Asthma exacerbations are acute worsening episodes in individuals with bronchial asthma, frequently necessitating emergency hospital care. Early differentiation between eosinophilic (≥150 eosinophils/mm³) and non-eosinophilic (<150 eosinophils/mm³) subtypes plays a crucial role in treatment decisions and identifying patients eligible for biologic therapies. The ExBA Study explored variations in complete blood count (CBC) parameters and derived cellular ratios—namely the neutrophil-to-lymphocyte (NLR), thrombocyte-to-lymphocyte (TLR), and eosinophil-to-leukocyte ratios (ELR)—in adults hospitalized with severe asthma exacerbations. Ninety patients were enrolled and categorized into eosinophilic (n = 38) and non-eosinophilic (n = 52) groups. Significant statistical differences were observed in the neutrophil and lymphocyte levels, as well as in all three ratios. ROC analysis highlighted the ELR as the most specific indicator of the eosinophilic phenotype (specificity 100%, AUC 0.938, cut-off 0.003), whereas the NLR and TLR showed stronger associations with the non-eosinophilic group (AUC 0.733 and 0.676). No meaningful differences emerged regarding arterial blood gas levels, length of hospital stay, treatment costs, or mortality. A notable association was found between a personal or family history of atopy and the eosinophilic subtype (p = 0.0181). This study underscores the relevance of CBC-based ratios in asthma phenotyping during exacerbation events.

Asthma is increasingly recognized as a heterogeneous syndrome where traditional management fails, particularly given spirometry’s limitations in assessing small airway dysfunction. This review synthesizes the transition from clinical phenotyping to deep molecular endotyping, establishing a framework for precision medicine. We highlight the insufficiency of absolute eosinophil counts, proposing eosinophil cationic protein (ECP) and eosinophil-derived neurotoxin (EDN) as superior activation metrics. Furthermore, we explore Type 2 drivers (IL-4/IL-13, periostin) and epithelial alarmins like TSLP. Beyond classical immunology, the text describes metabolic dysregulation, specifically asymmetric dimethylarginine (ADMA) in obese-asthma phenotypes where nitric oxide synthase uncoupling promotes oxidative stress. We also analyze YKL-40 and surfactant protein D (SP-D) as markers of remodeling and barrier permeability, alongside microRNAs—specifically miR-21—in corticosteroid resistance. We conclude that managing refractory asthma requires shifting from reactive symptom control to an integrated analysis of multi-omic biomarkers. Establishing this comprehensive molecular profile via specialized centers is fundamental for addressing current diagnostic limitations, selecting biological therapies, and modifying the disease trajectory through an endotype-driven strategy addressing inflammatory, metabolic, and structural pathologies.

Co-exposure to airborne pollen and fungal spores is increasingly recognized as a contributor to asthma and allergic rhinitis, especially as climatic shifts since 2020 have intensified their seasonal overlap. We systematically searched PubMed and Google Scholar for studies published between 2020 and 2025 that assessed simultaneous pollen–fungi exposure and respiratory outcomes. Screening was performed independently by two reviewers, resulting in 12 eligible studies out of 320 records. Meta-analysis was not feasible due to substantial heterogeneity in exposure definitions, taxa, outcome measures, and analytical approaches. Overall, the studies indicate that short-term co-exposure tends to worsen respiratory symptoms and increase emergency visits or asthma exacerbations, with stronger effects in children, polysensitized individuals, and urban settings. However, effect sizes varied considerably across regions and methodologies. Environmental and climatological papers provided context for seasonal overlap but did not contribute clinical data. Current evidence suggests a potential synergistic effect, though more standardized exposure metrics are needed to refine risk estimates.

Background: The increasing incidence of pediatric food allergy (FA) drives an imperative for mechanistically driven risk stratification beyond descriptive diagnostics. The current systematic review aims to assess the predictive and diagnostic value of early-life non-invasive biomarkers: cord blood IgE (CS-IgE), fecal calprotectin (FC), fecal zonulin (FZ) and secretory IgA (SIgA). Methods: In accordance with the PRISMA guidelines, we performed a systematic literature search on PubMed/MEDLINE and Scopus for English observational studies published in 2009–2025. The titles and abstracts were screened by two independent reviewers and methodological quality was assessed using the Newcastle–Ottawa Scale (NOS). Results: A total of 17 studies met the inclusion criteria. This synthesis demonstrates that CS-IgE reflects a systemic atopic predisposition rather than serving as a highly sensitive predictor for isolated FA. Fecal calprotectin was the most consistent marker of inflammatory activity in non-IgE-mediated food allergies, with median values in food allergy ranging from approximately 200 to 410 µg/g and proven useful in dietary monitoring. Fecal zonulin reflects epithelial barrier dysfunction; however, its clinical utility is limited by suboptimal assay specificity. SIgA primarily reflects mucosal immune maturation and tolerance development rather than serving as a direct diagnostic marker. Conclusions: Although CS-IgE, FC, FZ and SIgA exhibit potential in the risk stratification of early FA, their clinical implementation is complicated by methodological heterogeneity and concerns regarding analytical specificity, especially with respect to zonulin assays. We propose an integrated multi-biomarker risk stratification model as a conceptual hypothesis requiring prospective validation in future large-scale studies.

Allergic rhinitis induced by grass pollen affects 10-30% of the global population, with significant economic costs in Europe. Climate change is exacerbating the problem by increasing airborne pollen levels. Allergen-specific immunotherapy (AIT) is the only method that alters the course of the disease, providing immunological tolerance and reducing the risk of asthma. Cross-reactivity between grass species allows protection against a variety of allergens, needs that vary depending on the climate.

Background and Clinical Significance: Infective endocarditis (IE) is a serious condition with rising incidence, frequently caused by Staphylococcus aureus. However, cases involving rare congenital anomalies such as Gerbode’s defect are uncommon. Case Presentation: This report presents the first documented case of IE in a patient with a congenital Gerbode defect complicated by DRESS syndrome—a severe, drug-induced hypersensitivity reaction typically triggered by antibiotics like oxacillin. A 65-year-old woman developed infective endocarditis involving vegetations on the cardiac device lead, the tricuspid valve, and adjacent to a Gerbode defect. The diagnosis was confirmed by positive blood cultures and echocardiographic findings. She received treatment with oxacillin. Subsequently, she exhibited clinical features consistent with DRESS syndrome, including rash, eosinophilia, and multi-organ involvement. Rapid recognition and management, including corticosteroid therapy and antibiotic modification, led to clinical improvement. Conclusions: This case highlights the importance of vigilance for DRESS syndrome in prolonged antibiotic therapy for IE, especially in the context of rare congenital cardiac anomalies. In addition, guidelines are needed to optimize the diagnosis and treatment of this potentially lethal complication.