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Mattis, L; Young, R; Hampsey, J; Antonson, D; Vanderhoof, J; Saavedra, J

Journal of Pediatric Gastroenterology and Nutrition: October 2005 - Volume 41 - Issue 4 - p 562-563
doi: 10.1097/01.mpg.0000182080.32954.35
Abstracts: North American Society of Pediatric Gastroenterology, Hepatology, and Nutrition Annual Meeting October 20-22, 2005 Salt Lake City, Utah: APGNN Abstracts Presented During Poster Session II, Friday, October 21, 2005

Johns Hopkins University, Baltimore, MD; University of Nebraska, Omaha, NE

Vitamin B12 deficiency in patients with intestinal disease has been attributed to malabsorption, ileal resection, and small bowel bacterial overgrowth (SBBO). To the best of our knowledge, elevated serum vitamin B12 (VB12) levels in children with intestinal disease have not previously been reported. We report the incidence of elevated VB12 levels in this population.

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Laboratory and demographic data were collected for patients with short bowel syndrome (SBS) and intestinal dysmotility (ID) followed in the clinics at 2 institutions. Those who received tube feedings or a combination of parenteral nutrition (PN) and enteral nutrition (EN) for >3 months and whose VB12 levels were routinely monitored were included.

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A total of 139 subjects were identified and medical records reviewed. 96 instances of elevated VB12 levels (>900 pg/ml) were identified in 46 (33%) of 139 subjects; 20 instances of low VB12 levels (<150 pg/ml) were identified in only 7(5%). Elevated VB12 levels ranged from 903−>2000 pg/ml (limit of detection). Age range at initial high VB12 level:3-286 months; mean: 60 months. Primary diagnoses: SBS (33), gastroschisis (4), pseudo-obstruction (5), IBD (3), microvillus inclusion disease/SB transplant (1). 33 (72%) had partial or complete ileal resection; 31 (67%) had resection of ileocecal valve (ICV). 32 (33%) of elevated VB12 levels were found in 15 subjects while receiving no PN and no VB12 enterally beyond that in commercial formulas.

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Most children with SBS and ID receiving adequate nutrition have normal VB12 levels. Elevated VB12 levels were significantly more frequent (p < 0.05) than low levels, even in cases of ileal and ICV resection. These findings are contrary to the belief that VB12 deficiency is common in intestinal disease. Given that the source of VB12 (or its analogues) in humans is only dietary intake or bacterial synthesis in the gut lumen, we speculate that synthesis of VB12 from SBBO and absorption in the SB is responsible for the frequency of elevated VB12 levels in this population.

Note: * after the final id indicates Poster of Distinction.

© 2005 Lippincott Williams & Wilkins, Inc.