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BackgroundA number of biomarkers have been studied for the diagnosis of sepsis in paediatrics, but no gold standard has been identified. Procalcitonin (PCT) was demonstrated to be an accurate biomarker for the diagnosis of sepsis in adults and showed to be promising in paediatrics. Our study reviewed the diagnostic accuracy of PCT as an early biomarker of sepsis in neonates and children with suspected sepsis.MethodsA comprehensive literature search was carried out in Medline/Pubmed, Embase, ISI Web of Science, CINAHL and Cochrane Library, for studies assessing PCT accuracy in the diagnosis of sepsis in children and neonates with suspected sepsis. Studies in which the presence of infection had been confirmed microbiologically or classified as “probable” by chart review were included. Studies comparing patients to healthy subjects were excluded. We analysed data on neonates and children separately.Our primary outcome was the diagnostic accuracy of PCT at the cut-off of 2-2.5 ng/ml, while as secondary outcomes we analysed PCT cut-offs <2 ng/ml and >2.5 ng/ml. Pooled sensitivities and specificities were calculated by a bivariate meta-analysis and heterogeneity was graphically evaluated.ResultsWe included 17 studies, with a total of 1408 patients (1086 neonates and 322 children). Studies on neonates with early onset sepsis (EOS) and late onset sepsis (LOS) were grouped together. In the neonatal group, we calculated a sensitivity of 0.85, confidence interval (CI) (0.76; 0.90) and specificity of 0.54, CI (0.38; 0.70) at the PCT cut-off of 2.0-2.5 ng/ml. In the paediatric group it was not possible to undertake a pooled analysis at the PCT cut-off of 2.0-2.5 ng/ml, due to the paucity of the studies.ConclusionsPCT shows a moderate accuracy for the diagnosis of sepsis in neonates with suspected sepsis at the cut-off of 2.0-2.5 ng/ml. More studies with high methodological quality are warranted, particularly in neonates, studies considering EOS and LOS separately are needed to improve specificity.Trial registrationPROSPERO Identifier: CRD42016033809. Registered 30 Jan 2016.Electronic supplementary materialThe online version of this article (doi:10.1186/s12879-017-2396-7) contains supplementary material, which is available to authorized users.

In humans, the interaction of the natural killer group 2 member D (NKG2D)-activating receptor on natural killer (NK) and CD8(+) T cells with its major histocompatibility complex class I-related chain (MIC) and UL16 binding protein (ULBP) ligands (NKG2DLs) promotes recognition and elimination of stressed cells, such as tumor or infected cells. Here, we investigated the capacity of HIV-1 to modulate NKG2DL expression and escape NGK2D-mediated immunosurveillance. In CD4(+) T lymphocytes, both cell surface expression and release of MICA, MICB, and ULBP2 were up-regulated >2-fold by HIV-1 infection. In HIV-infected CD4(+) T lymphocytes or Jurkat T-cell lines, increased shedding of soluble NKG2DLs (sNKG2DLs) was impaired by a matrix metalloproteinase inhibitor (MMPI). Moreover, naive HIV(+) patients displayed increased plasma sMICA and sULBP2 levels and reduced NKG2D expression on NK and CD8(+) T cells compared to patients receiving highly active antiretroviral therapy (HAART) or healthy donors. In individual patients, HAART uptake resulted in the drop of sNKG2DL and recovery of NKG2D expression. Finally, sNKG2DLs in patients' plasma down-regulated NKG2D on NK and CD8(+) T cells and impaired NKG2D-mediated cytotoxicity of NK cells. Thus, NKG2D detuning by sNKG2DLs may promote HIV-1 immune evasion and compromise host resistance to opportunistic infections, but HAART and MMPI have the potential to avoid such immune dysfunction.

Attention deficit/hyperactivity disorder (ADHD) is the most common neurobehavioral disorder of childhood. There is an increasing need to find objective measures and markers of the disorder in order to assess the efficacy of the therapies and to improve follow-up strategies. Actigraphy is an objective method for recording motor activity and sleep parameters that has been used in many studies in ADHD. Our meta-analysis aimed to assess the current evidence on the role of actigraphy in both the detection of changes in motor activity and in sleep patterns in ADHD. A systematic review was carried out to find studies comparing children with unmedicated ADHD versus controls, using actigraphic measures as an outcome. The primary outcome measures were "sleep duration" and daytime "activity mean". As secondary outcome measures we analyzed "sleep onset latency", "sleep efficiency" and "wake after sleep onset". Twenty-four studies comprising 2179 children were included in this review. We show evidence that ADHD compared to typically developing children present a higher mean activity during structured sessions, a similar sleep duration, and a moderately altered sleep pattern. This study highlights the role of actigraphy as an objective tool for the ambulatory monitoring of sleep and activity in ADHD.

This study demonstrates the high mortality of hospital-acquired MDRGN bacteremia in children. International networks focusing on clinical management and outcomes of MDRGN in children are required. Study of novel antibiotics active against Gram-negative bacteria should include children early in the clinical trial development programs.

Aim: To evaluate the effect of gender, gestational age, birthweight, mode of delivery, 5′‐Apgar score and maternal conditions on calprotectin concentrations in meconium. Methods: Calprotectin was measured in 131 neonates, in the first passed meconium. Results: Calprotectin levels (mean ± SD) resulted in 145.2 ± 78.5 mg kg−1 meconium, significantly correlated with birthweight (r=–0.333; p < 0.001), gestational age (r =–0.206; p = 0.018) and 5′‐Apgar score (r= ‐0.243, p= 0.035). The estimated regression model was: calprotectin levels (mg kg−1) = 269.58–41.54 weight (kg); r = 0.383, p < 0.001. No differences were found in relation to gender, mode of delivery and maternal conditions. Conclusion: Calprotectin is already present in the first passed meconium, with higher levels in preterm and low birthweight neonates, as well as in neonates with some degree of perinatal asphyxia, as indicated by the negative correlation with 5′‐Apgar score. These findings are probably secondary to both the immaturity of the intestinal mucosa and its hypoxic‐ischaemic damage.

We describe the EEG findings of an infant with early‐onset epileptic encephalopathy with mutation of the KCNQ2 gene and a family history of neonatal seizures. The infant presented with multifocal drug‐resistant seizures with onset during the third day of life. Family history was positive for early‐onset neonatal seizures. Metabolic screening and neuroimaging were negative. Direct sequencing of KCQN2 from both the mother and child revealed a heterozygous cytosine‐to‐guanine mutation (Dedek et al., 2003). Interictal EEG showed a very discontinuous pattern which evolved towards a defined burst‐suppression pattern during sleep and a multifocal, random, attenuation pattern during wakefulness. Focal, tonic seizures with head deviation, sometimes followed by asynchronous and asymmetrical clonic jerks, eyelid myoclonias, and polypnoea, were recorded. Ictal EEG was characterised by focal, low‐voltage, fast activity, followed by recruiting theta rhythms and bilateral, focal, spike‐wave complexes, alternatively localised to one hemisphere and subsequently diffusing to the other. ACTH therapy was introduced, resulting in a significant improvement in EEG activity and gradual reduction in seizure frequency, with cessation at age 13 weeks. [Published with video sequences]

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