Energy- and protein-enriched formula improves weight gain in infants with malnutrition due to cardiac and noncardiac etiologies.

Background: We aimed to assess safety, tolerability, and improvement in weight gain with an energy- and protein-enriched formula (EPEF) in infants with poor growth.

Methods: Infants aged 1-8 months with poor growth received EPEF for 16 weeks. Our primary objective was improvement in weight as measured by change in weight-for-age z-score (WAZ) and weight gain velocity (grams per day) ≥ median for age.

Longitudinal Growth Outcomes Following First-line Treatment for Pediatric Patients With Eosinophilic Esophagitis.

Objectives: No formal comparative effectiveness studies have been conducted to evaluate the effect of eosinophilic esophagitis (EoE) treatment choice on long-term growth in pediatric patients. Long-term studies of inhaled corticoid steroids in asthma, however, suggest possible effects on linear growth. The aim of this study was to compare longitudinal, anthropometric growth in children with EoE according to treatment approach.

Practice Pattern Variation in Pediatric Eosinophilic Esophagitis in the Carolinas EoE Collaborative: A Research Model in Community and Academic Practices.

Objectives: Differences in the initial management of pediatric eosinophilic esophagitis (EoE) by practice setting have not been well characterized. We aimed to characterize these differences for sites in the Carolinas EoE Collaborative (CEoEC), a multicenter network of academic and community practices.

Methods: We performed a retrospective cohort study of pediatric EoE patients at five CEoEC sites: University of North Carolina (UNC) Hospital, Charlotte Asthma and Allergy Specialists, Greenville Health Systems, Wake Forest Baptist Medical Center, and the Medical University of South Carolina Hospital.

Combined and Alternating Topical Steroids and Food Elimination Diet for the Treatment of Eosinophilic Esophagitis.

Background: Few studies have examined combined or alternating treatment algorithms in eosinophilic esophagitis.

Aims: We conducted a retrospective cohort study to ascertain the efficacy and adherence to a combined and alternating treatment approach with topical corticosteroids and 2-food elimination diet for pediatric EoE.

Methods: Patients were prescribed a 2-food elimination diet (milk and soy) and topical corticosteroid (fluticasone or oral viscous budesonide) for 3 months, after which the steroid was discontinued and 2-food elimination diet continued for 3 months.

Mucosal-Associated Invariant T Cells in the Human Gastric Mucosa and Blood: Role in Helicobacter pylori Infection.

Mucosal-associated invariant T (MAIT) cells represent a class of antimicrobial innate-like T cells that have been characterized in human blood, liver, lungs, and intestine. Here, we investigated, for the first time, the presence of MAIT cells in the stomach of children, adults, and the elderly undergoing routine endoscopy and assessed their reactivity to Helicobacter pylori (H. pylori - Hp), a major gastric pathogen.

Remission of Refractory Celiac Disease With Infliximab in a Pediatric Patient.

Refractory celiac disease (RCD) is a rare but life-threatening complication of celiac disease (CD), and only 1 pediatric case has been reported. We report a case of a 14-year-old girl with CD presenting with persistent symptoms and positive tissue celiac-specific antibodies despite a gluten-free diet. Push enteroscopy showed jejunal scalloping and partial villous atrophy on histology.

Secretory phospholipase A2-mediated depletion of phosphatidylglycerol in early acute respiratory distress syndrome.

Introduction: Secretory phospholipases A2 (sPLA2) hydrolyze phospholipids in cell membranes and extracellular structures such as pulmonary surfactant. This study tests the hypothesis that sPLA2 are elevated in human lungs during acute respiratory distress syndrome (ARDS) and that sPLA2 levels are associated with surfactant injury by hydrolysis of surfactant phospholipids.

Methods: Bronchoalveolar lavage (BAL) fluid was obtained from 18 patients with early ARDS (<72 hours) and compared with samples from 10 healthy volunteers.

Pediatric celiac disease.

Purpose Of Review: Celiac disease is an extremely common, although underdiagnosed, disorder. Knowledge about the varied clinical manifestations and the proper approach to screening and diagnosing celiac disease will lead to appropriate early intervention in affected children

Recent Findings: New age-dependent algorithms are emerging to properly screen for celiac disease. There is new evidence on the patchy nature of celiac disease supporting the practice of multiple duodenal biopsies including the bulb of the duodenum.

Long-term treatment of primary sclerosing cholangitis in children with oral vancomycin: an immunomodulating antibiotic.

Background: Primary sclerosing cholangitis is a rare chronic cholestatic condition of unknown etiology, frequently associated with inflammatory bowel disease and characterized by diffuse fibrosing and inflammatory destruction of the intra- and/or extrahepatic biliary duct system.

Patients And Methods: The study involved 14 children with primary sclerosing cholangitis confirmed by either liver biopsy, endoscopic retrograde cholangiopancreatography, and/or magnetic resonance cholangiogram. In each of the 14 cases, liver histology showed characteristic features consistent with primary sclerosing cholangitis.

Lysophospholipid generation and phosphatidylglycerol depletion in phospholipase A(2)-mediated surfactant dysfunction.

Pulmonary surfactant's complex mixture of phospholipids and proteins reduces the work of breathing by lowering alveolar surface tension during respiration. One mechanism of surfactant damage appears to be the hydrolysis of phospholipid by phospholipases activated in the inflamed lung. Humans have several candidate secretory phospholipase A(2) (sPLA(2)) enzymes in lung cells and infiltrating leukocytes that could damage extracellular surfactant.

Surfactant phospholipid changes after antigen challenge: a role for phosphatidylglycerol in dysfunction.

In asthma, inflammation-mediated surfactant dysfunction contributes to increased airway resistance, but the mechanisms for dysfunction are not understood. To test mechanisms that alter surfactant function, atopic asthmatics underwent endobronchial antigen challenge and bronchoalveolar lavage (BAL). BAL fluids were sequentially separated into cells, surfactant, and supernatant, and multiple end points were analyzed.