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Related Experiment Videos

Calcium kinetics in the hyperprostaglandin E syndrome

L Shoemaker1, T R Welch, W Bergstrom

  • 1Department of Pediatrics, University of Cincinnati College of Medicine, Ohio 45229.

Pediatric Research
|January 1, 1993
PubMed
Summary

Hyperprostaglandin E syndrome in children causes high calcium levels in urine and bone loss. Indomethacin treatment significantly reduces these effects, improving calcium balance.

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Area of Science:

  • Pediatric Endocrinology
  • Nephrology
  • Metabolic Bone Disease

Background:

  • Hyperprostaglandin E syndrome is a rare condition affecting calcium metabolism.
  • Children with this syndrome exhibit hypercalciuria and bone density loss.

Observation:

  • Studies in three children with hyperprostaglandin E syndrome were conducted off and on indomethacin therapy.
  • Measurements included calcium kinetics using stable isotopes, urinary calcium and prostaglandin E excretion, serum calcitriol, and bone density.

Findings:

  • Off therapy, children showed hypercalciuria, hyperprostaglandinuria, elevated serum calcitriol, and diminished bone density.
  • Indomethacin treatment reduced serum calcitriol, prostaglandin E excretion, and urinary calcium excretion significantly.
  • Stable isotope studies revealed an indomethacin-sensitive dietary calcium component and an indomethacin-resistant bone resorptive component contributing to hypercalciuria.

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Implications:

  • Indomethacin effectively manages hypercalciuria and hyperprostaglandinuria in this syndrome.
  • The findings elucidate distinct mechanisms contributing to hypercalciuria, aiding in targeted therapeutic strategies.
  • Understanding these pathways is crucial for preventing skeletal demineralization in affected children.