Airway microbiome has been linked to asthma heterogeneity, yet little is known about the associations between airway microbiota and type 2 (T2) asthma phenotype and severity.

The small airways, also referred to as the lung's silent zone, are closely associated with poor symptom control and more frequent asthma exacerbations. The oscillometry technique superimposes sound or airwaves onto normal tidal breathing and provides information on resistance and reactance, that is, obstacles to airflow occurring inside and outside of the bronchi. More recently, a management paradigm based on so-called "treatable traits" has been proposed to personalize and improve asthma care for individuals by proactively identifying and targeting modifiable pulmonary, extrapulmonary, and behavioral traits affecting asthma control. In this review article, we evaluate the literature on small airways dysfunction as a potential treatable trait in persistent asthma. In particular, we discuss whole- and intrabreath oscillometry and the impact of extrafine inhaled corticosteroids and systemic biologics on the peripheral airways.

Eosinophilic granulomatosis with polyangiitis (EGPA) is a rare, chronic inflammatory disease characterized by asthma and small/medium vessel vasculitis. Mepolizumab is approved for use in EGPA disease management alongside oral corticosteroids (OCS), but evidence of its real-world impact is limited.

Previous studies have defined clinical phenotypes of allergic rhinitis (AR) after allergen exposure using the time course of the total nasal symptom score (TNSS).

The use of oscillometry has significantly advanced in recent years, thanks to the availability of more robust and portable measurement devices. However, one major drawback is the variability between different devices, which leads to non-interchangeable results. This lack of standardization has prevented the establishment of widely accepted reference equations, complicating the implementation of oscillometry in clinical practice. This review aims to clarify these areas, suggesting the adoption of specific guidelines based on the context.

Food protein-induced allergic proctocolitis (FPIAP) typically develops in infancy, a critical period for taste preference and feeding skill development. Eliminating culprit foods, along with limited food options and the child's distressing symptoms, can significantly impact mothers' parenting roles. However, research on behavioral feeding problems and parenting stress in toddlers with FPIAP is lacking.

Osteonecrosis, also referred to as avascular necrosis is a disease characterized by necrosis or death of bone secondary to impairment in blood supply. The condition affects the epiphyseal ends of bones such as the femur and the humerus, but can also involve the metacarpal and metatarsal bones, the patella, the knee, vertebrae and the jaw. A plethora of inflammatory, autoimmune, hematological, thrombotic and vascular diseases can lead to osteonecrosis. Corticosteroids are intimately linked to the development of osteonecrosis. The frequent use of systemic corticosteroids in patients with asthma, eczema, nasal polyposis, sinusitis, urticaria and angioedema, or anaphylaxis make this disease of great relevance to the practicing allergist and pulmonologist. Untreated, bone necrosis leads to frustrated bone remodeling and angiogenesis, leading to subchondral fractures and collapse of the articular heads of bones, and culminating in debilitating osteoarthritis, often requiring arthroplasty. Recent studies have shed light on the molecular mechanisms underlying osteonecrosis and on the role of glucocorticoids. The gold standard test in patients suspected of having the disease is MRI scanning, with plain radiographs having a lower sensitivity and specificity. Early diagnosis and intervention are essential. The allergist should avoid the frequent use of glucocorticoids and consider early introduction of steroid-sparing alternatives for asthma or sinusitis. Smoking and alcohol ingestion need to be addressed, and the management of glucocorticoid-induced osteoporosis may be helpful. It is essential for allergists to familiarize themselves with the disease and its diagnosis and consider early referral to an orthopedic surgeon for surgical intervention.

Chronic spontaneous urticaria (CSU) is an inflammatory disorder manifesting with hives, angioedema, or both, and lasting ≥6 weeks. Although certain elements of CSU pathogenesis are well defined, others remain unclear. We discuss our current understanding of underlying CSU endotypes, distinct clinical phenotypes, and predictive biomarkers. It is increasingly recognized that CSU comprises a spectrum of different underlying pathogenic mechanisms and distinct clinical presentations. Broadly, 2 endotypes that drive CSU pathogenesis have been identified: type I (autoallergic) and type IIb (autoimmune). However, a subpopulation has evidence of both types, and some patients show evidence of neither. Multiple identified biomarkers have been associated with these endotypes or with disease features such as CSU severity and duration. There is a lack of connectivity among identified biomarkers, genetic risk loci, phenotypes, and corresponding endotypes, with each frequently considered independently of the others. These identifiable features have also been associated with response, or lack thereof, to available therapies. Future investigations should optimize the endotyping of CSU using point-of-care, noninvasive, accessible biomarkers and assess differences in response to therapy. With multiple treatments in late-stage development, establishing clearly defined CSU endotypes will facilitate future treatment decision-making and tailored treatment approaches, and will inform optimal trial design.