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.

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).

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.