Background: Vitamin D deficiency and low bone mineral density (BMD) are complications of inflammatory bowel disease. Vitamin D deficiency is more prevalent among African Americans compared with whites. There are little data comparing differences in serum 25-hydroxyvitamin D (25OHD) concentrations and BMD between African American and white children with Crohn disease (CD).
Methods: We compared serum 25OHD concentrations of African American children with CD (n = 52) to white children with CD (n = 64) and healthy African American controls (n = 40). We also analyzed BMD using dual-energy x-ray absorptiometry results from our pediatric CD population.
Results: African American children with CD had lower serum 25OHD concentrations (16.1 [95% confidence interval, CI 14.5–17.9] ng/mL) than whites with CD (22.3 [95% CI 20.2–24.6] ng/mL; P < 0.001). African Americans with CD and controls exhibited similar serum 25OHD concentration (16.1 [95% CI 14.5–17.9] vs 16.3 [95% CI 14.4–18.4] ng/mL; NS). African Americans with CD exhibited no difference in serum 25OHD concentration when controlling for seasonality, disease severity, and surgical history, although serum 25OHD concentration was significantly decreased in overweight children (body mass index ≥85%, P = 0.003). Multiple regression analysis demonstrated that obese African American girls with CD had the lowest serum 25OHD concentrations (9.6 [95% CI 6.8–13.5] ng/mL). BMD was comparable between African American and white children with CD (z score −0.4 ± 0.9 vs −0.7 ± 1.2; NS).
Conclusions: African American children with CD are more likely to have vitamin D deficiency compared with white children with CD, but have similar BMD. CD disease severity and history of surgery do not affect serum 25OHD concentrations among African American children with CD. African American children have low serum 25OHD concentrations, independent of CD, compared with white children. Future research should focus on how race affects vitamin D status and BMD in children with CD.
*Department of Pediatrics, Division of Gastroenterology, Hepatology, and Nutrition, Emory School of Medicine and Children's Healthcare of Atlanta
†Department of Medicine, Division of Endocrinology, Metabolism, and Lipids
‡Department of Human Genetics, Emory University School of Medicine, Atlanta, GA.
Address correspondence and reprint requests to Subra Kugathasan, MD, Emory University School of Medicine, Division of Pediatric Gastroenterology, Emory Children's Center, 2015 Uppergate Drive, Rm 248, Atlanta, GA 30322 (e-mail: email@example.com).
Received 29 March, 2013
Accepted 22 May, 2013
This work was supported, in part, by grants from the National Institutes of Health: T32 DK007734 (to JAA), K23 AR054334 (to VT), K24 DK096574 (to TRZ), R01 DK 087694 (to SK) and UL1 TR000454 (Atlanta Clinical and Translational Science Institute).
The authors report no conflicts of interest.