Diagnosis and Management of Vitamin D Dependent Rickets
Front. Pediatr., 12 June 2020 | https://doi.org/10.3389/fped.2020.00315
Michael A. Levine*
Center for Bone Health and Division of Endocrinology and Diabetes, The Children's Hospital of Philadelphia and University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, United States
Rickets almost eradicated in counties giving free Vitamin D, perhaps the world can learn – Dec 2019
Overview of Rickets and vitamin D contains the following summary
Rate of rickets is usually < 0.1% of births, unless dark skin, breastfed, preemie, twin, Mongolian, or Russian
Rate of rickets has greatly increased with the drop in vitamin D levels during the past 40 years
400 IU can prevent/treat most rickets Turkey gave vitamin D to EVERY child and eliminated Rickets
Can have rickets without a low serum level of vitamin D (~20% of the time)
Giving enough Vitamin D to the mother (before and after birth) PREVENTS most forms of Rickets
Rate of rickets in some countries varies from 10% to 70% (typically poor health overall)
Rickets has been more than doubling in many countries
Rickets is strongly associated with severe breathing problems (weak ribs)
Bowed legs is not the primary indication of rickets (3 other indications of rickets are seen more often)
Rickets is typically due to low cellular Vitamin D - April 2024
Some Rickets is due to poor genes - Vitamin D needed lifelong – June 2020
Vitamin D and Rickets consensus took 80 years
Genetics has the following chart
The items in both Rickets and Genetics are listed here:
The items in both Rickets and Vitamin D Receptor are listed here:
Download the PDF from VitaminDWiki
Note by VitaminDWiki - Vitamin D values seem to be about 40X too large - perhaps should be IU, not micrograms
The term “vitamin D dependent rickets” describes a group of genetic disorders that are characterized by early-onset rickets due to the inability to maintain adequate concentrations of active forms of vitamin D or a failure to respond fully to activated vitamin D. Although the term is now admittedly a pathophysiological misnomer, there remains clinical relevance for its continued use, as patients have a lifelong “dependency” on administration of specialized regimens of vitamin D replacement. This review provides an update on the molecular bases for the three forms of vitamin D dependent rickets, and summarizes current protocols for management of affected subjects.
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