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

Authors

  • Aaron R. Prosnitz MD,

    1. Department of Pediatrics, Yale-New Haven Children's Hospital, New Haven, Connecticut
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  • Mary B. Leonard MD, MSCE,

    1. Department of Pediatrics, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania
    2. Department of Biostatistics and Epidemiology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania
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  • Justine Shults PhD,

    1. Department of Biostatistics and Epidemiology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania
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  • Babette S. Zemel PhD,

    1. Department of Pediatrics, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania
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  • Bruce W. Hollis PhD,

    1. Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina
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  • Lee A. Denson MD,

    1. Department of Pediatrics, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio
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  • Robert N. Baldassano MD,

    1. Department of Pediatrics, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania
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  • Aaron B. Cohen BS,

    1. Department of Pediatrics, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania
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  • Meena Thayu MD, MSCE

    Corresponding author
    1. Department of Pediatrics, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania
    2. Department of Biostatistics and Epidemiology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania
    • Division of Gastroenterology, Hepatology, and Nutrition, Children's Hospital of Philadelphia, 34th and Civic Center Blvd., Philadelphia, PA 19104
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  • Disclosure: B.W.H. is an academic consultant to Diasorin Corp.

Abstract

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. (Inflamm Bowel Dis 2012;)

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