Whole-blood-free choline and choline metabolites in infants who require chronic parenteral nutrition therapy.

BACKGROUND AND AIM: Choline deficiency is associated with hepatic dysfunction. Parenteral nutrition (PN) and lipid emulsions contain phosphatidylcholine (PtdCho) but insignificant free choline (FCho). PtdCho is sequentially degraded to glycerolphosphocholine (GPCho), phosphocholine (PCho), and finally to FCho. Biosynthesis of FCho may be insufficient during PN therapy. The aim of the study was to examine the status of FCho and related metabolites in infants on prolonged (> or =4 weeks) PN. METHODS: Whole blood concentrations of FCho, PtdCho, GPCho, and PCho were measured and compared in infants on PN and infants on enteral feeds (controls). RESULTS: Infants on PN (n = 14) had higher birth weight but same postnatal age as controls (n = 14) (mean +/- standard deviation) 8.3 +/- 3.9 versus 7.4 +/- 3.6 weeks. Parenteral nutrition was associated with increased PtdCho 1761 +/- 452 versus 1471 +/- 221 nmol/mL, P = 0.04. Mean whole blood FCho, GPCho, and PCho concentrations did not differ significantly in PN versus controls: 40.0 +/- 15.4 versus 50.8 +/- 49.7, 16.4 +/- 14.5 versus 25.2 +/- 29.3, and 15.3 +/- 13.5 versus 22.0 +/- 14.8 nmol/mL, respectively. However, PCho was positively correlated with GPCho in controls (r = 0.91, P < 0.01) but not PN (r = 0.24, P = NS), and infants receiving >90% of daily energy intake from PN (n = 6) had decreased PCho, 5.7 +/- 4.1 nmol/mL, compared with those receiving <90% of daily energy intake (n = 8) 22.5 +/- 13.7 nmol/mL, P < 0.05, and controls, 22.0 +/- 14.8 nmol/mL, P < 0.01. CONCLUSIONS: Decreased whole-blood concentrations of choline suggest possible evidence of choline deficiency as illustrated by decreased whole-blood PCho. Choline supplementation should be investigated in infants who require prolonged PN, and whole-blood PCho can be used to monitor response.

Nutritional deficiencies in intestinal failure.

Intestinal failure (IF) is the ultimate malabsorption state, with multiple causes, requiring long-term therapy with enteral or intravenous fluids and nutrient supplements. The primary goal during management of children with potentially reversible IF is to promote intestinal autonomy while supporting normal growth, nutrient status, and preventing complications from parenteral nutrition therapy. This article presents how an improved understanding of digestive pathophysiology is essential for diagnosis, successful management, and prevention of nutrient deficiencies in children with IF.

Vitamin D status in children, adolescents, and young adults with Crohn disease.

BACKGROUND: Crohn disease (CD) and vitamin D deficiency are associated with decreased bone mineralization. OBJECTIVE: We examined the prevalence of and risk factors for hypovitaminosis D in children, adolescents, and young adults with CD. DESIGN: Growth, clinical characteristics, vitamin D intake ( micro g/d), and bone mineral density (g/cm(2)) were measured in a cross-sectional study of 112 subjects (44 females) who had CD and were 5-22 y of age. Hypovitaminosis D was defined as a serum concentration of 25-hydroxyvitamin D [25(OH)D] < 38 nmol/L. RESULTS: The mean (+/- SD) serum concentration of 25(OH)D was 59.7 +/- 26.9 nmol/L, and 16% (95% CI: 9.3%, 23%) of the subjects had hypovitaminosis D. Hypovitaminosis D was most prevalent during the winter (31%; P = 0.02), among the African Americans (56%; P = 0.01), in the subjects with CD confined to the upper gastrointestinal tract (44%; P = 0.05), and in the subjects with a greater lifetime exposure to glucocorticoid therapy (23.7 +/- 13.5 compared with 17.5 +/- 12.2 mg/d; P = 0.05). There was no association between hypovitaminosis D and either bone mineral density (P = 0.10) or average dietary intake of vitamin D (4.6 +/- 3.6 micro g/d; P = 0.87). CONCLUSIONS: In this sample of pediatric patients with CD, hypovitaminosis D was common and was associated with the winter season, African American ethnicity, CD confined to the upper gastrointestinal tract, and magnitude of lifetime exposure to glucocorticoid therapy. The occurrence of these factors should prompt assessment of 25(OH)D status and clinical care optimized by supplementing subjects who have low serum concentrations. The physiologic relevance of ethnicity on 25(OH)D status in children with CD remains to be determined.