The adverse effects of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) are not limited to the related infectious disease. In children and adolescents, serious risks due to the coronavirus disease 2019 (COVID-19) pandemic are also related to its indirect effects. These include an unbalanced diet with an increased risk of weight excess or nutritional deficiencies, increased sedentary lifestyle, lack of schooling, social isolation, and impaired mental health.Pediatricians should be aware of the side effects of the COVID-19 pandemic on children’s diet, physical mental health and advise the families according to their nutritional needs and financial resources. Moreover, the lack of a targeted therapy able to offer protection against the deleterious effects of SARS-CoV-2 infection should require a greater effort by scientific societies to find a more effective prevention strategy. In this context, much interest should be given to nutritional support, able to contrast malnutrition and to stimulate the immune system.

Obesity is one of the greatest health challenges affecting children of all ages and ethnicities. Almost 19% of children and adolescents worldwide are overweight or obese, with an upward trend in the last decades. These reports imply an increased risk of fat accumulation in hepatic cells leading to a series of histological hepatic damages gathered under the acronym NAFLD (Non-Alcoholic Fatty Liver Disease). Due to the complex dynamics underlying this condition, it has been recently renamed as ‘Metabolic Dysfunction Associated Fatty Liver Disease (MAFLD)’, supporting the hypothesis that hepatic steatosis is a key component of the large group of clinical and laboratory abnormalities of Metabolic Syndrome (MetS). This review aims to share the latest scientific knowledge on MAFLD in children in an attempt to offer novel insights into the complex dynamics underlying this condition, focusing on the novel molecular aspects. Although there is still no treatment with a proven efficacy for this condition, starting from the molecular basis of the disease, MAFLD’s therapeutic landscape is rapidly expanding, and different medications seem to act as modifiers of liver steatosis, inflammation, and fibrosis.

pathogenesis. Clinical heterogeneity and confounding factors also impair the search for alternative mechanisms. Therefore, we studied the CSF of 13 patients with neurological symptoms during the acute phase of their hospitalization, looking for clues suggesting a specific dysimmune phenomenon. MethodsCSF underwent conventional analysis and RT-PCR for SARS-CoV-2; a in-house HEK293 cell-based assay was also arranged to identify anti-spike antibodies. Albumin ratio, IgG index and oligoclonal bands were also assessed, along with a screening for autoimmune antibodies. First, commercial immunofluorescence and lineblot were used to detect common neuronal surface and intracellular antibodies, respectively; secondly, immunohistochemistry was performed on rat brain sections; lastly, CSF was incubated with fixed murine neuron and astrocyte cultures to confirm a potential auto-reactivity. ResultsCSF analysis disclosed a slightly increased protein level with a non-significant cell count (0-10 cells/uL). Neither SARS-CoV-2 nor common neuronal antibodies were detectable in the CSF, but we recognized anti-spike IgGs. 69% of the samples also showed neuropil staining, some of which had a common staining pattern involving the hippocampal dentate gyrus. Rodent primary cultures confirmed the presence of autoreactive antibodies against epitopes that are expressed in cortical neurons and/or astrocytes in most samples. ConclusionsA strong immunoreactivity against spike protein was found in the CSF of those patients, even without a significant blood brain barrier permeability. The detection of auto reactivity with two different techniques could thus represent a dysimmune response to COVID-19 infection, perhaps suggesting molecular mimicry.

Introduction Metabolic Syndrome (MetS) represents a common dysmetabolic state in children with obesity. Although data in youth show a role of gut hormones (GH) in the risk of developing MetS, no data are available during the prepubertal age, especially across clusters of MetS. Methods We characterized components of MetS and changes in GH concentrations in 90 prepubertal children with obesity compared to 30 healthy age-and gender matched peers. Children with obesity were divided into three groups according to the number of the components of MetS (group 1: 30 obese without components of MetS; group 2: 30 obese with 1 component of MetS; group 3: 30 obese with 2 or more components of MetS). Anthropometric parameters, blood pressure (BP), fasting insulin and glycaemia, lipid profile, transaminases and GH concentration were determined. Differences across the groups were evaluated by Kruskal-Wallis test and post-hoc analysis by Mann-Whithney test. Results Fasting glycaemia and insulin, HOMA-IR, Triglycerides, BP progressively increased and High Density Lipoprotein (HDL) progressively decreased across the groups of children with obesity compared to controls, showing worse values in group 3. GLP-1 and Ghrelin values progressively decreased and Obestatin progressively increased. The more components of the Mets were presents, the further GH concentrations deviated from standard values. Discussion and Conclusion Components of MetS and GH concentrations are impaired in prepubertal children with obesity compared to controls. The close association between progressive alterations in GH levels and increasing number of components of the MetS might indicate a role of these hormones in the determination of metabolic risk.

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