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A neonate presents with severe skeletal undermineralization, respiratory distress, and hypercalcemia. Alkaline phosphatase level is very low. The baby has "punched out" lesions on skull X-ray.

AR (severe) or AD (mild); ALPL (tissue non-specific alkaline phosphatase)

  • Defective bone mineralization
  • LOW alkaline phosphatase (opposite of most bone disorders)
  • Elevated phosphoethanolamine and pyridoxal-5'-phosphate (PLP) in blood/urine
  • Spectrum from lethal perinatal to mild adult (dental only)
  • Premature loss of deciduous teeth (roots intact)
  • Craniosynostosis, rachitic changes
  • LOW serum alkaline phosphatase for age is the key biochemical clue
  • Elevated substrates: pyridoxal-5'-phosphate (PLP) in blood, phosphoethanolamine (PEA) in urine
  • Radiographs: undermineralization, rachitic-appearing metaphyses, "punched out" skull lucencies in severe forms
  • ALPL sequencing confirms and clarifies inheritance (AR in severe, AD in milder forms)
  • Asfotase alfa (enzyme replacement therapy)

This comparison table differentiates X-linked hypophosphatemia (PHEX) from hypophosphatasia (ALPL) across genetics, mechanism, lab findings, clinical features, and treatment.

X-linked hypophosphatemia vs hypophosphatasia comparison: genes (PHEX vs ALPL), mechanism, lab findings (phosphate, calcium, ALP, PLP, urine phosphoethanolamine), clinical features, and treatment
X-linked hypophosphatemia vs hypophosphatasia comparison: genes (PHEX vs ALPL), mechanism, lab findings (phosphate, calcium, ALP, PLP, urine phosphoethanolamine), clinical features, and treatment

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