In our study the efficacy on symptom control and lung function of the combination of a long-acting bronchodilator with inhaled corticosteroid is equal to doubling the dose of the inhaled corticosteroid in children still symptomatic on a moderate dose of inhaled corticosteroid.

European Union's Seventh Framework programme.

Since its first identification in Scotland, over 1000 cases of unexplained pediatric hepatitis in children have been reported worldwide, including 278 cases in the UK 1 . Here we report investigation of 38 cases, 66 age-matched immunocompetent controls and 21 immunocompromised comparator subjects, using a combination of genomic, transcriptomic, proteomic and immunohistochemical methods. We detected high levels of adeno-associated virus 2 (AAV2) DNA in liver, blood, plasma or stool from 27/28 cases. We found low levels of Adenovirus (HAdV) and Human Herpesvirus 6B (HHV-6B), in 23/31 and 16/23 respectively of the cases tested. In contrast, AAV2 was infrequently detected at low titre in blood or liver from control children with HAdV, even when profoundly immunosuppressed.AAV2, HAdV and HHV-6 phylogeny excluded emergence of novel strains in cases. Histological analyses of explanted livers showed enrichment for T-cells and B-lineage cells.Proteomic comparison of liver tissue from cases and healthy controls, identified increased expression of HLA class 2, immunoglobulin variable regions and complement proteins.HAdV and AAV2 proteins were not detected in the livers. Instead, we identified AAV2 DNA complexes reflecting both HAdV and HHV-6B-mediated replication. We hypothesize that high levels of abnormal AAV2 replication products aided by HAdV and in severe cases HHV-6B, may have triggered immune-mediated hepatic disease in genetically and immunologically predisposed children.

Recognition of this disease and differentiation from juvenile idiopathic arthritis is important to avoid unnecessary investigations and treatment. Follow-up of renal function is indicated.

We report the first case of community-acquired bacteremia with Burkholderia fungorum , a newly described member of the Burkholderia cepacia complex. A 9-year-old girl sought treatment with septic arthritis in her right knee and ankle with soft tissue involvement. Commercial identification systems did not identify the causative microorganism.

Background: An epimeric form of 25-hydroxyvitamin D 3 (25(OH)D 3 ) has recently been detected in clinical samples, with relatively high levels in infants. Little is known on 3-epi-25(OH) D 3 formation and physiological function. Our objective was to study dynamics of 3-epi-25(OH)D 3 formation during infancy. Methods: 25(OH)D 3 and 3-epi-25(OH)D 3 levels were measured by liquid chromatography-tandem mass spectrometry in 22 preterm (aged 34-37 wk), 15 early preterm (aged <34 wk), and 118 term infants up to 2 y of age. All infants were prescribed vitamin D 400 IU/day after the first week of life. results: At birth, 3-epi-25(OH)D 3 levels were 3 (1-7) nmol/l, <10% of total 25(OH)D 3 . From the second week to 3 mo of age, both 25(OH)D 3 and 3-epi-25(OH)D 3 increased, with highest 3-epi-25(OH)D 3 contribution in early preterm infants (up to 55% of total 25(OH)D 3 vs. 36% in term infants, P < 0.0001). After 3 mo of age, 3-epi-25(OH)D 3 normalized to <10% in all infants. conclusions: At birth, all infants showed low contribution of 3-epi-25(OH)D 3 , increasing the week after starting vitamin D supplementation, until 3 mo of age. Highest levels of 3-epi-25(OH)D 3 were found in early preterm infants, supporting the hypothesis that hepatic immaturity plays a role in 3-epi-25(OH) D 3 formation.

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Chronic renal failure during childhood may be associated with delayed cognitive development. From 10 children with chronic renal failure, aged 2–59 months, plasma and cerebrospinal fluid (CSF) purines and pyrimidines have been determined. A marked increase of pseudouridine and cytidine was demonstrated in CSF of 10 and 8 children, respectively. The plasma concentration of pseudouridine was increased in a varying degree to a maximal value of more than 10 times the upper limit of normal. The plasma concentration of cytidine showed only moderately elevated values. In 3 children the study of CSF and plasma was repeated 6 weeks after the start of continuous ambulatory peritoneal dialysis. The abnormal concentrations of pseudouridine and cytidine were still present in CSF and plasma. Further studies are necessary to elucidate the cause of this unknown biochemical aberration of the central nervous system.