Thanks to improvements in asthma care and availability of new biologic treatments, a relatively novel population of adolescents and young adults (AYA) with severe asthma (SA) is growing. Transition from pediatric to adult care represents a critical phase in the management of SA. We herein describe clinical outcomes, therapeutic adjustments and disease management in a group of SA patients transitioning from the pediatric to the adult care center. This is a retrospective study in which demographic and clinical (comorbidities, baseline treatment, number of asthma attacks, spirometry, airway inflammation [fractional exhaled nitric oxide (FeNO) measurements], patient’s compliance) data of four SA patients during visits in the Pediatric center as well as after transition into the Adult Center, were retrospectively recollected. All patients transitioned at 18 years of age. Clinical parameters, spirometry and FeNO showed significant improvement following the addition of biologics to baseline asthma regimen during pediatric follow-up and the early transition phase. Several months after transition to the Adult Center, two males experienced SA exacerbations following voluntary discontinuation of the biologic treatment. Symptom control was gained after a phenotype driven re-introduction of a biologic drug in the regimen. Male patients were less compliant and independent than females in the adult setting. Transition from pediatric to adult care for patients with SA can be effectively managed with coordinated and structured transition processes. While some patients maintain stable clinical and respiratory outcomes, others risk to lose asthma control. A personalized approach supporting both patient’s independence and adherence to treatment is requested for a successful long-term management.

A high percentage of patients with severe asthma also suffer from nasal polyposis, with dupilumab, an anti-IL-4R antibody both diseases can be treated due to its role in type 2 (T2) inflammation. When these conditions are associated with eosinophilic vasculitis, they may be classified as eosinophilic granulomatosis with polyangiitis (EGPA), which can be treated with mepolizumab. This case report presents an atypical form of EGPA, following an unusual course that began with the final signs and symptoms and then proceeded backward to the prodromal stages. Our patient, indeed, a 46-year-old woman, was asymptomatic throughout her youth, with the exception of nasal polyps. Later, at the age of 34, she developed late onset asthma, which became increasingly difficult to treat, until old and previously unacknowledged evidence of vasculitis was discovered, giving a twist to our patient’s medical history and, subsequently, to the therapeutic strategy adopted to treat her. This case report aims to highlight the importance of conducting a thorough anamnesis in patients suffering from both severe asthma and nasal polyposis, taking into account the high prevalence of EGPA in this category of patients, as well as its wide range of clinical manifestations, not to mention the various available therapeutic strategies, including mepolizumab.

Telemedicine (TM) is rapidly gaining recognition as a valuable tool for accessing medical treatments globally. The article aimed to review the latest literature on the role of TM in asthma care. It has been shown that TM offers numerous advantages for patients and clinicians, facilitating an easier access to healthcare resulting in higher patient satisfaction. Telemedicine technology, pushed by the COVID-19 pandemic, has improved asthma management, notably treatment adherence. Smart inhalers, wearable gadgets, and smartphone apps allow doctors to make data-driven decisions and empower patients to manage their diseases. Real-world research shows that TM is effective and patient-friendly. Infrastructure constraints, data security issues, and long-term patient engagement must be addressed. In conclusion, a hybrid strategy combining TM and in-person visits, enabled by AI and secure digital solutions, can provide equal, efficient, and comprehensive asthma management.

Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by a compromised epidermal barrier and heightened immunoglobulin E (IgE) levels, often associated with filaggrin (FLG) gene mutations. Genetic factors like FLG mutations and environmental influences, including microbial exposure and pollutants, contribute to the disease’s progression, leading to itchy, inflamed skin. AD frequently coexists with allergic conditions, severely affecting the quality of life. The disease’s pathogenesis involves complex interactions between genetic predispositions, immune responses, and environmental triggers. Despite advances, the development of effective treatments remains challenging due to an incomplete understanding of how FLG mutations influence immune pathways and the variability in AD presentation. Current biomarkers are insufficient to fully capture disease complexity or predict therapeutic responses, highlighting the need for novel biomarkers and personalized approaches. Emerging therapies such as chimeric antigen receptor (CAR)-T cell therapy, stem cell therapy, and regenerative medicine show promise in addressing AD’s root causes. This review explores key aspects of AD pathogenesis, focusing on epidermal barrier dysfunction, immune mechanisms, and the need for innovative therapeutic strategies to improve patient outcomes.

Gelatin is extracted from beef, pork, and fish tissues. An increasing number of cases of gelatin-induced anaphylaxis are associated with α-Gal syndrome (AGS). Only a few cases of anaphylaxis to bovine gelatin (BG) without AGS (BG-woAG) have been described. We report two new cases of anaphylaxis to BG-woAG, highlight the characteristics of this entity, and propose a procedure in cases of suspected anaphylaxis to BG. We selected articles on gelatin allergy between 1987 and 2024. Results: we report two new cases of severe anaphylaxis BG-woAG. Diagnosis was established using skin tests (ST), IgE, and basophil activation tests (BAT). We confirm the existence of allergies to BG-woAG. The main characteristic of these allergies seems to be the presence of BG IgE which differentiates them from AGS-related allergies. These initial data need to be confirmed by larger case series. We propose a diagnostic algorithm for better patient management. To confirm the diagnosis, ST and IgE to BG and α-Gal should be performed. The role of BAT to Gelofusine^® in the diagnostic strategy remains to be defined.

In a previous study, we conducted an in vitro comparison of two sublingual allergy immunotherapy products, namely, house dust mite (HDM) Staloral 300 IR/mL produced by Stallergenes Greer, and HDM Osiris 300 IR/mL produced by ALK-Abelló. Although both products are labeled with the same unit, that is, the index of reactivity (IR), the definition of this unit is different depending on the product. This resulted in HDM Staloral 300 IR/mL displaying a higher total allergenic activity (TAA) and higher contents in major allergens and proteins. The aim of this study was to extend the comparison to cat sublingual extracts, that is, to cat Staloral 300 IR/mL from Stallergenes Greer and cat Osiris 300 IR/mL from ALK-Abelló. While both cat allergen extracts were qualitatively similar, in that they exhibited similar protein and allergen profiles, cat Staloral 300 IR/mL displayed a 2 times higher TAA than cat Osiris 300 IR/mL (according to an in-house method) and contained 1.6 time more proteins, 1.3 and 1.9 time more major allergens Fel d 1 and Fel d 4, respectively. No conclusions on clinical efficacy or safety can be drawn from these data.

Glucagon-like peptide-1 (GLP-1) is a hormone that regulates blood glucose levels and is produced by the enteroendocrine glands in the large and small intestines in response to the consumption of foods that contain carbohydrates, fats, and proteins. When GLP-1 is secreted, it acts on the pancreas to increase insulin production and secretion, while decreasing pancreatic glucagon secretion in order to lower serum glucose. However, GLP-1 also regulates metabolism through the gut-brain axis. While GLP-1 is primarily produced in the gut and released into the bloodstream, small quantities of it can also be synthesized in distinct areas of neurons located in the hindbrain. Recent studies have proposed that GLP-1 receptor (GLP-1R) agonists (GLP-1RAs) may protect against neuroinflammatory diseases. GLP-1RAs may also be a therapeutic target for asthma as animal models show that these drugs reduce allergen-induced airway inflammation, as the GLP-1R is expressed on lung epithelial and endothelial cells. There is a notable association between insulin resistance and the onset of asthma, particularly among obese people, with this association suggesting that metabolic dysfunction may play a role in asthma development. There is also evidence that there may be a link between asthma pathobiology and neuroinflammation, suggesting that GLP-1 and its analogs may regulate neuroinflammatory pathways that contribute to asthma pathogenesis. Interest is growing, though research remains limited, in how inflammation in the nervous system and lung might be linked. This review will explore how GLP-1R signaling could inhibit interdependent inflammation in both the lung and nervous system. This review will first focus on the inflammation that is known to exist in asthma, then pivot to the current state of neural regulation of asthma, and finally speculate on how GLP-1RA signaling could inhibit both neural and lung inflammation in asthma treatment.

Atopic dermatitis (AD) is a prevalent chronic inflammatory skin disorder affecting millions worldwide, with significant variations in clinical presentation influenced by socioeconomic, racial, and environmental factors. This review explores the current understanding of AD pathophysiology, emphasizing immune dysregulation, epithelial barrier dysfunction, and the role of cytokines, particularly interleukin (IL)-4 and IL-13, in disease progression. Safety and efficacy concerns limit traditional corticosteroids, phototherapy, and systemic immunosuppressants, prompting interest in innovative therapies. New biologic agents, including monoclonal antibodies (mAbs) and Janus kinase (JAK) inhibitors (JAKis), target specific immune pathways, promising outcomes in moderate-to-severe AD cases. Biologics like dupilumab and emerging JAKis have shown substantial efficacy and safety in clinical trials, with notable reductions in inflammation and pruritus. However, these advancements present challenges, including hypersensitivity risks and the high costs of biologics, underscoring the need for further research on long-term safety and accessibility. The shift toward precision medicine in AD management marks a significant evolution, with future approaches likely to integrate targeted therapies alongside multidisciplinary care to enhance patient outcomes and quality of life (QoL).

Severe pediatric asthma is a very challenging type of asthma for both physicians and patients. Precision medicine in severe pediatric asthma has undergone important developments in recent years. This therapeutic approach requires an adequate diagnosis and clinical phenotyping of patients and is useful for predicting the prognosis and response to treatment in this type of patient. This article summarizes the scientific information of the last five years in the diagnosis of severe pediatric asthma, focusing on topics such as genetic markers, biomarkers, lung function, radiological techniques, and bronchoscopy.

This review delves into the complex role of 12/15-lipoxygenase (12/15-LOX) in asthma pathogenesis, focusing on its contributions to mitochondrial dysfunction, oxidative stress, epithelial injury, and airway remodeling. We provide new insights into potential therapeutic strategies aimed at improving asthma management. Additionally, we examine the pro-inflammatory functions of interleukin-4 (IL-4) and its regulatory mechanisms that upregulate 12/15-LOX, leading to increased oxidative stress and airway remodeling. Key interventions such as vitamin E, esculetin, and baicalein are highlighted for their potential to inhibit 12/15-LOX activity, reduce oxidative stress, and restore mitochondrial function. Vitamin E suppresses IL-4 transcription, reducing 12/15-LOX expression and its inflammatory metabolites, while esculetin and baicalein directly inhibit 12/15-LOX, mitigating inflammation and oxidative damage. These antioxidants also promote mitochondrial biogenesis, protect mitochondrial DNA, and enhance respiratory efficiency, contributing to improved cellular metabolism and reduced apoptosis. This comprehensive approach emphasizes the therapeutic potential of targeting 12/15-LOX pathways to alleviate asthma symptoms and improve patient outcomes, paving the way for novel treatment strategies that significantly enhance asthma therapy.

Bronchiectasis is a heterogeneous chronic lung disease, characterised by irreversible dilatation of the airways and attributed to a wide spectrum of other underlying conditions, usually underdiagnosed and inadequately treated with a high burden for both the patients and the healthcare system. The way bronchiectasis is viewed by physicians has drastically changed over the last decades, with the topic of eosinophilia in the context of the disease being one of the substantially highlighted. Eosinophilia was traditionally considered as a means for distinguishing bronchiectasis from asthma, whereas bronchiectasis was primarily associated with neutrophilic inflammation. However, eosinophilic bronchiectasis is nowadays identified as a distinct disease endotype and is associated with a specific clinical course and response to treatment. Further research is needed to better characterise this endotype and improve its personalised investigation and management in daily clinical practice.

Asthma is a complex inflammatory airway disease affecting a significant global population, spanning from childhood through adulthood. Despite advances in treatment modalities, a significant subset of patients, approximately 10%, grapple with severe asthma, characterized by increased healthcare utilization and diminished quality of life. Tezepelumab, a monoclonal antibody targeting thymic stromal lymphopoietin (TSLP), offers promising therapeutic potential. TSLP is a protein released by a variety of cells, with a predominance of epithelial cells, in reaction to plenty of stimuli, such examples as viruses, aeroallergens, and others. Its action is upstream and pertains to initiating numerous subsequent innate and adaptive immune reactions, contributing to the continuation of asthma pathophysiological processes. Tezepelumab’s unique efficacy spans diverse severe asthma phenotypes, significantly reducing exacerbation rates across eosinophilic and non-eosinophilic subtypes. Its favorable safety profile and clinically meaningful improvements in asthma control, accompanied by reductions in cytokine levels and baseline biomarkers, underscore its broad impact on asthma inflammation. Its efficacy, irrespective of type 2 (T2) endotype, reinforces the idea that TSLP blockade broadly inhibits pathways crucial to asthma pathophysiology, rather than narrowly focusing on individual downstream factors, as previous biological treatments have. This review discusses the rationale for TSLP blockade and the efficacy of tezepelumab in severe asthma using data from key trials.

Chronic rhinosinusitis (CRS) is an inflammatory disorder of the paranasal sinuses and the nasal cavity lasting longer than 12 weeks. This disease is a common clinical syndrome with significant monetary burden due to the high costs of medical visits, diagnostic tests, medications, and surgical therapies. CRS without nasal polyposis (CRSsNP) is the most common subtype of CRS, accounting for about 70% of all patients. Other subtypes include CRS with nasal polyposis (CRSwNP) and allergic fungal rhinosinusitis (AFRS). CRSwNP has the worldwide prevalence of 2% to 4% and is often accompanied by type 2 inflammation and asthma as a comorbid condition. Pediatric chronic sinusitis is distinct from adult chronic sinusitis and is currently considered an infectious process, characterized by persistent inflammation representing an exaggerated immune response to an external stimulus. The medical and surgical management of CRS has been remarkably modified in the past two decades. The aim of this study was to present an update on CRS based on the recent years’ literature.