Prevalence of childhood obesity is progressively increasing, reaching worldwide levels of 5.6% in girls and of 7.8% in boys. Several evidences showed that obesity is a major preventable risk factor and disease modifier of some respiratory conditions such as asthma and Obstructive Sleep Apnea Syndrome (OSAS). Co-occurrence of asthma and obesity may be due to common pathogenetic factors including exposure to air pollutants and tobacco smoking, Western diet, and low Vitamin D levels. Lung growth and dysanapsis phenomenon in asthmatic obese children play a role in impaired respiratory function which appears to be different than in adults. Genes involved in both asthma and obesity have been identified, though a gene-by-environment interaction has not been properly investigated yet. The identification of modifiable environmental factors influencing gene expression through epigenetic mechanisms may change the natural history of both diseases. Another important pediatric respiratory condition associated with obesity is Sleep-Disordered Breathing (SDB), especially Obstructive Sleep Apnea Syndrome (OSAS). OSAS and obesity are linked by a bidirectional causality, where the effects of one affect the other. The factors most involved in the association between OSAS and obesity are oxidative stress, systemic inflammation, and gut microbiota. In OSAS pathogenesis, obesity’s role appears to be mainly due to mechanical factors leading to an increase of respiratory work at night-time. However, a causal link between obesity-related inflammatory state and OSAS pathogenesis still needs to be properly confirmed. To prevent obesity and its complications, family education and precocious lifestyle changes are critical. A healthy diet may lead to an improved quality of life in obese children suffering from respiratory diseases. The present review aimed to investigate the links between obesity, asthma and OSAS, focusing on the available evidence and looking for future research fields.

Asthma exacerbations are associated with significant childhood morbidity and mortality. Recurrent asthma attacks contribute to progressive loss of lung function and can sometimes be fatal or near-fatal, even in mild asthma. Exacerbation prevention becomes a primary target in the management of all asthmatic patients. Our work reviews current advances on exacerbation predictive factors, focusing on the role of non-invasive biomarkers and genetics in order to identify subjects at higher risk of asthma attacks. Easy-to-perform tests are necessary in children; therefore, interest has increased on samples like exhaled breath condensate, urine and saliva. The variability of biomarker levels suggests the use of seriate measurements and composite markers. Genetic predisposition to childhood asthma onset has been largely investigated. Recent studies highlighted the influence of single nucleotide polymorphisms even on exacerbation susceptibility, through involvement of both intrinsic mechanisms and gene-environment interaction. The role of molecular and genetic aspects in exacerbation prediction supports an individual-shaped approach, in which follow-up planning and therapy optimization take into account not only the severity degree, but also the risk of recurrent exacerbations. Further efforts should be made to improve and validate the application of biomarkers and genomics in clinical settings.

Over the past few decades, an increase in the prevalence of asthma and food allergy has been observed in the pediatric population. In infants, food sensitization, particularly to egg, has increased the risk of developing allergic asthma. This is even more likely if sensitization to food allergens occurs early within the first few years of life. It is indeed known that both diseases may be present simultaneously in the pediatric population, but coexistence may negatively influence the severity of both conditions by increasing the risk of life-threatening asthmatic episodes as well as food-related anaphylaxis. Therefore, an accurate clinical and phenotype characterization of this high-risk group of children with both asthma and food allergy and a more aggressive management might lead to reducing related morbidity and mortality. The aim of this review is to provide an updated overview on the close link between food allergy and asthma and their negative mutual influence.

Non-cystic fibrosis bronchiectasis is an emergent disease characterized by endobronchial suppuration, dilated airways with neutrophilic inflammation and chronic wet cough due to recurrent lower airway infections. A regular clinical follow-up and adequate management of exacerbations are essential to reduce symptoms and the worsening of lung injury. We report a retrospective study comprising 15 children and adolescents with NCFB followed in our hospital center of pediatric pulmonology. We retrospectively analyzed the main comorbidities associated with the presence of NCFB, the radiological aspect associated with the different etiologies and the therapeutic approach used. We also emphasized the importance of an effective preventive strategy to reduce and prevent pulmonary exacerbations.

Asthma is a complex and heterogeneous disease, caused by the interaction between genetic and environmental factors with a predominant allergic background in children. The role of specific genes in asthmatic bronchial reactivity is still not clear, probably because of the many common pathways shared with other allergic disorders. This study is focused on 11 SNPs possibly related to asthma that were previously identified in a GWAS study. The genetic variability of these SNPs has been analysed in a population of 773 Italian healthy controls, and the presence of an association between the polymorphisms and the asthma onset was evaluated performing genotyping analysis on 108 children affected with asthma compared with the controls. Moreover, a pool of 171 patients with only allergic rhinoconjunctivitis has been included in the case–control analysis. The comparison of allele frequencies in asthmatic patients versus healthy controls identified two SNPs—rs1162394 (p = 0.019) and rs25681 (p = 0.044)—associated with the asthmatic condition, which were not differentially distributed in the rhinoconjunctivitis group. The rs25681 SNP, together with three other SNPs, also resulted in not being homogenously distributed in the Italian population. The significantly higher frequency of the rs25681 and rs1162394 SNPs (located, respectively, in the C5 and SRGAP3 genes) in the asthmatic population suggests an involvement of these genes in the asthmatic context, playing a role in increasing the inflammatory condition that may influence asthma onset and clinical course.

Background: Advances in pediatric care have increased the survival of children with life-limiting conditions, leading to a growing population requiring pediatric palliative care (PPC). Respiratory tract infections are among the leading causes of hospitalization in these patients. This study aimed to describe the features of respiratory infections in children eligible for PPC. Methods: The present study is a monocentric retrospective study including pediatric patients eligible for PPC with an Assessment of Complex Clinical-Care Needs in Pediatrics (ACCAPED) score ≥30 who were followed by a third-level hospital in Bologna, Italy. Hospitalizations for respiratory infections occurring between January 2019 and February 2025 were analyzed. Clinical, microbiologic, laboratory and therapeutic data were collected. Results: Among 319 eligible PPC patients, 99 experienced at least 1 infectious hospitalization, accounting for 117 admissions due to respiratory infections in 56 children. Lower respiratory tract infections predominated (86.3%), with viral pathogens identified in most cases. Respiratory support required escalation in 76.9% of admissions, while 6% required pediatric intensive care, and mortality was 1.7%. Pseudomonas aeruginosa was the most frequently isolated bacterial pathogen, especially among tracheostomized patients. Multivariate analysis identified an Assessment of Complex Clinical-Care Needs in Pediatrics score ≥75 [odds ratio (OR): 2.43; 95% confidence interval (CI): 1.04–5.68; P = 0.041] and C-reactive protein ≥8 mg/dL (OR: 3.85; 95% CI: 1.48–10.00; P = 0.0058) as independent predictors of respiratory support escalation. Conclusions: Respiratory infections represent a major cause of hospitalization in children receiving PPC. High clinical complexity and elevated inflammatory markers independently predict worsening respiratory status, supporting their use for early risk stratification and individualized management.