Vitamin D-Binding Protein Deficiency and Homozygous Deletion of the GC Gene.
Clark M HendersonSusan L FinkHanan BassyouniBob ArgiropoulosLindsay BrownThomas J LahaKonner J JacksonRaymond LewkoniaPatrick FerreiraAndrew N HoofnagleJulien L MarcadierPublished in: The New England journal of medicine (2019)
A 58-year-old woman with debilitating ankylosing spondylitis who was born to consanguineous parents was found to have an apparent severe vitamin D deficiency that did not respond to supplementation. Liquid chromatography-tandem mass spectrometry showed the absence of circulating vitamin D-binding protein, and chromosomal microarray confirmed a homozygous deletion of the group-specific component (GC) gene that encodes the protein. Congenital absence of vitamin D-binding protein resulted in normocalcemia and a relatively mild disruption of bone metabolism, in this case complicated by severe autoimmune disease. (Funded by the National Institutes of Health and the University of Washington.).
Keyphrases
- binding protein
- liquid chromatography tandem mass spectrometry
- ankylosing spondylitis
- copy number
- simultaneous determination
- genome wide
- public health
- ms ms
- rheumatoid arthritis
- healthcare
- solid phase extraction
- disease activity
- multiple sclerosis
- drug induced
- genome wide identification
- quality improvement
- health information
- replacement therapy
- computed tomography
- low birth weight
- systemic lupus erythematosus
- dna methylation
- human health
- high resolution
- bone regeneration
- social media