Vitamin D metabolites are lower with active Crohn's disease and spontaneously recover with development of remission.
Crohn’s disease
inflammatory bowel disease
vitamin D
Journal
Therapeutic advances in gastroenterology
ISSN: 1756-283X
Titre abrégé: Therap Adv Gastroenterol
Pays: England
ID NLM: 101478893
Informations de publication
Date de publication:
2019
2019
Historique:
received:
05
04
2019
accepted:
28
06
2019
entrez:
7
8
2019
pubmed:
7
8
2019
medline:
7
8
2019
Statut:
epublish
Résumé
Vitamin D deficiency is associated with active Crohn's disease (CD). However, it remains unclear if lower 25-hydroxyvitamin D [25(OH)D] concentration is the cause, or consequence, of intestinal inflammation. Existing literature has focused on circulating 25(OH)D rather than the active metabolite 1,25(OH) Fifty-four patients with CD and not on corticosteroids or vitamin D supplements, were enrolled in a 6-month prospective cohort study. Sera were collected on enrolment and at 6 months and tested for 25(OH)D, 1,25(OH) There were no differences in 25(OH)D or 1,25(OH) Levels of 24,25(OH)
Sections du résumé
BACKGROUND
BACKGROUND
Vitamin D deficiency is associated with active Crohn's disease (CD). However, it remains unclear if lower 25-hydroxyvitamin D [25(OH)D] concentration is the cause, or consequence, of intestinal inflammation. Existing literature has focused on circulating 25(OH)D rather than the active metabolite 1,25(OH)
METHODS
METHODS
Fifty-four patients with CD and not on corticosteroids or vitamin D supplements, were enrolled in a 6-month prospective cohort study. Sera were collected on enrolment and at 6 months and tested for 25(OH)D, 1,25(OH)
RESULTS
RESULTS
There were no differences in 25(OH)D or 1,25(OH)
CONCLUSION
CONCLUSIONS
Levels of 24,25(OH)
Identifiants
pubmed: 31384306
doi: 10.1177/1756284819865144
pii: 10.1177_1756284819865144
pmc: PMC6661794
doi:
Types de publication
Journal Article
Langues
eng
Pagination
1756284819865144Déclaration de conflit d'intérêts
Conflict of interest statement: The author(s) declare that there is no conflict of interest.
Références
J Clin Endocrinol Metab. 1999 Oct;84(10):3666-72
pubmed: 10523012
J Clin Endocrinol Metab. 2003 Oct;88(10):4623-32
pubmed: 14557432
Photochem Photobiol. 2004 Jan;79(1):32-9
pubmed: 14974713
Aliment Pharmacol Ther. 2010 Aug;32(3):377-83
pubmed: 20491740
Anal Bioanal Chem. 2010 Sep;398(2):779-89
pubmed: 20628873
J Crohns Colitis. 2010 Feb;4(1):7-27
pubmed: 21122488
J Bone Miner Res. 2011 Jul;26(7):1609-16
pubmed: 21416506
JPEN J Parenter Enteral Nutr. 2011 May;35(3):308-16
pubmed: 21527593
J Clin Endocrinol Metab. 2011 Jul;96(7):1911-30
pubmed: 21646368
J Clin Endocrinol Metab. 2011 Dec;96(12):3838-45
pubmed: 21956424
Photochem Photobiol. 2013 Jan-Feb;89(1):219-26
pubmed: 22891914
J Crohns Colitis. 2013 Nov;7(10):e407-13
pubmed: 23403039
N Engl J Med. 2013 Nov 21;369(21):1991-2000
pubmed: 24256378
Am J Epidemiol. 2014 Apr 1;179(7):864-74
pubmed: 24573539
Inflamm Bowel Dis. 2016 Oct;22(10):2456-64
pubmed: 27631600
Aliment Pharmacol Ther. 2017 Mar;45(5):653-659
pubmed: 28074487
Inflamm Bowel Dis. 2018 Feb 15;24(3):633-640
pubmed: 29462382
J Dig Dis. 2018 Apr;19(4):215-224
pubmed: 29542862
J Crohns Colitis. 2018 Jul 30;12(8):963-972
pubmed: 29726893
J Clin Endocrinol Metab. 2018 Sep 1;103(9):3267-3277
pubmed: 29947775
Sci Rep. 2018 Jul 31;8(1):11511
pubmed: 30065252
Endocr Rev. 2019 Aug 1;40(4):1109-1151
pubmed: 30321335
J Gastroenterol. 2019 Apr 30;:null
pubmed: 31041545
Gut. 1985 Nov;26(11):1197-203
pubmed: 3877663