Identification of specific foods responsible for inflammation in children with eosinophilic esophagitis successfully treated with empiric elimination diet.

OBJECTIVES: Eosinophilic esophagitis (EoE) is an immune-mediated chronic inflammatory disorder triggered by food antigen(s). A 6-food elimination diet (SFED) excluding cow's milk, soy, wheat, egg, peanuts/tree nuts, and seafood has been shown to induce remission in a majority of children with EoE. The goal of the present study was to identify specific food antigens responsible for eosinophilic esophageal inflammation in children with EoE who had achieved histological remission with the SFED. PATIENTS AND METHODS: In this analysis, we retrospectively analyzed children with EoE who completed subsequent single-food reintroductions that led to identification of foods causing disease recurrence. Repeat upper endoscopy with biopsies was performed after single-food introductions. Recurrence of esophageal eosinophilia following a food reintroduction identified that food antigen as a cause of EoE. RESULTS: A total of 36/46  (25 M/11F) children who were initially successfully treated with SFED completed this trial; the mean age was 7.6  ±  4.3 years. The most common foods identified were 25 to cow's milk (74%), 8 to wheat (26%), 4 to eggs (17%), 3 to soy (10%), and 1 to peanut (6%). Milk was 8 times more likely to cause EoE compared with wheat, the next most common food (95% confidence interval 2.41-26.62, P = 0.0007). CONCLUSIONS: Serial single-food reintroductions following induction of histological remission with the SFED can lead to the identification of specific causal food antigen(s) in EoE. Cow's milk was the most common food identified in subjects with EoE treated with SFED. A subset of children with EoE may develop tolerance to their food sensitivities while on the SFED.

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.

Intestinal permeability and effects of Lactobacillus rhamnosus therapy in children with short bowel syndrome.

BACKGROUND: The present study was conducted to investigate the effects of Lactobacillus rhamnosus (also known as LGG) on intestinal permeability (IP) in children with short bowel syndrome (SBS). PATIENTS AND METHODS: In a double-blind, placebo-controlled crossover clinical trial, baseline IP (ie, lactulose-to-mannitol ratio) was measured in subjects with SBS and healthy control subjects. Subjects with SBS received LGG or placebo for 4 weeks, followed by a 3-week washout before therapy was crossed over for another 4 weeks. IP, quantitative fecal cultures for Lactobacillus species (in colony-forming units [cfu] per gram of stool) and hydrogen breath test (HBT) were performed during LGG and placebo phases of therapy. RESULTS: Twenty-one children (SBS, n = 9; control, n = 12) with a median age of 4.5 years (range 1.6-16.4 years) enrolled. Baseline IP measurements were similar in patients with SBS and control subjects: 0.08 +/- 0.06 (mean +/- SD) versus 0.07 +/- 0.05 (P = 1.0). IP was correlated with age in control subjects (r = -0.83, P = 0.001) but not among patients with SBS (r = -0.55, P = 0.16). Fecal colonization with Lactobacillus species did not differ during LGG versus placebo therapy (median 1.4 x 10(9) cfu/g [range 4.0 x 10(5) to 4.0 x 10(9) cfu/g] vs 6.0 x 10(9) cfu/g [1.0 x 10(3) to 1.0 x 10(10) cfu/g], respectively; P = 0.83). LGG therapy had no consistent effects on IP (P = 0.58) or its relationship with age (r = -0.40, P = 0.29), and was associated with conversion to positive HBT results in 1 subject. CONCLUSIONS: In this sample of children with SBS, the IP was within normal limits but did not correlate with age. LGG therapy had no consistent effects on IP. These findings do not support empiric LGG therapy to enhance IP in children with SBS.

Colonic Necrosis in a 4-Year-Old with Hyperlipidemic Acute Pancreatitis.

Here we report the case of a 4-year-old male with severe acute pancreatitis due to hyperlipidemia, who presented with abdominal pain, metabolic abnormalities, and colonic necrosis. This colonic complication was secondary to the extension of a large peripancreatic fluid collection causing direct serosal autodigestion by pancreatic enzymes. Two weeks following the initial presentation, the peripancreatic fluid collection developed into a mature pancreatic pseudocyst, which was percutaneously drained. To our knowledge, this is the youngest documented pediatric case of colonic necrosis due to severe pancreatitis and the first descriptive pediatric case of a colonic complication due to hyperlipidemia-induced acute pancreatitis.

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.

Drug-induced nutrient deficiencies.

Good clinical care extends beyond mere diagnosis and treatment of disease to appreciation that nutrient deficiencies can be the price of effective drug therapy. The major risk factors for developing drug-induced nutrient deficiencies are lack of awareness by the prescribing physician and long duration of drug therapy. The field of pharmacogenomics has potential to improve clinical care by detecting patients at risk for complications from drug therapy. Further improvements in patient safety rely on physicians voluntarily reporting serious suspected adverse drug reactions.

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.

Effect of six-food elimination diet on clinical and histologic outcomes in eosinophilic esophagitis.

BACKGROUND & AIMS: In children, eosinophilic esophagitis (EE) is predominantly, but not exclusively, a food-hypersensitivity disorder. A crystalline amino acid-based elemental diet (ELED) formula currently remains the most effective nutritional treatment in inducing clinical and histologic remission. However, compliance with an exclusive, poor-tasting liquid formulation is difficult. METHODS: This retrospective observational study assessed the short-term clinical and histologic responses of 2 cohorts of children with EE evaluated during 2 different time periods: one was treated with the standard 6-food elimination diet (SFED) and the other was treated with ELED. Of the 60 children who met the inclusion criteria and were compliant with the dietary protocol, 35 were treated with a diet excluding cow-milk protein, soy, wheat, egg, peanut, and seafood while allowing all other table foods and 25 were treated exclusively with ELED. Repeat esophageal biopsy specimens were obtained at least 6 weeks later. RESULTS: Twenty-six of 35 (74%) in the SFED group and 22 of 25 (88%) in the ELED group achieved significant improvement of esophageal inflammation (

The use of oral rehydration solutions in children and adults.

The observation that the intestinal Na(+)-glucose cotransporter remains intact in most diarrheal illnesses led to development of the life-saving, low-cost technology of oral rehydration salt (ORS) solutions. The primary therapeutic role of ORS solutions is in prevention and treatment of dehydration during management of acute gastroenteritis. Successful oral rehydration therapy involves early use of ORS with maintenance or timely resumption of regular feeding. Since the inception of the oral rehydration approach more than three decades ago, the widespread use of ORS solutions has revolutionized the management and outcomes of acute gastroenteritis in children and adults. The efficacy of the World Health Organization ORS solution and of commercial ORS formulations has been enhanced by reducing osmolarity. Newer formulations of ORS are under active investigation, with promise of added benefits, including promotion of intestinal healing. This article reviews fluid and electrolyte transport in the gastrointestinal tract, the pathophysiologic mechanisms of acute diarrhea, and the basis and formulation of current and newer ORS solutions. Guidelines for efficacious use of ORS in the management of acute gastroenteritis and short gut syndrome are also provided.