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.

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).

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.

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.

Atopic dermatitis (AD) represents the most common inflammatory skin disease with a highly intricated immune fingerprint. Until recently, AD management mostly relied on topical corticosteroids, calcineurin inhibitors, and systemic immunosuppressants, with a range of safety and tolerability concerns including toxicity, drug interactions, and contraindications. With the onset of biologics, safer and more targeted therapeutics have become available, displaying various degrees of success in treating AD, but not yet able to meet all the needs of AD patients. Some of the challenges encountered included variability of responses among patients, long-term safety, and limited access due to prohibitive costs. As the pathophysiology of AD has been increasingly understood within the last years, new approaches are explored, leading to an unprecedented diversification of therapeutic options to address these hurdles. This review highlights current immunotherapeutic strategies developed towards AD, whether already in the clinical pipeline or still in preclinical exploration.

Asthma is a common chronic inflammatory disease of the airways that affects more than 330 million people globally. Severe asthma, despite being 5–10% of the total asthmatic population presents significant morbidity and high cost due to health care utilization. The management of severe asthma has dramatically changed with the use of biologics. However, biologics have been approved only for patients with severe asthma with type-2 mediated inflammation. Eosinophils are central in the T2 inflammatory process in asthma and this stands true for the severe form of the disease as well. In this review, we discuss basic insights into the pathogenesis of severe asthma related to eosinophilic inflammation and the pivotal role of T2 cytokines which have also become along with eosinophils the target of biologics. Novel biologics such as tezepelumab have demonstrated efficacy regardless of the blood eosinophil count and have shown promise for T2 low asthma, although to a lesser degree.

A granulomatous vasculitis of the medium and large vessels, giant cell arteritis (GCA) is a persistent, idiopathic condition. The overlapping phenotypes of this condition include conventional cranial arteritis and extra-cranial GCA, also known as large-vessel GCA. Vascular problems linked with considerable vessel involvement may partly be caused by delayed diagnosis, emphasizing the necessity of early detection and the fast beginning of appropriate therapy. The cornerstone of treatment for GCA is glucocorticoids, but using them for an extended period has numerous, often severe, side effects. We aim to explore the most recent literature on GCA therapies to investigate the current and potential therapeutic options for induction and maintaining treatment in GCA. By now, only tocilizumab is approved for GCA treatment, but several other biological drugs may be efficient and safe for GCA patients, like abatacept, baricitinib and upadacitinib, mavrilimumab, secukinumab, ustekinumab, and anakinra.

Allergic and immunologic skin diseases are becoming increasingly common and this requires clinicians to be able to recognize and diagnose them. A joint meeting (GET TOGETHER 2022) of the Italian Society of Allergy, Asthma and Clinical Immunology (SIAAIC) and the Italian Society of Allergological, Occupational and Environmental Dermatology (SIDAPA) aimed to review the current knowledge on the differential diagnosis of contact dermatitis, atopic dermatitis, hereditary angioedema, urticaria, and cutaneous mastocytosis. The most important aspects to take into consideration when faced with a new cutaneous manifestation are the clinical features of the lesions, their distribution, age of onset, and comorbidities/aggravating factors. The document does not aim to provide an exhaustive and comprehensive description of all allergic and immunologic skin diseases. Instead, it should be a reference tool for the clinician who is faced with the onset of a new skin manifestation and its differential diagnosis.

Atopic dermatitis (AD) is a chronic inflammatory skin disease that primarily affects the barrier function of the skin in patients. The condition has been documented to cause xerosis in patients from birth onwards. In order to protect the skin barrier in AD, it is of the utmost importance to moisturize the skin. Moisturizers and emollients play a pivotal role in the prevention and treatment of AD. Concordantly, the use of moisturizers and emollients can facilitate the reduction in the necessity for the application of topical treatments such as corticosteroids. An understanding of the use of moisturizers and emollients, in conjunction with an appreciation of the pathophysiology of the skin barrier, will prove invaluable in the treatment of AD.

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.

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.

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.

Asthma is a prevalent chronic respiratory condition in children, often exacerbated by allergic reactions, with house dust mites (HDMs) being a significant trigger. Traditional asthma management primarily involves inhaled corticosteroids and bronchodilators, which do not address the underlying allergic mechanisms. Allergen immunotherapy, including subcutaneous and sublingual immunotherapy (SLIT), has emerged as a strategy to induce immune tolerance to allergens. This review evaluates the efficacy of HDM immunotherapy in paediatric asthma, focusing on reductions in asthma exacerbations, improvements in lung function, decreases in medication use, and enhancements in quality of life (QoL). The review highlights that both subcutaneous immunotherapy (SCIT) and SLIT significantly reduce asthma exacerbations in children, with SCIT showing superior efficacy in lung function improvement. Combination therapies, particularly SCIT with biologics, demonstrate enhanced outcomes, including exacerbations and medication use reductions. SCIT has also been shown to improve lung function more effectively than SLIT, particularly in children with high baseline levels of HDM-specific IgE. In terms of safety, both SCIT and SLIT are generally well-tolerated, though SCIT is associated with more localized and systemic reactions, which can be mitigated by combination with biologics. Furthermore, HDM immunotherapy significantly enhances the QoL in paediatric patients by reducing asthma symptoms and improving sleep, leading to long-lasting benefits. Despite these positive outcomes, there remain gaps in knowledge, particularly regarding the optimal duration of therapy and long-term effects post-treatment. Future research should standardize treatment protocols, explore personalized approaches, and investigate the long-term sustainability of treatment benefits to fully optimize the use of HDM immunotherapy in paediatric asthma.

In the context of severe asthma, one of the causes of poor disease control has been identified in mucus plugs, which are real obstacles to the physiological flow of air in the bronchi. This clinical case will present the efficacy of dupilumab, as measured by respiratory function and chest computed tomography (CT) imaging, in reducing mucus plugs with consequent improvement in symptoms and function.