Long COVID, also known as post-acute sequelae of SARS-CoV-2 infection (PASC), is increasingly recognized as a condition affecting not only adults but also children and adolescents. While children often experience milder acute COVID-19 symptoms compared to adults, some develop persistent physical, psychological, and neurological symptoms lasting for weeks or months after initial infection. The most commonly reported symptoms include debilitating fatigue, respiratory issues, headaches, muscle pain, gastrointestinal disturbances, and cognitive difficulties, which significantly impact daily activities, schooling, and social interactions. Additionally, many children with long COVID experience psychological symptoms, such as anxiety, depression, mood swings, and irritability, likely exacerbated by prolonged illness and lifestyle disruptions. Risk factors for long COVID in children include pre-existing health conditions such as asthma, obesity, and neurological disorders, with adolescents and females seemingly more affected. Hypothesized mechanisms underlying long COVID include chronic immune dysregulation, persistent viral particles stimulating inflammation, autonomic nervous system dysfunction, and mitochondrial impairment, which may collectively contribute to the variety of observed symptoms. Long-term outcomes remain uncertain; however, long COVID can lead to school absenteeism, social withdrawal, and psychological distress, potentially affecting cognitive development. Severe cases may develop chronic conditions such as postural orthostatic tachycardia syndrome (POTS) and reduced exercise tolerance. This review synthesizes the existing literature on long COVID in children, examining its prevalence, symptomatology, risk factors, and potential mechanisms, with an emphasis on the need for further clinical studies. While existing research largely relies on surveys and self-reported data, clinical assessments are essential to accurately characterize long COVID in pediatric populations and to guide effective management strategies.

Background: The increasing rate of obesity and overweight among children has highlighted nonalcoholic fatty liver disease (NAFLD) as the most common cause of chronic pediatric liver diseases. There are many publications supporting the idea that gut microbiota is altered in NAFLD. The aim of this study was to evaluate the prevalence of NAFLD among overweight and obese children with and without small intestinal bacterial overgrowth (SIBO) compared to a control group and to assess if intestinal dysbiosis represents a risk factor for NAFLD.Methods: One hundred and twenty-five overweight and obese children aged 10–18 years and 120 controls matched for age and gender were enrolled. SIBO was assessed by glucose hydrogen breath test (GHBT) in all subjects. NAFLD was assessed in all children using abdominal imaging and laboratory findings.Results: Of 125 obese children enrolled, 47 (37.6%) presented intestinal dysbiosis and 78 (62.4%) were SIBO negative. Only four (3.3%) controls were SIBO positive. NAFLD was detected in 28/47 (59.5%) of the SIBO positive obese group, compared to 8/78 (10.2%) of the SIBO negative obese group (p<0.001) and 0/120 (0%) controls (p<0.001). Children from the SIBO positive obese group had higher rates of elevated aminotransferases levels: aspartate aminotransferases (ASAT) (53.1% vs. 6.4%; p<0.001) and alanine aminotransferase (ALAT) (59.5% vs. 7.6%; p<0.001), hypertension (23.4% vs. 5.1%; p=0.002) and metabolic syndrome (44.6% vs. 9%; p=0.002) compared to the SIBO negative obese group.Conclusions: Obese children with SIBO have an increased risk for developing NAFLD. The relationship between intestinal dysbiosis and diet can influence the gut-liver axis.

Non-invasive techniques for liver fibrosis assessment were developed for adults and recent researches tested their accuracy in children. The only validated elastographic method for non-invasive liver fibrosis evaluation in children is Transient Elastography (TE). The aim of our study was to investigate the feasibility of liver stiffness (LS) measurement in paediatric patients with chronic liver diseases by means of Acoustic Radiation Force Impulse Elastography (ARFI) and 2D-Shear Wave Elastography (2D-SWE), compared to TE as reference method. Material and methods: We enrolled 54 consecutive children and adolescents with different chronic liver diseases. All patients were examined by means of TE, ARFI, and 2D-SWE. All measurements were performed in the right liver lobe, in the same session, in fasting condition. We considered reliable LS elastographic measurements as follows: for TE and ARFI - the median value of ten measurements with a success rate≥60% and an interquartile range70%, we found a significant correlation between TE and ARFI (Kappa correlation factor=0.761, p=0.001). Conclusions: Overall, 2D-SWE correlate better with TE compared to ARFI in children. Excluding patients with less satisfactory technical parameters, we obtained significant correlations between all three methods. Both SWE and ARFI are non-invasive techniques feasible of performing on paediatric patients along with TE.

Background: Inflammatory bowel diseases (IBDs) have seen an exponential increase in incidence, particularly among pediatric patients. Psychological stress is a significant risk factor influencing the disease course. This review assesses the interaction between stress and disease progression, focusing on articles that quantified inflammatory markers in IBD patients exposed to varying degrees of psychological stress. Methods: A systematic narrative literature review was conducted, focusing on the interaction between IBD and stress among adult and pediatric patients, as well as animal subjects. The research involved searching PubMed, Scopus, Medline, and Cochrane Library databases from 2000 to December 2023. Results: The interplay between the intestinal immunity response, the nervous system, and psychological disorders, known as the gut–brain axis, plays a major role in IBD pathophysiology. Various types of stressors alter gut mucosal integrity through different pathways, increasing gut mucosa permeability and promoting bacterial translocation. A denser microbial load in the gut wall emphasizes cytokine production, worsening the disease course. The risk of developing depression and anxiety is higher in IBD patients compared with the general population, and stress is a significant trigger for inducing acute flares of the disease. Conclusions: Further large studies should be conducted to assess the relationship between stressors, psychological disorders, and their impact on the course of IBD. Clinicians involved in the medical care of IBD patients should aim to implement stress reduction practices in addition to pharmacological therapies.

Celiac disease (CD) is an immune-mediated enteropathy caused by exposure to gluten and related prolamins in genetically susceptible individuals. It is a complex genetic disorder with multiple contributing genes. Linkage studies have identified several genomic regions that probably contain CD susceptibility genes. The most important genetic factors are HLA-DQ2 and DQ8. Several known environmental triggers promote the onset of CD at any age after gluten introduction in individuals with a genetic background, such as viral infections and intestinal dysbiosis. Recent publications have described the interference of the intestinal microbiome in gluten metabolism, modulation of local immune reactions, and in maintaining normal gut permeability. These results have promoted further lines of research on the benefit of probiotic administration to prevent disease onset or alleviate clinical symptoms along with a gluten-free diet (GFD). The relationship between gut microbiome changes and the onset of CD is incompletely understood, still being the subject of current research. This narrative review analyzes the interplay between environmental factors, intestinal microbiome alterations, and the course of CD. Furthermore, this review sets out to discuss if modulation of intestinal microflora with pre- and probiotics along with a GFD could represent a reliable therapeutic target for celiac patients.

Inflammatory bowel disease (IBD) is a complex disorder influenced by genetic, environmental, and microbial factors, with emerging evidence highlighting the gut microbiome’s role in disease pathogenesis. This study investigates the impact of microbiome-targeted interventions in pediatric IBD by integrating multi-omics analysis, including metagenomics, metabolomics, transcriptomics, and clinical biomarkers, to identify microbial dysbiosis patterns and potential therapeutic targets. A cohort of pediatric IBD patients underwent a personalized intervention involving dietary modifications, probiotic supplementation, and selective antibiotic therapy. Microbiome composition, inflammatory markers (fecal calprotectin, CRP), and disease activity scores (PCDAI/PUCAI) were assessed before and after treatment. At the 3-month follow-up, patients showed significant clinical improvement, with reduced stool frequency (p = 0.004) and improved stool consistency (p < 0.001). Symptoms such as bloating and abdominal pain decreased, while energy levels increased (p < 0.001). Dietary changes included higher fruit, meat, and dairy intake, and lower fast-food and sweets consumption (p < 0.001). Physician assessments classified 90% as “improved”, reinforcing the effectiveness of personalized microbiome interventions. Microbiome-targeted interventions (diet, probiotics, and selective antibiotics) improved pediatric IBD outcomes by reducing pathogenic bacteria and increasing short-chain fatty acid (SCFA)-producing species, lowering inflammation and symptoms. Early-life factors (cesarean birth, and formula feeding) influence IBD risk. Personalized diets enhanced microbial balance. Integrating multi-omics supports precision medicine, offering microbiome-based biomarkers and reducing immunosuppressive reliance.