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ORIGINAL RESEARCH COMMUNICATION |
1 From the Department of Pediatrics, University of California, San Francisco, San Francisco, CA (MBH, EAG, and FAJ); the School of Public Health, University of California, Berkeley, Berkeley, CA (NS, KH, and NH); the Children's Hospital and Research Center, Oakland, CA (PH and ES); the Children's Center for Digestive Health Care, Atlanta, GA (SAH); the Pediatrics, Emory University School of Medicine, Atlanta, GA (SAC and BDG); Pediatrics, MassGeneral Hospital for Children, Boston, MA (HSW); Pediatrics, Children's Hospital of Philadelphia, Philadelphia, PA (RNB); the University of Chicago Comer Children's Hospital, Chicago, IL (BSK); and the Texas Children's Hospital, Baylor College of Medicine, Houston, TX (GDF). 2 The contents are solely the responsibility of the authors and do not necessarily represent the official view of the National Center for Research Resources of the National Institutes of Health. Information on the National Center for Research Resources is available at http://www.ncrr.nih.gov/. Information on Re-engineering the Clinical Research Enterprise can be obtained from http://nihroadmap.nih.gov/clinicalresearch/overview-translational.asp. 3 Supported in part by NIH grants R03 DK063187 (to MBH, NH, and PH), M01 RR01271, and UL1 RR024131 (Pediatric Clinical Research Centers at UCSF and Children's Hospital Oakland); K24 DK060617 (to MBH); T32 DK007762-31S1 (to FAJ); the family of Joel Barnett (to BSK); and the family of John Fullerton (to MBH). 4 Reprints not available. Address correspondence to MB Heyman, 500 Parnassus Avenue, MU 4-East, Box 0136, University of California, San Francisco, San Francisco, CA 94143-0136. E-mail: mheyman{at}peds.ucsf.edu.
Background: Folate is postulated to protect against cell injury and long-term risk of cancer. Folate deficiency has been shown to be associated with inflammatory bowel disease (IBD). However, folate concentrations are poorly delineated in children with IBD.
Objective: The objective was to compare folate concentrations between children with newly diagnosed IBD and healthy controls.
Design: Red blood cell folate (RBCF) and whole-blood folate (WBF) concentrations were measured in 78 children (mean age: 12.8 ± 2.7 y): 22 patients with newly diagnosed untreated Crohn disease, 11 patients with ulcerative colitis, 4 patients with indeterminate colitis, and 41 controls. Vitamin supplementation and dietary intakes determined by food-frequency questionnaire were recorded for 20 IBD patients and 28 controls.
Results: RBCF concentrations were 19.4% lower in controls (587.0 ± 148.6 ng/mL) than in patients (728.7 ± 185.8 ng/mL; P = 0.0004), and WBF concentrations were 11.1% lower in controls (218.2 ± 49.7 ng/mL) than in patients (245.3 ± 59.1 ng/mL; P = 0.031). Total folate intake was 18.8% higher in controls (444.7 ± 266.7 µg/d) than in IBD patients (361.1 ± 230.6 µg/d), but this difference was not statistically significant (P = 0.264). Folate intakes were below the Recommended Dietary Allowance (200–400 µg/d), adjusted for age and sex, in 35.4% of study subjects.
Conclusions: In contrast with previous evidence of folate deficiency in adult IBD patients, our data indicate higher folate concentrations in children with newly diagnosed untreated IBD than in controls. This finding was unexpected, especially in light of the higher dietary folate intakes and hematocrit values in children without IBD. The influence of IBD therapy on folate metabolism and the long-term clinical implications of high RBCF and WBF concentrations at the time of IBD diagnosis should be explored further.
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