Search Results (105)

Background/Objectives: Leptin is a pleiotropic adipokine linking energy metabolism with innate and adaptive immunity. Its relationship with clinical severity across distinct airway disease phenotypes remains insufficiently characterized. This study examined serum leptin concentrations in adults with allergic rhinitis, non-allergic asthma, and allergic asthma associated with allergic rhinitis. Methods: This single-center retrospective observational study analyzed fully anonymized clinical and laboratory data from 88 adults: patients with allergic rhinitis (n = 31), non-allergic asthma (n = 15), or allergic asthma with allergic rhinitis (n = 22) and healthy controls (n = 20). Serum leptin was measured using a quantitative sandwich enzyme-linked immunosorbent assay. Disease severity was classified using the Allergic Rhinitis and its Impact on Asthma and Global Initiative for Asthma frameworks applicable during the study period. Statistical analyses were performed using IBM SPSS Statistics, version 26.0 (IBM Corp., Armonk, NY, USA), and available original statistical outputs were summarized using retained t statistics and two-sided p values. Results: Stage-specific mean serum leptin concentrations were heterogeneous and non-monotonic. Statistically significant relationships between leptin concentration and disease stage were reported for allergic rhinitis (t = 2.844; p = 0.008), non-allergic asthma (t = 4.240; p = 0.001), and allergic asthma with allergic rhinitis (t = 2.700; p = 0.013). In the allergic rhinitis subgroup, 64.5% of participants had normal weight, 32.3% were overweight, and 3.2% had grade II obesity; weight category was not significantly related to rhinitis stage. Conclusions: The retained analyses indicate statistically significant relationships between serum leptin concentration and clinical disease stage across the investigated airway phenotypes. However, the stage-specific descriptive means were heterogeneous and non-monotonic and therefore do not support a uniform progressive increase in leptin with increasing disease severity. Because complete model outputs and covariate-adjusted estimates were unavailable, these findings should be regarded as exploratory and require prospective validation with appropriate adjustment for adiposity and other relevant metabolic confounders. Full article

Asthma prevalence in school-age children varies widely by geography, from below 5% in some regions to above 20% in others, averaging 10–12% across industrialized countries, but genetic factors account for less than 40% of disease liability. Gut microbiota is increasingly recognized as a critical intermediary between early-life dietary exposure and immunological trajectories that determine asthma susceptibility. Through the production of short-chain fatty acids (SCFAs), particularly butyrate, propionate, and acetate, commensal bacteria regulate dendritic cell function, promote T-regulatory (Treg) cell differentiation, and attenuate Th2-polarized airway inflammation via the gut–lung axis. Epidemiological cohorts including CHILD, WHEALS, and PASTURE associate early-life dysbiosis and reduced Lactobacillus, Bifidobacterium, and Faecalibacterium prausnitzii with increased asthma risk, while dietary patterns rich in fermentable fibre, omega-3 polyunsaturated fatty acids, and diverse plant-based foods are associated with preserved microbial diversity and, in preclinical models, attenuated type-2 inflammatory signalling. This narrative review synthesizes mechanistic and epidemiological evidence on how nutritional exposures shape gut microbiota composition and influences asthma onset and severity in paediatric populations, including the distinct obesity-related asthma phenotype. Critical gaps, insufficient dietary intervention trials with microbiome endpoints, methodological heterogeneity across cohorts, and the paucity of data from non-Western populations are discussed, with implications for preventive nutritional counselling in paediatric allergology practice. Full article

Background: Children with obesity-related asthma exhibit poorer symptom control and more frequent exacerbations than their normal-weight peers, but the underlying metabolic mechanisms are unclear. This study aimed to identify drivers of obesity-related asthma through untargeted plasma metabolomic and lipidomic profiling. Methods: Plasma was obtained from normal weight (NW) asthmatic (n = 95) and non-asthmatic (n = 67) and overweight/obese (OO) asthmatic (n = 99) and non-asthmatic (n = 100) children (6–17 years). We assessed metabolic and lipidomic differences between asthmatics and controls within each BMI group using orthogonal partial least squares discriminant analysis (OPLS-DA), examined overlap with the adult Qatar Biobank cohort, and mapped metabolic–clinical interactions using Gaussian Graphical Models. Results: In the fitted OPLS-DA models, separation between asthmatic and control groups was stronger in the NW group (R²Y = 0.72/0.52) than in OO (R²Y = 0.65/0.63) children. Asthma was associated with altered tricarboxylic acid (TCA) intermediates, ether-linked phosphatidylethanolamines, and sphingomyelins (SM) in NW, and with phosphatidylcholines, lysophosphatidylcholines, and phosphatidylethanolamines in OO. Integrating metabolomic, lipidomic, and clinical data revealed connections between altered SMs and interleukins, and TCA intermediates and electrolytes, all associated with elevated leptin in NW. An increased residual volume to total lung capacity ratio in OO was associated with phospholipid shifts. The overall dynamics in lipid metabolism with asthma, conditioned on BMI, was also observed in the adult Qatar Biobank cohort. Conclusions: Among NW children with asthma, we found enhanced TCA cycle activity and inflammation linked to altered SM metabolism, whereas in OO, the findings suggest oxidative stress arising from chronic obesity-related inflammation. These data reveal BMI-specific metabolic mechanisms of pediatric asthma that might inform precision approaches to disease management. Full article

Background/Objectives: The co-occurrence of asthma and obesity presents a significant clinical challenge, but the underlying mechanisms remain unclear. Reduced adiponectin and vitamin D levels have been associated with both conditions, suggesting that their potential modulatory roles warrant further investigation. This study aimed to evaluate whether vitamin D and adiponectin levels differ among pediatric groups defined by their asthma and obesity status, to better characterize the metabolic and inflammatory profile of the obesityasthma phenotype. Methods: A total of 120 participants aged 6–18 were enrolled and categorized into four groups: Asthma (n = 30), Obesity (n = 30), Asthma + Obesity (n = 30), and Control group (n = 30). All participants underwent lung function testing, anthropometric assessment and measurement of fraction of exhaled nitric oxide (FeNO). Participants were further categorized according to BMI percentiles. Adiponectin levels were measured using ELISA, while vitamin D levels were detected using HPLC. Results: Vitamin D levels and lung function parameters did not differ across groups, although deficiency was most prevalent in the obesity group. FeNO was elevated in asthmatics relative to obese children (p = 0.038) and in obese asthmatics compared with both controls (p = 0.040) and obese children (p = 0.021). Adiponectin levels were lower in obese asthmatic children compared to the controls (p = 0.024). A similar difference was observed between the controls and obese asthmatics among children with low vitamin D levels (p = 0.014). Conclusions: The dominant mechanisms underlying the obesity–asthma phenotype remain unclear; however, our findings indicate a link between adiponectin dysregulation and heightened airway inflammation, as evidenced by increased FeNO levels, though the precise pathways involved are still not well-understood. The role of vitamin D appears less consistent. These results highlight the need for further research to clarify the interplay between metabolic and inflammatory pathways and to support more personalized management strategies in children with obesity-related asthma. Full article

Background and objective: Obstructive sleep apnea (OSA) is a common pediatric sleep disorder, most often caused by adenotonsillar hypertrophy. Although adenotonsillectomy (AT) is the standard first–line treatment, a substantial proportion of children experience residual OSA (rOSA). This systematic review aimed to synthesize current evidence on risk factors associated with rOSA in children following AT. Materials and Methods: A systematic review was conducted in accordance with PRISMA guidelines. PubMed and the Cochrane Library were searched without date restrictions using English–language terms related to rOSA, children, and adenotonsillectomy. Studies assessing postoperative persistence of OSA and associated risk factors were included. Results: Thirteen studies published between 2010 and 2024 met the inclusion criteria. The reported prevalence of rOSA varied widely (18.6–85.0%), reflecting heterogeneity in study design, patient populations, baseline disease severity, and follow–up methods. Obesity emerged as the most consistently identified risk factor, with significantly higher rOSA rates reported among children with elevated body mass index. Age also influenced outcomes, with both very young (<3 years) and older (>7 years) children demonstrating an increased likelihood of persistent disease. Comorbid conditions, particularly asthma and Down syndrome, were associated with poorer postoperative improvement. Additional contributors included craniofacial or developmental abnormalities and higher preoperative apnea–hypopnea index. Limited evidence also suggested that socioeconomic and environmental factors may affect postoperative outcomes. Conclusions: Residual OSA is common following adenotonsillectomy in children. Obesity, age, and comorbidities are key predictors, underscoring the need for comprehensive preoperative risk stratification and structured postoperative follow–up. Full article

Background: Severe asthma exacerbations (SAEs) significantly contribute to asthma-related morbidity, mortality, and healthcare burden. Despite therapeutic advances, a subset of patients remains exacerbation-prone. This review aims to summarize current evidence on risk factors, phenotypes, and biomarkers associated with SAEs, and explore personalized strategies for their acute management. Methods: We conducted a comprehensive literature review focusing on clinical, inflammatory, and environmental drivers of SAE. Special attention was given to Type 2 (T2) biomarkers—blood eosinophil count (BEC) and fractional exhaled nitric oxide (FeNO)—as tools for phenotyping and treatment guidance. Emerging evidence on the use of biologics during exacerbations was also analyzed. Results: SAEs are heterogeneous in etiology and inflammatory profile. Respiratory infections, allergen exposure, obesity, and comorbidities increase exacerbation risk. T2-high SAEs respond well to corticosteroids and biologics, whereas T2-low SAEs show limited treatment benefit. BEC and FeNO reliably predict exacerbation risk and corticosteroid responsiveness. Recent case reports suggest potential roles for anti-IL-5 and anti-thymic stromal lymphopoietin (TSLP) biologics in acute care. Conclusions: Biomarker-guided management of SAEs may enhance therapeutic precision and avoid overtreatment. Integrating phenotypic (observable characteristics) and endotypic (biological markers) assessment into acute care could improve patient outcomes and optimize resource use. Prospective trials are needed to confirm these approaches. Full article

Asthma is a multifactorial respiratory condition affected by demographic, clinical, and lifestyle factors. Recognizing sex-related differences in risk factors may help develop personalized preventive strategies and ultimately enhance clinical outcomes. This study aims to compare the characteristics of male and female patients with asthma and to identify the primary risk factors linked to the condition in each group as well. A comparative analysis was conducted using regression models to evaluate the association between asthma and potential risk factors. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated to estimate the strength of associations for men and women separately. In females, obesity (OR, 1.85; 95% CI, 1.24–2.75), chronic obstructive pulmonary disease (COPD) (OR, 3.37; 95% CI, 1.77–6.43), chronic sinusitis (OR, 4.37; 95% CI, 1.02–18.64), and hypothyroidism (OR, 1.79; 95% CI, 1.09–2.94) were significantly associated with asthma. In males, COPD was the strongest predictor (OR, 4.35; 95% CI, 1.18–15.97), while other factors showed weaker or non-significant associations. Age was not a significant predictor in either sex. The findings highlight important sex differences in the risk profile for asthma. These results underscore the need for sex-specific approaches in the prevention, diagnosis, and management of asthma. Full article

Background: Overweight and obesity frequently occur as comorbid conditions in people with asthma, particularly among those with poor disease control or more severe clinical profiles. However, the extent to which exposure to grey spaces may influence the link between overweight/obesity and asthma remains insufficiently explored. Aim: To assess the association between overweight/obesity and asthma in an Italian general population sample and the influence of residential grey space on such relationship. Methods: A total of 2841 individuals (54.7% women; age range 8–97 years) residing in Pisa, Italy, were surveyed in 1991–1993 using a standardised questionnaire on health conditions and relevant risk factors. The proportion of grey space within a 1000 m buffer around each participant’s home was quantified using the CORINE Land Cover database. Multinomial logistic regression models were applied to assess the association between asthma status (1. asthma symptoms without doctor diagnosis, 2. diagnosis ± symptoms, 3. no diagnosis/symptoms − reference category) and overweight/obesity, adjusting for sex, age, educational level, smoking, physical activity and grey space exposure. Analyses were further stratified according to high vs. low grey space exposure (above vs. below 63%, corresponding to the second tertile). Mediation and interaction analyses were also performed. Results: The prevalence of asthma diagnosis ± symptoms, overweight and obesity was 18.7%, 35.8% and 12.8%, respectively. In the full sample, asthma symptoms without medical diagnosis were positively associated with overweight (Odds Ratio—OR 1.43; 95% Confidence Interval—CI 1.08–1.88), obesity (OR 1.99; 95% CI 1.38–2.88) and residential grey space (OR 1.06; 95% CI 1.01–1.13). Stratified models showed that, among participants with high exposure to grey areas, asthma symptoms were linked to both overweight (OR 2.03; 95% CI 1.29–3.19) and obesity (OR 2.57; 95% CI 1.36–4.86). In individuals with low grey space exposure, an association was observed only with obesity (OR 1.80; 95% CI 1.15–2.82). Mediation analysis did not reveal any weight-related effect modification. Measures of additive interaction indicated that 32% of asthma symptoms were attributable to the interaction between excess body weight and high grey space exposure. Conclusions: This study showed that overweight/obesity and grey space exposure are factors associated with asthma symptoms. These findings advocate for an early identification of overweight/obese-asthma symptom phenotype since it may help prevent the onset or worsening of asthma, particularly in urban environments. These insights highlight the need for integrated public health and urban planning strategies to promote more sustainable, health-supportive environments. Full article

Plastic production and subsequent environmental contamination have increased substantially in recent decades, resulting in pervasive human exposure to microplastics (MPs), nanoplastics (NPs), and plastic-associated additives such as bisphenols and phthalates. These substances are known to induce toxic effects via multiple biological mechanisms, including oxidative stress, inflammation, apoptosis, immune system disruption, and genotoxicity. While exceptions exist, current research generally indicates that these exposures may adversely affect fertility. Notably, children constitute the most vulnerable demographic due to behavioral tendencies, higher intake-to-body-weight ratios, underdeveloped detoxification systems, and critical developmental periods of susceptibility. Evidence demonstrates that exposure commences in utero, with MPs, NPs, and additives identified in placental tissue, amniotic fluid, cord blood, and meconium—factors associated with impaired fetal growth and reduced gestational duration. After birth, additional exposure occurs through diet, inhalation, household dust, feeding equipment, toys, and consumer products. Experimental and epidemiological studies suggest that plastics may adversely affect multiple physiological systems. Reported outcomes include altered pubertal development, reduced fertility, neurodevelopmental abnormalities, respiratory diseases such as asthma, and increased risks of metabolic disorders, including obesity and insulin resistance. However, substantial knowledge gaps remain: the relative toxicity of different polymers and additives, dose–response relationships, critical exposure periods, and long-term consequences are not yet fully defined. Given growing concern and mounting evidence of harm, precautionary measures are warranted. Reducing nonessential plastic use, strengthening regulatory actions, improving product labeling, and promoting public awareness are urgent priorities, particularly in vulnerable and resource-limited communities. Further mechanistic studies and longitudinal human research are essential to clarify health risks, guide safer material substitutions, and inform evidence-based policies aimed at protecting children from avoidable plastic-related toxicity. Full article

Asthma and obesity are two common chronic diseases of growing clinical and social importance. One of the recognised phenotypes of asthma is obesity-related asthma, which is characterised by a more severe course, resistance to glucocorticosteroids, increased inflammation and poorer symptom control. This article discusses the complex pathophysiological mechanism of this phenotype, considering the role of chronic inflammation, immune dysregulation and metabolic disorders resulting from obesity. The potential role of glucagon-like peptide-1(GLP-1) receptor analogues as an innovative therapeutic option in the treatment of asthma in obese individuals, both with and without type 2 diabetes mellitus (T2DM), is also analysed. A literature review indicates that glucagon-like peptide-1 receptor analogue (GLP-1RA) drugs, in addition to their hypoglycaemic and weight-reducing effects, also exhibit anti-inflammatory activity in the respiratory system and may reduce the frequency of asthma exacerbations and improve asthma control. The article reviews current data from experimental and clinical studies, emphasising the need for further research on the use of GLP-1RA as an adjunct to conventional asthma therapy in the context of the obese asthma phenotype. Full article

Background/Objectives: This study aimed to assess the anthropometric and body composition characteristics, blood profiles and fitness-related parameters of emergency medical services (EMS) professionals. Methods: A total of 39 EMS professionals participated in the study, consisting of 18 males (age: 37.78 ± 10.62 years, height 180.87 ± 6.00 cm, weight 105.42 ± 25.40 kg) and 21 females (age: 33.05 ± 7.44 years, height 167.29 ± 3.89 cm, weight 90.63 ± 21.20 kg). The testing included anthropometric measurements, blood profiling, handgrip and low back strength assessments, vertical jump evaluation, flexibility testing, sit-up and push-up assessments, as well as timed performance measurements for a 300 m sprint and a 1.5-mile run. Results: According to the body mass index (BMI), 41% of the EMS professionals were classified as obese. Self-reported data indicated a smoking prevalence of 23%, while diabetes (n = 3), asthma (n = 2), and hypertension (n = 2) were also reported. Our results reveal that a great proportion of EMS professionals demonstrated suboptimal body composition and performance levels, with many failing to meet recommended health and performance standards. Elevated BMI, waist and hip circumferences, and body fat percentages were observed, along with relatively low performance in the strength and endurance tests. Conclusions: These findings highlight the need for targeted interventions among EMS professionals, who are expected to maintain adequate levels of aerobic capacity, flexibility, muscular strength and endurance. Full article

Asthma is a chronic respiratory disease affecting over 262 million people worldwide, with obesity-associated asthma emerging as a distinct endotype of increasing prevalence characterized by metabolic inflammation and airway remodeling. Unlike allergic asthma, this phenotype is driven by chronic low-grade inflammation, originating from hypertrophic and hypoxic adipose tissue. This dysregulated state leads to the activation of pro-inflammatory pathways and the secretion of cytokines, contributing to airway dysfunction and remodeling. Recent evidence highlights non-coding RNAs (ncRNAs) as key regulators of these processes. MicroRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs) influence inflammation and remodeling by modulating immune cell polarization, cytokine secretion, extracellular matrix composition, and airway smooth muscle cell (ASMC) proliferation. Notably, H19, MEG3, GAS5, miR-26a-1-3p, and miR-376a-3p have been implicated in both asthma and obesity, suggesting their role in linking metabolic dysfunction with airway pathology. Moreover, ncRNAs regulate Treg/Th17 balance, fibroblast activation, and autophagy-related pathways, further influencing airway remodeling. Our in silico analysis highlighted the IGF1R signaling pathway as a key enriched mechanism, linking selected ncRNAs with metabolic dysregulation and inflammation in obesity-related asthma. This paper reviews how ncRNAs regulate inflammation and airway remodeling in obesity-associated asthma, emphasizing their potential molecular links between metabolic dysfunction and airway pathology. Full article

Neutrophilic asthma (NA) is an inflammatory phenotype of asthma, characterized by predominantly neutrophilic infiltrations in bronchial mucosa. It is usually diagnosed on the basis of high neutrophil count in induced sputum (from >40% to >76%) with low eosinophils (<2%). The prevalence of NA ranges from 16% to 28% of the adult asthma population depending on the definitions and study methods applied. A clinical picture of NA is characterized by late onset of symptoms, higher exacerbation rate, lower level of symptoms control, and poorer response to steroids compared to eosinophilic phenotype. Comorbidities such as obesity and GERD as well as the influence of environmental factors (air pollution, smoking, bacterial infections) contribute to the development and severe course of the disease. NA is T2-low disease with predominantly Th1/Th17-type inflammation. Neutrophils are key cells responsible for initiating and sustaining inflammation. In addition to their primary functions like phagocytosis, degranulation, and NETosis, neutrophils release several pro-inflammatory cytokines (IL-1α, IL-1β, IL-6, TNF) and chemokines (CXCL-1, -2, -8, -9, -10) responsible for the recruitment of other neutrophils or T cells. Increasing knowledge about the biology of neutrophiles and their role in asthma results in new potential therapies that could improve control of NA, particularly new biologicals targeting Th1/Th17-related cytokines. In this review, we discuss the prevalence, mechanisms, and clinical features of neutrophilic asthma. Furthermore, current therapeutic options and some promising perspectives for the near future are presented. Full article

Over several decades, childhood asthma has emerged as a significant global public health concern, with the highest prevalence reported in industrialized countries. The rapid rise in asthma incidence and loss of control when the diagnosis is established can be related to environmental and lifestyle changes, especially during early infancy. Current evidence indicates a potential link to an imbalance in immune system responses, influenced by tobacco smoke, traffic-related air pollution, outdoor and indoor allergens, gut microbiome, viral infection, obesity, sedentary lifestyle and dietary patterns. This narrative review aims to explore the landscape of contemporary environmental risk factors for childhood asthma, with a focus on their interplay and the relative importance. Full article

Background: Dupilumab, a monoclonal antibody targeting the IL-4/IL-13 receptor, has shown significant efficacy in improving asthma control and reducing exacerbations in patients with severe eosinophilic asthma. However, there is a lack of knowledge about real-world data on clinical remission rates and their predictors. Objective: This study aimed to evaluate clinical outcomes, remission rates, and predictive factors of remission in a real-life cohort of patients with severe eosinophilic asthma treated with dupilumab. Methods: We conducted a retrospective, bicentric, observational study including 52 patients with severe eosinophilic asthma treated with dupilumab. Clinical, functional, and biomarkers were assessed at baseline, 6 months, and 12 months. Statistical analyses included logistic regression to identify independent predictors of clinical remission. Results: After 12 months of treatment, 48.2% of patients achieved clinical remission. Dupilumab significantly improved asthma control and lung function (including FVC and FEF_25–75), reduced exacerbation rates, and maintenance therapy. High blood eosinophil levels (>490 cells/µL), high FeNO levels (>25 ppb), a history of CRSwNP, and better baseline FEV1 were associated with asthma remission. Conversely, obesity (BMI > 30) and related comorbidities (such as GERD, OSAS, and hypertension) and bronchiectasis were associated with a lower likelihood of remission. Multivariate analysis confirmed higher baseline FEV1 (OR 2.94; IC 1.13–7.6), positive history of CRSwNP (OR 8.03; IC 1.41–45.5), and higher baseline blood eosinophils (OR 1.003 IC 1.001–1.006) as independent predictors of clinical remission. Conclusions: These results are in line with the known effectiveness of dupilumab in severe eosinophilic asthma and identified a history of CRSwNP, higher baseline FEV1, and elevated blood eosinophils as key predictors of clinical remission. These findings may contribute to a more personalized approach to treatment selection, emphasizing the importance of comorbidity assessment together with type 2 inflammation biomarkers. Further prospective studies are needed to validate these results. Full article