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Crohn's disease kids are 2X more likely to have low vitamin D, intervention helps – April 2012

Changes in vitamin D and parathyroid hormone metabolism in incident pediatric Crohn's disease

Aaron R. Prosnitz MD1, Mary B. Leonard MD, MSCE2,3, Justine Shults PhD3, Babette S. Zemel PhD2, Bruce W. Hollis PhD4, Lee A. Denson MD5, Robert N. Baldassano MD2, Aaron B. Cohen BS2, Meena Thayu MD, MSCE2,3,*
1 Department of Pediatrics, Yale-New Haven Children's Hospital, New Haven, Connecticut
2 Department of Pediatrics, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania
3 Department of Biostatistics and Epidemiology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania
4 Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina
5 Department of Pediatrics, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio
Email: Meena Thayu MD, MSCE (thayu@email.chop.edu)

*Division of Gastroenterology, Hepatology, and Nutrition, Children's Hospital of Philadelphia, 34th and Civic Center Blvd., Philadelphia, PA 19104
† Disclosure: B.W.H. is an academic consultant to Diasorin Corp.
Article first published online: 5 APR 2012; DOI: 10.1002/ibd.22969
Copyright © 2012 Crohn's & Colitis Foundation of America, Inc.

Background:
Prior studies of vitamin D metabolism in Crohn's disease (CD) did not include controls or examine changes following diagnosis. This study examined associations among 25-hydroxyvitamin D [25(OH)D], 1,25-dihydroxyvitamin D [1,25(OH)2D], and parathyroid hormone (PTH) levels in incident pediatric CD, compared with controls, and following diagnosis.

Methods:
Serum vitamin D and PTH were measured at diagnosis (n = 78), 6, 12, and a median of 43 months (n = 52) later in CD participants, and once in 221 controls. Multivariate regression was used to examine baseline associations and quasi-least squares regression to assess subsequent changes.

Results:
At diagnosis, 42% of CD participants were 25(OH)D-deficient (<20 ng/mL). The odds ratio for deficiency was 2.1 (95% confidence interval CI: 1.1, 3.9; P < 0.05) vs. controls, adjusted for age, race, and season. 1,25(OH)2D was lower in CD vs. controls (P < 0.05), adjusted for 25(OH)D, tumor necrosis factor alpha (TNF-?), and PTH. TNF-? was associated with lower 1,25(OH)2D (P < 0.05), and the positive association between PTH and 1,25(OH)2D in controls was absent in CD (interaction P = 0.02). Among participants with 25(OH)D <30 ng/mL, CD was associated with lower PTH (P < 0.05) vs. controls.
Following diagnosis, 25(OH)D and 1,25(OH)2D improved (P < 0.001).
At the final visit, 3% were 25(OH)D-deficient, PTH was no longer low relative to 25(OH)D, and 1,25(OH)2D was significantly elevated (P < 0.001) compared with controls.

Conclusions:
Incident CD was associated with 25(OH)D and 1,25(OH)2D deficiency and a relative hypoparathyroidism that resolved following diagnosis.
Inflammatory cytokine suppression of PTH and renal 1-?-hyroxylase may contribute to these alterations. (Inflamm Bowel Dis 2012;)
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Unfortunately the abstract does not say how much, or what type of vitamin D intervention. Have requested information from the authors

Suspect that a type of vitamin D that can be absorbed by poorly functioning gut was used, such as
Bio-D-Mulsion Forte or
Inter-muscular injection

See also VitaminDWiki

see wikipage such as http://www.vitamindwiki.com/tiki-index.php?page_id=2582
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