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Changes in Vitamin D and Parathyroid Hormone Metabolism in Incident Pediatric Crohn's Disease

Prosnitz, Aaron R. MD*; Leonard, Mary B. MD, MSCE†,‡; Shults, Justine PhD; Zemel, Babette S. PhD; Hollis, Bruce W. PhD§; Denson, Lee A. MD; Baldassano, Robert N. MD; Cohen, Aaron B. BS; Thayu, Meena MD, MSCE†,‡

doi: 10.1002/ibd.22969
Original Clinical Articles

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-α), and PTH. TNF-α 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-α-hyroxylase may contribute to these alterations.

Article first published online 5 April 2012

*Department of Pediatrics, Yale-New Haven Children's Hospital, New Haven, Connecticut

Department of Pediatrics, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania

Department of Biostatistics and Epidemiology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania

§Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina

Department of Pediatrics, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.

Reprints: Meena Thayu, MD, MSCE, Division of Gastroenterology, Hepatology, and Nutrition, Children's Hospital of Philadelphia, 34th and Civic Center Blvd., Philadelphia, PA 19104 (e-mail:

Grant support: National Institutes of Health (NIH) R01DK60030, K23 DK082012, K24 DK076808, and R01 DK068164; North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition; and the Children's Hospital of Philadelphia Clinical Translational Research Center UL1 RR024134. Disclosure: B.W.H. is an academic consultant to Diasorin Corp.

Received February 24, 2012

Accepted March 08, 2012

© Crohn's & Colitis Foundation of America, Inc.
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