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Background: Atopic dermatitis (AD) is a common pediatric skin condition with significant morbidity. It is unclear what factors contribute to racial differences in disease prevalence. Methods: A single‐site, retrospective cohort study of infants born from June 1, 2011, to April 30, 2017, was performed. Results: Of the 4016 infants included, 39.2% (n = 1574) were Black, 38.5% (n = 1543) White (non‐Hispanic), 7.1% (n = 286) Hispanic, 5.3% (n = 213) Asian, 6.5% (n = 262) "other" race, 3.4% (n = 135) multiracial, and 0.1% (n = 3) not reported. Prevalence of AD differed by race, with 37.0% (n = 583) of Black, 25.8% (n = 55) of Asian, 24.1% (n = 69) of Hispanic, 23.0% (n = 31) of multiracial, 19.1% (n = 50) of "other" race, and 17.9% (n = 276) of White patients diagnosed (P < 0.0001). Delivery mode, NICU stay, and gestational age were all significantly associated with race. In modeling AD with logistic regression, race was significantly associated with the development of AD (P < 0.0001, OR Black = 2.6 [2.2‐3.2], OR Asian = 1.6 [1.1‐2.2], OR Hispanic = 1.4 [1.0‐1.9], OR multiracial 1.4 [0.91‐2.2], OR "other" 0.97 [0.67‐1.4], and OR White 1.0). Conclusions: Racial differences in rates of AD arise early in life. Diagnosis is associated with race rather than delivery mode, insurance type, and gestational age. Further investigation into these disparities and interventions to mitigate them should focus on infancy and early childhood. [ABSTRACT FROM AUTHOR]

Despite advances in our understanding of the human microbiome, there exist significant knowledge gaps in our understanding of the skin microbiome of the preterm neonate. Herein, we describe skin microbiome sampling of six preterm neonates at multiple timepoints, and compare the skin microbiome samples to environmental (crib/isolette swabs) and negative controls. Samples of the same type (skin, crib, control) were more similar than when compared by week or by patient. [ABSTRACT FROM AUTHOR]

Background/Objectives: Premature infants have lower rates of atopic dermatitis (AD) compared with full‐term infants, though little is known about the factors contributing to this association. We explored the infant and environmental factors that may contribute to the association between prematurity and atopic dermatitis, including mode of delivery, birthweight, gestation, and duration of stay in the neonatal intensive care unit (NICU). Methods: This was a single‐center retrospective study. Independent samples t tests or chi‐square tests were used to compare groups on continuous and categorical variables, respectively. Logistic regression then examined the association of the predictor variables with AD. Results: Four thousand sixteen mother‐infant dyads were included. Infants had a higher risk of developing AD if they were delivered vaginally (P =.013), did not stay in the NICU (P <.001), had a longer gestation (P =.001), or had a higher birthweight (P =.002). In modeling atopic dermatitis with the predictor variables, only NICU length of stay remained significantly associated with a lower risk of AD (P =.004). Conclusion: Infants had a lower risk of developing AD if they had a longer stay in the NICU. [ABSTRACT FROM AUTHOR]

Recent focus on the neonatal intestinal microbiome has advanced our knowledge of the complex interplay between the intestinal barrier, the developing immune system, and commensal and pathogenic organisms. Despite the parallel role of the infant skin in serving as both a barrier and an interface for priming the immune system, large gaps exist in our understanding of the infantile cutaneous microbiome. The skin microbiome changes and matures throughout infancy, becoming more diverse and developing the site specificity known to exist in adults. Delivery method initially determines the composition of the cutaneous microbiome, though this impact appears transient. Cutaneous microbes play a critical role in immune system development, particularly during the neonatal period, and microbes and immune cells have closely intertwined, reciprocal effects. The unique structure of newborn skin influences cutaneous microbial colonization and the development of dermatologic pathology. The development of the infantile skin barrier and cutaneous microbiome contributes to future skin pathology. Atopic dermatitis flares and seborrheic dermatitis have been linked to dysbiosis, while erythema toxicum neonatorum is an immune response to the establishment of normal bacterial skin flora. Physicians who care for infants should be aware of the impact of the infantile skin microbiome and its role in the development of pathology. A better understanding of the origin and evolution of the skin microbiome will lead to more effective prevention and treatment of pediatric skin disease. [ABSTRACT FROM AUTHOR]

Three recent papers have provided sequential methods for meta-analysis of two-treatment randomized clinical trials. This paper provides an alternate approach that has three desirable features. First, when carried out prospectively (i.e., we only have the results up to the time of our current analysis), we do not require knowledge of the information fraction (the fraction of the total information that is available at each analysis). Second, the methods work even if the expected values of the effect sizes vary from study to study. Finally, our methods have easily interpretable metrics that make sense under changing effect sizes. Although the other published methods can be adapted to be 'group sequential' (recommended), meaning that a set number and timing of looks are specified, rather than looking after every trial, ours can be used in both a continuous or group sequential manner. We provide an example on the role of probiotics in preventing necrotizing enterocolitis in preterm infants. Copyright © 2013 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Necrotizing enterocolitis (NEC) is a leading cause of mortality and morbidity in neonatal intensive care units. Here we review selected manifestations of NEC, risk factors involved in its pathophysiology as well as putative mechanisms associated with how an immature gut might be more susceptible to NEC. Treatment and potential preventive strategies are discussed. [ABSTRACT FROM AUTHOR]

The increased survival of very-low-birth-weight infants has resulted in the need to better understand the immaturities that challenge optimal nutrition for these infants and how to surmount them. This is critical if we are to prevent short and long term morbidity associated with poor nutrition. Here we describe several of these immaturities including those related to digestion and absorption, suck-swallow incoordination, delayed gastric emptying, and intestinal motility and how they lead to the common problem of feeding intolerance. Scientifically based strategies for introducing, stopping and continuing enteral feedings in association with parenteral nutrition are presented. [ABSTRACT FROM AUTHOR]

Objective: Type 1 diabetes is an autoimmune disorder that occurs in genetically susceptible individuals. It has been hypothesized that the disease could be triggered by environmental agents that gain entry into the body through small intestinal absorption. Increased intestinal permeability has been reported both in spontaneous animal models of type 1 diabetes and human type 1 diabetes. In these studies, we examined both the physical and functional permeability characteristics of the small intestine in diabetes-prone and control rats.Methods: In a series of studies, BioBreeding diabetes-prone(n = 31), BioBreeding diabetes-resistant (n = 20) and control Wistar (n = 25) rats were examined at intervals from 21 to 125 days of age.Results: The percentage of goblet cells and the mucosal crypt depth were significantly greater in BioBreeding diabetes-prone than BioBreeding diabetes-resistant rats (P < 0.001 and P = 0.01, respectively). BioBreeding diabetes-prone and BioBreeding diabetes-resistant rats expressed less of the tight junction protein claudin (P < 0.05) and exhibited greater intestinal permeability (P < 0.001) than did Wistar rats. Intestinal permeability measured both in vivo and ex vivo decreased in all rat strains as age increased (P < 0.001).Conclusions: In a genetically susceptible rodent model of diabetes, early increased intestinal permeability might allow unregulated passage of environmental antigens that could potentially trigger the autoimmune response leading to type 1 diabetes. [ABSTRACT FROM AUTHOR]

Objectives: Critically ill neonates often have their enteral intake severely limited shortly after birth. Whether glutamine (Gln) or glutamate (Glu) can preserve intestinal structure and function in the neonate undergoing limited enteral feeding is not clear. We hypothesize that Gln and Glu can similarly preserve intestinal structure in the developing small intestine of infant rats fed a low protein diet.Methods: Using a gastrostomy-fed "pup-in-a-cup" rat model, the effects of Gln and Glu on the developing rat small intestine were examined. Four groups of 6- to 7-day-old pups were fed rat milk substitute (RMS) via gastrostomy tube. One group was provided 100% and three were provided 25% of the protein normally received from their mothers. Two of the groups fed 25% protein received additional Gln or Glu for 6 days.Results: Pups receiving the 100% protein RMS were larger than pups receiving the 25% protein RMS with or without Gln/Glu supplementation (P < 0.001). Average villus height (P < 0.01) and area (P < 0.01) were greater in pups receiving 100% protein RMS than in pups given 25% protein RMS formula. There was no significant difference among the groups in mucosal maltase or alkaline phosphatase activities. Tight junction protein claudin-1 was significantly higher in the group fed 100% protein RMS diet, while occludin did not differ among the 4 groups. Neither Gln nor Glu increased claudin-1 or occludin in rats fed 25% protein.Conclusions: These results suggest that neither Gln nor Glu supplementation can substitute effectively for whole protein in the developing rat small intestine for the outcomes that were evaluated. [ABSTRACT FROM AUTHOR]