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[Rickets resistant to calcitropic hormones]

M Vainsel1, R Bouillon

  • 1Hôpital Saint-Pierre, Bruxelles.

Revue Medicale De Bruxelles
|November 1, 1995
PubMed
Summary

Vitamin D resistance, distinct from phosphate issues, stems from receptor defects or post-receptor problems. Early diagnosis is crucial for rickets cases with normal 25-hydroxyvitamin D levels.

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Area of Science:

  • Endocrinology and Metabolism
  • Molecular Biology
  • Pediatric Bone Diseases

Context:

  • Vitamin D deficiency rickets is common, but vitamin D resistance presents unique diagnostic challenges.
  • Historical misattributions to phosphate deficiency have complicated the understanding of true vitamin D resistance.
  • Rickets diagnosis requires differentiating between simple deficiency and genuine resistance for appropriate management.

Purpose:

  • To clarify the distinct causes of vitamin D resistance, including receptor defects and post-receptor alterations.
  • To emphasize the diagnostic importance of distinguishing true vitamin D resistance from other causes of rickets.
  • To highlight the clinical utility of 25-hydroxyvitamin D levels in diagnosing vitamin D resistance.

Summary:

  • True vitamin D resistance arises from vitamin D receptor (VDR) abnormalities, including lack of the receptor or structural defects in its hormone or DNA-binding sites.
  • Post-receptor resistance mechanisms have also been identified in some cases.
  • Diagnosis is critical for rickets cases not caused by simple vitamin D deficiency, often indicated by normal 25-hydroxyvitamin D levels despite clinical signs of rickets.

Impact:

  • Facilitates accurate diagnosis of vitamin D resistance, enabling targeted therapeutic strategies.
  • Improves patient outcomes by ensuring correct treatment for complex rickets cases.
  • Advances the understanding of VDR function and its role in calcium-phosphate homeostasis.

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