired, tumor-related cause of low phosphate, combining different localization approaches may improve the chance of finding the source. [3]

What remains uncertain is how these results translate to other hospitals, since the study was small and access to newer imaging varied. [3] Even so, it provides a clearer explanation for why a scan alone may not give a firm answer in suspected tumor-related cases, and why repeat review or additional testing might be considered in research and specialized settings. [3]