Sufficient evidence was noted showing that ethanol locks reduced CRBSIs and catheter replacements. Our findings raise questions about the effect of the ethanol lock on catheter integrity based on the noted increase in repair rate. This requires further prospective evaluation and may support selective application of ethanol locks to patients with documented CRBSIs.

The histologic diagnosis of LE is associated with pediatric CD and was found in 28% of CD patients. If LE is identified in pediatric CD, it is likely a manifestation of UGI-CD rather than esophagitis due to other etiologies or a variant of normal.

TNFalpha signaling through TNFR1 is protective in the trinitrobenzene sulfonic acid mouse model of inflammatory bowel disease.

N onalcoholic steatohepatitis (NASH) and nonalcoholic fatty liver disease (NAFLD) have been recognized entities in adult and pediatric medicine for more than 2 decades (1,2). Longterm follow-up studies of adults with NASH have confirmed that fibrosis can progress to cirrhosis (3). Individuals with NAFLD who have hepatic fibrosis and/or inflammation at presentation can progress to more severe fibrosis or cirrhosis and have a higher mortality when compared with individuals with steatosis alone (4-6).Nonalcoholic fatty liver disease is recognized as the most common cause of elevated liver enzymes in children. A recent autopsy series demonstrated that the estimated prevalence of NASH was 2.96% (22/742) in children. Furthermore, 23% of children with NAFLD in this study had NASH, whereas bridging fibrosis or cirrhosis was seen in 9% of children with NASH in this study (7).Long-term natural history data of pediatric NAFLD or NASH are not available. Certain components of routine laboratory tests may be predictive of NAFLD pattern and advanced fibrosis, but these serologic markers do not at present have adequate sensitivity or specificity to replace liver biopsy data to distinguish NASH from NAFLD (8). Serum alanine aminotransferase (ALT) and aspartate animotransferase (AST), for example, are not reliable measures of histological improvement in NASH (9).Thus, liver tissue histology becomes a critical requirement for accurate diagnosis and evaluation of fibrosis progression in patients with NAFLD or NASH. The invasive nature and inherent risk of percutaneous liver biopsy, coupled with the debatable benefit of liver biopsies in guiding therapy or changing clinical outcomes, have prevented gaining a full understanding of the natural history and progression rates of NASH in both children and adults. This report presents 2 children with NASH whose serial liver biopsies demonstrate progression of hepatic fibrosis in a short period of time. This report attempts to highlight that worsening of hepatic fibrosis can occur within childhood in patients with NASH.

Tumor necrosis factor (TNF)-alpha, a cardinal molecule in the cascade of sepsis-induced host injury, binds to two distinct receptors: tumor necrosis factor receptor (TNFR) 1 and TNFR2. We used the cecal ligation and puncture model of polymicrobial sepsis to elucidate the role of these receptors in sepsis pathogenesis. Mice lacking TNFR1 had prolonged survival with less hypothermia, whereas mice lacking TNFR2-/- had shortened survival and more profound hypothermia than wild-type mice. TNFR1-/- and TNFR2-/- mice had increased serum concentrations of interleukin (IL) 1beta and total TNF-alpha (free plus receptor bound) compared with wild-type mice, but there were no differences in IL6 or IL10 concentrations. Furthermore, free TNF-alpha was markedly elevated in the serum and peritoneal fluid of mice lacking TNFR2, supporting a role for this receptor in regulating the concentration of TNF-alpha. Lastly, apoptosis of ileal crypt epithelial cells was increased in mice lacking TNFR1, but there were no differences in lymphocyte apoptosis. These data suggest that in sepsis, TNFR1 mediates much of the TNF-alpha-induced pathology, whereas TNFR2 mediates protective effects.

There is variation in diagnostic and therapeutic interventions in the management of pediatric Crohn disease, and gaps exist between recommended and actual care.

Objectives Endoscopic mucosal improvement is the gold standard for assessing treatment efficacy in clinical trials of Crohn’s disease. Current endoscopic indices are not routinely used in clinical practice. The lack of endoscopic information in large clinical registries limits their use for research. A quick, easy, and accurate method is needed for assessing mucosal improvement for clinicians in real-world practice. We developed and tested a novel simplified endoscopic mucosal assessment for Crohn’s disease (SEMA-CD). Methods We developed a 5-point scale for ranking endoscopic severity of ileum and colon based on Simple Endoscopic Score for Crohn’s disease (SES-CD). Central readers were trained to perform SES-CD and SEMA-CD. Pediatric patients with Crohn’s disease undergoing colonoscopy were enrolled. Video recordings of colonoscopies were de-identified and randomly assigned to blinded central readers. The SES-CD and SEMA-CD were scored for each video. The SES-CD was considered the validated standard for comparison. Correlation was assessed with Spearman rho, inter- and intrarater reliability with kappa statistics. Results Fifty-seven colonoscopies were read a total of 212 times. Correlation between SEMA-CD and SES-CD was strong (rho = 0.98, P < 0.0001). Inter-rater reliability for SEMA-CD was 0.80, and intrarater reliability was 0.83. Central readers rated SEMA-CD as easier than SES-CD. Conclusion The SEMA-CD accurately and reproducibly correlates with the standard SES-CD. Central readers viewed SEMA-CD as easier than SES-CD. Use of SEMA-CD in practice should enable collecting mucosal improvement information in large populations of patients. This will improve the quality of research that can be conducted in clinical registries. External validation is needed.

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