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Non-steroidal anti-inflammatory drug (NSAID)-exacerbated respiratory disease (N-ERD) is a respiratory illness characterized by chronic eosinophilic airway inflammation. Although a typical clinical history of asthma, chronic rhinosinusitis with nasal polyps (CRSwNP), and respiratory reactions to NSAIDs may strongly suggest the diagnosis, history alone is often unreliable due to NSAID avoidance, atypical reactions, or incomplete symptom recognition. In this context, aspirin provocation tests remain the diagnostic gold standard for confirming N-ERD. Beyond diagnostic confirmation, aspirin provocation testing provides critical insights into disease heterogeneity and phenotyping. Different challenge routes—nasal, bronchial, and oral—allow assessment of organ-specific sensitivity and inflammatory dominance. Nasal aspirin provocation primarily reflects upper airway involvement and is particularly informative in patients with severe CRSwNP, whereas inhalational lysine-aspirin challenges highlight lower-airway bronchial hyperresponsiveness. Oral aspirin provocation, through systemic exposure, captures the full spectrum of respiratory and extra-respiratory responses and therefore best reflects global disease severity. The pattern, timing, and intensity of reactions observed during provocation testing contribute to the identification of clinically relevant N-ERD subphenotypes, such as upper-airway-dominant disease, bronchial-predominant disease, or blended reactions involving both compartments. These phenotypic distinctions have direct therapeutic implications, influencing the selection of targeted treatments, including aspirin desensitization, biologic therapies, or surgical interventions. Moreover, provocation testing remains essential prior to aspirin desensitization to ensure both diagnostic accuracy and patient safety. Aspirin provocation tests are not merely confirmatory tools but represent a cornerstone of precision-based evaluation of N-ERD, enabling refined phenotyping, risk stratification, and individualized treatment planning in this complex and heterogeneous disease.
Non-steroidal anti-inflammatory drug (NSAID)-exacerbated respiratory disease (N-ERD) is a respiratory illness characterized by chronic eosinophilic airway inflammation. Although a typical clinical history of asthma, chronic rhinosinusitis with nasal polyps (CRSwNP), and respiratory reactions to NSAIDs may strongly suggest the diagnosis, history alone is often unreliable due to NSAID avoidance, atypical reactions, or incomplete symptom recognition. In this context, aspirin provocation tests remain the diagnostic gold standard for confirming N-ERD. Beyond diagnostic confirmation, aspirin provocation testing provides critical insights into disease heterogeneity and phenotyping. Different challenge routes—nasal, bronchial, and oral—allow assessment of organ-specific sensitivity and inflammatory dominance. Nasal aspirin provocation primarily reflects upper airway involvement and is particularly informative in patients with severe CRSwNP, whereas inhalational lysine-aspirin challenges highlight lower-airway bronchial hyperresponsiveness. Oral aspirin provocation, through systemic exposure, captures the full spectrum of respiratory and extra-respiratory responses and therefore best reflects global disease severity. The pattern, timing, and intensity of reactions observed during provocation testing contribute to the identification of clinically relevant N-ERD subphenotypes, such as upper-airway-dominant disease, bronchial-predominant disease, or blended reactions involving both compartments. These phenotypic distinctions have direct therapeutic implications, influencing the selection of targeted treatments, including aspirin desensitization, biologic therapies, or surgical interventions. Moreover, provocation testing remains essential prior to aspirin desensitization to ensure both diagnostic accuracy and patient safety. Aspirin provocation tests are not merely confirmatory tools but represent a cornerstone of precision-based evaluation of N-ERD, enabling refined phenotyping, risk stratification, and individualized treatment planning in this complex and heterogeneous disease.
DOI: https://doi.org/10.37349/eaa.2026.1009121
This article belongs to the special issue Update on Chronic Rhinosinusitis
Occupational allergens are an important cause of diseases emerging in the workplace, both indoor and outdoor, causing conditions such as allergic asthma, dermatitis, and rhinitis. Numerous national and international institutions focus on sensitizing agents able to induce allergies in workplaces, which are also considered by the International Classification of Diseases (ICD)-11, underlining their increasing worldwide importance. There is thus the need to develop and implement new, multidisciplinary approaches to study and monitor these agents, taking into account different sources of exposure, environmental concentrations, co-factors of exposure, and individual susceptibility. This includes the integration between traditional and innovative methodologies applied to environmental and biological matrices, as well as the use of “omic” techniques. In this picture, information, training, and communication emerge as fundamental for workers. This kind of approach will permit us to attain a better management of exposure to allergens in the workplace, improving the well-being of workers worldwide.
Occupational allergens are an important cause of diseases emerging in the workplace, both indoor and outdoor, causing conditions such as allergic asthma, dermatitis, and rhinitis. Numerous national and international institutions focus on sensitizing agents able to induce allergies in workplaces, which are also considered by the International Classification of Diseases (ICD)-11, underlining their increasing worldwide importance. There is thus the need to develop and implement new, multidisciplinary approaches to study and monitor these agents, taking into account different sources of exposure, environmental concentrations, co-factors of exposure, and individual susceptibility. This includes the integration between traditional and innovative methodologies applied to environmental and biological matrices, as well as the use of “omic” techniques. In this picture, information, training, and communication emerge as fundamental for workers. This kind of approach will permit us to attain a better management of exposure to allergens in the workplace, improving the well-being of workers worldwide.
DOI: https://doi.org/10.37349/eaa.2026.1009120
This article belongs to the special issue Environment, Infectious Diseases, and Allergy
Climate change is reshaping the aeroallergen landscape, with rising temperatures, elevated CO2, shifting precipitation, and land-use change extending pollen seasons, increasing pollen loads and allergenicity, and expanding the geographic range of allergenic plants. These changes are accompanied by escalating air pollution from fossil fuel combustion and wildfires that act as an adjuvant with co-exposure with allergen exacerbate allergic airway disease. Vulnerable populations—particularly those in socioeconomically disadvantaged and marginalized communities in the US—experience disproportionate exposure to pollutants and allergens due to structural inequities that result in some populations being exposed to more environmental hazards than other groups. Climate-amplified aeroallergen exposure and air pollution are associated with higher sensitization, symptom burden, exacerbations, and healthcare use. Structural inequities magnify exposures to allergens and air pollution, while also influencing the social environment through concentration of poverty and diminished access to resources. This review synthesizes evidence linking climate change-related effects on aeroallergens and air pollution with allergic disease risk and the modification of this relationship by social vulnerability, with a focus on Europe and North America. We also highlight established and emerging strategies to mitigate the effects of climate change on allergic disease prevalence and morbidity, including anticipatory guidance, digital forecasting, community adaptation measures, and local, regional, and national policies that promote responsible land use, healthy housing, and equity-focused public health initiatives.
Climate change is reshaping the aeroallergen landscape, with rising temperatures, elevated CO2, shifting precipitation, and land-use change extending pollen seasons, increasing pollen loads and allergenicity, and expanding the geographic range of allergenic plants. These changes are accompanied by escalating air pollution from fossil fuel combustion and wildfires that act as an adjuvant with co-exposure with allergen exacerbate allergic airway disease. Vulnerable populations—particularly those in socioeconomically disadvantaged and marginalized communities in the US—experience disproportionate exposure to pollutants and allergens due to structural inequities that result in some populations being exposed to more environmental hazards than other groups. Climate-amplified aeroallergen exposure and air pollution are associated with higher sensitization, symptom burden, exacerbations, and healthcare use. Structural inequities magnify exposures to allergens and air pollution, while also influencing the social environment through concentration of poverty and diminished access to resources. This review synthesizes evidence linking climate change-related effects on aeroallergens and air pollution with allergic disease risk and the modification of this relationship by social vulnerability, with a focus on Europe and North America. We also highlight established and emerging strategies to mitigate the effects of climate change on allergic disease prevalence and morbidity, including anticipatory guidance, digital forecasting, community adaptation measures, and local, regional, and national policies that promote responsible land use, healthy housing, and equity-focused public health initiatives.
DOI: https://doi.org/10.37349/eaa.2026.1009119
This article belongs to the special issue Climate Change, Allergy, and Immunotherapy
The composition and biophysical characteristics of the plasma membrane are pivotal in regulating mast cell immune functions by influencing receptor distribution, activation, and intracellular signaling pathways. This article highlights the impact of plasma membrane components, such as cholesterol and lipid rafts, on the function of the Mas-related G protein-coupled receptor X2 (MRGPRX2), a key mediator of IgE-independent mast cell activation and pseudoallergic reactions. We discuss how variations in membrane fluidity, lipid composition, and microdomain organization influence MRGPRX2 conformational dynamics, ligand accessibility, and downstream signaling efficiency. These membrane-driven effects may help explain the heterogeneity of mast cell responsiveness across tissues and disease states. Integrating insights from structural biology, biophysics, and clinical immunology emphasizes that plasma membrane composition and dynamics regulate MRGPRX2-mediated signaling, positioning the membrane environment as a promising therapeutic target for modulating mast-cell hyperreactivity. By outlining this conceptual framework, we introduce a unifying hypothesis that membrane-driven regulation is a critical, yet underrecognized, determinant of MRGPRX2 responsiveness in different tissues and disease states.
The composition and biophysical characteristics of the plasma membrane are pivotal in regulating mast cell immune functions by influencing receptor distribution, activation, and intracellular signaling pathways. This article highlights the impact of plasma membrane components, such as cholesterol and lipid rafts, on the function of the Mas-related G protein-coupled receptor X2 (MRGPRX2), a key mediator of IgE-independent mast cell activation and pseudoallergic reactions. We discuss how variations in membrane fluidity, lipid composition, and microdomain organization influence MRGPRX2 conformational dynamics, ligand accessibility, and downstream signaling efficiency. These membrane-driven effects may help explain the heterogeneity of mast cell responsiveness across tissues and disease states. Integrating insights from structural biology, biophysics, and clinical immunology emphasizes that plasma membrane composition and dynamics regulate MRGPRX2-mediated signaling, positioning the membrane environment as a promising therapeutic target for modulating mast-cell hyperreactivity. By outlining this conceptual framework, we introduce a unifying hypothesis that membrane-driven regulation is a critical, yet underrecognized, determinant of MRGPRX2 responsiveness in different tissues and disease states.
DOI: https://doi.org/10.37349/eaa.2026.1009118
This article belongs to the special issue Bridging Experimental and Translational Allergology
APPaRENT2 was a multi-country, cross-sectional, online survey of patients with asthma and physicians conducted in five countries (Argentina, Brazil, France, Mexico, and Italy), aimed at assessing physicians’ and patients’ preferred treatment strategies and goals. Education level, age, and place of residence differed between European and Latin American patients; furthermore, most Italian doctors worked within the Public Health Service. For the purpose of identifying the critical issues in the management of asthma in Italy, the data were analysed in greater detail, comparing those collected in Italy with those from Latin American countries and those provided by Italian patients and doctors. The data are reported as frequencies or means. The differences found in comparing data were not analysed for statistical significance, given the absence of any a priori hypothesis in the original paper. The Italian results were consistently within the range of the Latin American countries’ results. In Italy, despite the physicians’ prioritization of symptom control, many patients had poor asthma control but gave a surprisingly optimistic evaluation of their disease, given the high frequency of symptoms and limitations in everyday life. Physicians and patients had quite different evaluations of symptoms and outcomes of asthma. Finally, the combination of ICS/LABA with SABA as needed was the preferred treatment compared with the maintenance and reliever therapy (MART) strategy, suggested as preferential in the Global Initiative for Asthma (GINA) document. In conclusion, the absence of shared assessments and expectations between doctors and patients appears to be the primary issue to address in order to improve asthma treatment in Italy.
APPaRENT2 was a multi-country, cross-sectional, online survey of patients with asthma and physicians conducted in five countries (Argentina, Brazil, France, Mexico, and Italy), aimed at assessing physicians’ and patients’ preferred treatment strategies and goals. Education level, age, and place of residence differed between European and Latin American patients; furthermore, most Italian doctors worked within the Public Health Service. For the purpose of identifying the critical issues in the management of asthma in Italy, the data were analysed in greater detail, comparing those collected in Italy with those from Latin American countries and those provided by Italian patients and doctors. The data are reported as frequencies or means. The differences found in comparing data were not analysed for statistical significance, given the absence of any a priori hypothesis in the original paper. The Italian results were consistently within the range of the Latin American countries’ results. In Italy, despite the physicians’ prioritization of symptom control, many patients had poor asthma control but gave a surprisingly optimistic evaluation of their disease, given the high frequency of symptoms and limitations in everyday life. Physicians and patients had quite different evaluations of symptoms and outcomes of asthma. Finally, the combination of ICS/LABA with SABA as needed was the preferred treatment compared with the maintenance and reliever therapy (MART) strategy, suggested as preferential in the Global Initiative for Asthma (GINA) document. In conclusion, the absence of shared assessments and expectations between doctors and patients appears to be the primary issue to address in order to improve asthma treatment in Italy.
DOI: https://doi.org/10.37349/eaa.2026.1009117
Allergic conjunctivitis (AC) is an inflammatory disorder of the ocular surface caused by allergic reactions to environmental substances. It presents with symptoms such as itching, redness of the eye, excessive tearing, and swelling/irritation in the eyes and eyelids. While many AC episodes occur on their own and go away, some forms of this disease are present in a chronic fashion or have the potential to cause serious loss of vision. In recent years, AC has been viewed as primarily an episodic irritative condition to a mucosal inflammatory condition in which the ocular surface provides an environment for the initiation and perpetuation of local immune responses. The molecular basis of AC represents a phase-linked inflammatory cascade: an immediate (minutes) mediator-driven response followed by a late (6–12 hours) cytokine/chemokine-driven cellular recruitment phase that can sustain symptoms and, in severe phenotypes, contribute to tissue remodeling. The initial response is due to the activation of mast cells via IgE-dependent pathways, producing the early phase response. The sustained response seen in the late phase of the disease is mediated by the action of lipid mediators and cytokines/chemokines involved in the recruitment of eosinophils and Th2-associated leukocytes. This narrative review synthesizes evidence on epithelial “alarmins” (TSLP, IL-33, IL-25) as upstream signals that may amplify type-2 inflammation in a phenotype-dependent manner, particularly in more severe or chronic disease, alongside established IgE/mast-cell biology. Further, we discuss neuroimmune mechanisms implicated in histamine-independent itch and symptom persistence, while noting that their clinical contribution likely varies across AC phenotypes. Finally, we will discuss how the mechanistic pathways relate to current limitations and to developing new therapeutic approaches.
Allergic conjunctivitis (AC) is an inflammatory disorder of the ocular surface caused by allergic reactions to environmental substances. It presents with symptoms such as itching, redness of the eye, excessive tearing, and swelling/irritation in the eyes and eyelids. While many AC episodes occur on their own and go away, some forms of this disease are present in a chronic fashion or have the potential to cause serious loss of vision. In recent years, AC has been viewed as primarily an episodic irritative condition to a mucosal inflammatory condition in which the ocular surface provides an environment for the initiation and perpetuation of local immune responses. The molecular basis of AC represents a phase-linked inflammatory cascade: an immediate (minutes) mediator-driven response followed by a late (6–12 hours) cytokine/chemokine-driven cellular recruitment phase that can sustain symptoms and, in severe phenotypes, contribute to tissue remodeling. The initial response is due to the activation of mast cells via IgE-dependent pathways, producing the early phase response. The sustained response seen in the late phase of the disease is mediated by the action of lipid mediators and cytokines/chemokines involved in the recruitment of eosinophils and Th2-associated leukocytes. This narrative review synthesizes evidence on epithelial “alarmins” (TSLP, IL-33, IL-25) as upstream signals that may amplify type-2 inflammation in a phenotype-dependent manner, particularly in more severe or chronic disease, alongside established IgE/mast-cell biology. Further, we discuss neuroimmune mechanisms implicated in histamine-independent itch and symptom persistence, while noting that their clinical contribution likely varies across AC phenotypes. Finally, we will discuss how the mechanistic pathways relate to current limitations and to developing new therapeutic approaches.
DOI: https://doi.org/10.37349/eaa.2026.1009116
This article belongs to the special issue Innate Immune Mechanisms in Allergic Diseases
Background:
Adolescence is a vulnerable and constantly changing stage of life. Experiencing chronic illnesses such as bronchial asthma during this period can lead to heightened physical, psychological, and social problems in addition to the wide scope of challenges that coincide with the stage. The objective of this research was to identify risk and protective factors for mental health disorders, as well as the preventive and treatment strategies recommended to preserve mental health in adolescents with asthma (AA).
Methods:
A search was conducted in Medline, Web of Science, EBSCO Host, PsycINFO, ScienceDirect, and Scopus for articles published in English between 2020 and 2025 using the following search terms: i) asthma in adolescents and ii) psychosocial or emotional problems. The items were checked using the PRISMA checklist.
Results:
Thirty-eight articles were found: eight on mental health problems, fourteen on biopsychosocial risk factors, ten on biopsychosocial protection factors, and six on biopsychosocial interventions in AA.
Discussion:
Internalizing problems such as anxiety and depression, or externalizing problems such as attention deficit hyperactivity disorder (ADHD) or conduct disorders, are prevalent in AA. Several biopsychosocial risk factors, both individual and familial, have been identified as being related to mental health problems in AA. Protective biopsychosocial factors have also been found in AA, such as certain personal characteristics, family types or structures, friends, or schoolmates. Prevention or treatment strategies for mental health problems in AA should consider a personalized approach, taking into account the family system, friendships, and the school environment.
Background:
Adolescence is a vulnerable and constantly changing stage of life. Experiencing chronic illnesses such as bronchial asthma during this period can lead to heightened physical, psychological, and social problems in addition to the wide scope of challenges that coincide with the stage. The objective of this research was to identify risk and protective factors for mental health disorders, as well as the preventive and treatment strategies recommended to preserve mental health in adolescents with asthma (AA).
Methods:
A search was conducted in Medline, Web of Science, EBSCO Host, PsycINFO, ScienceDirect, and Scopus for articles published in English between 2020 and 2025 using the following search terms: i) asthma in adolescents and ii) psychosocial or emotional problems. The items were checked using the PRISMA checklist.
Results:
Thirty-eight articles were found: eight on mental health problems, fourteen on biopsychosocial risk factors, ten on biopsychosocial protection factors, and six on biopsychosocial interventions in AA.
Discussion:
Internalizing problems such as anxiety and depression, or externalizing problems such as attention deficit hyperactivity disorder (ADHD) or conduct disorders, are prevalent in AA. Several biopsychosocial risk factors, both individual and familial, have been identified as being related to mental health problems in AA. Protective biopsychosocial factors have also been found in AA, such as certain personal characteristics, family types or structures, friends, or schoolmates. Prevention or treatment strategies for mental health problems in AA should consider a personalized approach, taking into account the family system, friendships, and the school environment.
DOI: https://doi.org/10.37349/eaa.2026.1009115
This article belongs to the special issue Asthma and its Relationship with Psychological and Psychopathological Factors
Aim:
To describe the first major epidemic thunderstorm asthma (ETSA) event detected in France in June 2023.
Methods:
Data on local meteorology, visits to the emergency room (ER) for asthma and hospitalization after a visit, aerobiological composition of the atmosphere (pollens and spores), phenological information on the flowering of grasses, and regional air pollution were collected, aggregated, and analyzed.
Results:
The ETSA was centered on the Paris region. An excess of 1,900 emergency visits for asthma was recorded over the period 10, 11, and 12 June. The people most affected were men aged 14 to 44. The hospitalization rate following a visit to the ER for asthma increased to 13%. ER visits for asthma began at around 6 pm on 10 June, just after an intense gust (15 m/s) triggering a PM10 resuspension episode, and peaked at around 10 pm on 11 June. Concentrations of mold spores (Cladosporium and Ascosporium) rose sharply during the night of 10–11 June, at the same time as the intake peak. The ETSA occurred during the grass and Urticaceae pollen season, with pollen concentrations lower (< 100 pollen grains/m3) compared to the days preceding the event (> 200 pollen grains/m3). A fraction of the pollen was observed without cytoplasm, but there was no apparent link with the ETSA. Phenological observations in the Paris pollinarium showed that the ETSA coincided with the start of the Lolium perenne (ryegrass) pollen season.
Conclusions:
Although the data collected did not allow the identification of a single cause for the occurrence of the ETSA, they pointed to multifactorial causes such as the occurrence of an ozone pollution episode, strong winds before the storm, an episode of resuspension of PM10 particles, the presence of broken pollen, and the significant increase in mold spores just after the stormy episode.
Aim:
To describe the first major epidemic thunderstorm asthma (ETSA) event detected in France in June 2023.
Methods:
Data on local meteorology, visits to the emergency room (ER) for asthma and hospitalization after a visit, aerobiological composition of the atmosphere (pollens and spores), phenological information on the flowering of grasses, and regional air pollution were collected, aggregated, and analyzed.
Results:
The ETSA was centered on the Paris region. An excess of 1,900 emergency visits for asthma was recorded over the period 10, 11, and 12 June. The people most affected were men aged 14 to 44. The hospitalization rate following a visit to the ER for asthma increased to 13%. ER visits for asthma began at around 6 pm on 10 June, just after an intense gust (15 m/s) triggering a PM10 resuspension episode, and peaked at around 10 pm on 11 June. Concentrations of mold spores (Cladosporium and Ascosporium) rose sharply during the night of 10–11 June, at the same time as the intake peak. The ETSA occurred during the grass and Urticaceae pollen season, with pollen concentrations lower (< 100 pollen grains/m3) compared to the days preceding the event (> 200 pollen grains/m3). A fraction of the pollen was observed without cytoplasm, but there was no apparent link with the ETSA. Phenological observations in the Paris pollinarium showed that the ETSA coincided with the start of the Lolium perenne (ryegrass) pollen season.
Conclusions:
Although the data collected did not allow the identification of a single cause for the occurrence of the ETSA, they pointed to multifactorial causes such as the occurrence of an ozone pollution episode, strong winds before the storm, an episode of resuspension of PM10 particles, the presence of broken pollen, and the significant increase in mold spores just after the stormy episode.
DOI: https://doi.org/10.37349/eaa.2026.1009114
This article belongs to the special issue Climate Change, Allergy, and Immunotherapy
This review describes the eosinophil journey through the various physiological and pathophysiological phases, from production, maturation, and activation by chemokines and cytokines [especially eotaxin, interleukin (IL)-5, IL-3, and granulocyte-macrophage colony-stimulating factor (GM-CSF)], to interaction with the innate and adaptive immune system and tissue homing. Excessive production and activation of eosinophils lead to the release of granule proteins, such as major basic protein, eosinophil cationic protein, eosinophil peroxidase, and others, resulting in inflammation, cell cytotoxicity, and oxidative stress. The pathogenesis, clinical features, diagnostic processes, and the latest therapeutic approaches to the resulting diseases—which affect the upper and lower airways, gastrointestinal tract, skin, myocardium, and may occur systemically—are discussed.
This review describes the eosinophil journey through the various physiological and pathophysiological phases, from production, maturation, and activation by chemokines and cytokines [especially eotaxin, interleukin (IL)-5, IL-3, and granulocyte-macrophage colony-stimulating factor (GM-CSF)], to interaction with the innate and adaptive immune system and tissue homing. Excessive production and activation of eosinophils lead to the release of granule proteins, such as major basic protein, eosinophil cationic protein, eosinophil peroxidase, and others, resulting in inflammation, cell cytotoxicity, and oxidative stress. The pathogenesis, clinical features, diagnostic processes, and the latest therapeutic approaches to the resulting diseases—which affect the upper and lower airways, gastrointestinal tract, skin, myocardium, and may occur systemically—are discussed.
DOI: https://doi.org/10.37349/eaa.2026.1009111
Eosinophilic esophagitis (EoE) is a chronic, immune-mediated inflammatory disease of the esophagus that has emerged as a major cause of esophageal dysfunction in all ages. Over the past two decades, its frequency has increased worldwide, reflecting both heightened recognition and a rise in occurrence. EoE predominantly affects males and frequently coexists with atopic conditions, underscoring its relationship with allergy. The pathogenesis involves genetic susceptibility, epithelial barrier dysfunction, and dysregulated type 2 immune responses. Variants in genes related to epithelial integrity and immune signaling, such as TSLP and CAPN14, predispose susceptible individuals to aberrant immune responses to food antigens, leading to eosinophil recruitment, mast cell activation, and chronic inflammation, which in turn promotes tissue remodeling and progression toward fibrostenotic disease. Clinical presentation varies with age. Infants and younger children often exhibit feeding difficulties, vomiting, and abdominal pain, whereas older children and adolescents usually present with dysphagia and food impaction. Diagnosis requires integration of clinical symptoms with histologic confirmation of esophageal eosinophilia (≥ 15 eosinophils per high-power field) and exclusion of alternative causes. Management of pediatric EoE aims to achieve and maintain clinical and histologic remission while preventing long-term complications and preserving quality of life. First-line therapeutic options include proton pump inhibitors, swallowed topical corticosteroids, and dietary elimination strategies. Biologic therapy has expanded treatment options for severe or refractory disease. Because symptom improvement alone does not reliably reflect disease control, objective reassessment with endoscopy and biopsies is recommended after treatment and during follow-up. Long-term outcomes of EoE are strongly influenced by diagnostic timing and adequacy of treatment. Early diagnosis, sustained anti-inflammatory therapy, and transition from pediatric to adult care are critical components of an appropriate management. Future directions include the development of precision medicine, identification of biomarkers to guide therapy selection, non-invasive tools for disease monitoring, and strategies aimed at disease modification.
Eosinophilic esophagitis (EoE) is a chronic, immune-mediated inflammatory disease of the esophagus that has emerged as a major cause of esophageal dysfunction in all ages. Over the past two decades, its frequency has increased worldwide, reflecting both heightened recognition and a rise in occurrence. EoE predominantly affects males and frequently coexists with atopic conditions, underscoring its relationship with allergy. The pathogenesis involves genetic susceptibility, epithelial barrier dysfunction, and dysregulated type 2 immune responses. Variants in genes related to epithelial integrity and immune signaling, such as TSLP and CAPN14, predispose susceptible individuals to aberrant immune responses to food antigens, leading to eosinophil recruitment, mast cell activation, and chronic inflammation, which in turn promotes tissue remodeling and progression toward fibrostenotic disease. Clinical presentation varies with age. Infants and younger children often exhibit feeding difficulties, vomiting, and abdominal pain, whereas older children and adolescents usually present with dysphagia and food impaction. Diagnosis requires integration of clinical symptoms with histologic confirmation of esophageal eosinophilia (≥ 15 eosinophils per high-power field) and exclusion of alternative causes. Management of pediatric EoE aims to achieve and maintain clinical and histologic remission while preventing long-term complications and preserving quality of life. First-line therapeutic options include proton pump inhibitors, swallowed topical corticosteroids, and dietary elimination strategies. Biologic therapy has expanded treatment options for severe or refractory disease. Because symptom improvement alone does not reliably reflect disease control, objective reassessment with endoscopy and biopsies is recommended after treatment and during follow-up. Long-term outcomes of EoE are strongly influenced by diagnostic timing and adequacy of treatment. Early diagnosis, sustained anti-inflammatory therapy, and transition from pediatric to adult care are critical components of an appropriate management. Future directions include the development of precision medicine, identification of biomarkers to guide therapy selection, non-invasive tools for disease monitoring, and strategies aimed at disease modification.
DOI: https://doi.org/10.37349/eaa.2026.1009112
This article belongs to the special issue Beyond Eosinophilic Gastrointestinal Diseases: Pathogenetic Mechanisms and Therapeutic Strategies
Scombroid syndrome is a frequent cause of fish poisoning and typically presents with mild, self-limiting symptoms. Severe anaphylaxis-like reactions are uncommon, and a biphasic clinical course has not previously been reported. We describe the case of a 19-year-old woman who developed flushing, headache, generalized urticaria, facial edema, dyspnea, and hypotension approximately 30 minutes after ingesting raw amberjack tartare. Emergency treatment with adrenaline, antihistamines, corticosteroids, and intravenous fluids led to initial clinical improvement; however, three hours later, she experienced a recurrence of cutaneous, respiratory, and gastrointestinal symptoms, consistent with a biphasic reaction. The patient subsequently developed chest pain associated with transient electrocardiographic changes and mild troponin elevation, prompting further evaluation for suspected Kounis syndrome. Allergy assessment, including specific IgE testing and skin-prick testing with fresh fish, was negative, supporting a toxic rather than IgE-mediated mechanism. This case expands the clinical spectrum of scombroid syndrome by documenting a biphasic anaphylaxis-like presentation and underscores the importance of considering histamine fish poisoning in the differential diagnosis of severe food-related reactions. Careful evaluation is essential to prevent misdiagnosis and unnecessary long-term dietary restrictions.
Scombroid syndrome is a frequent cause of fish poisoning and typically presents with mild, self-limiting symptoms. Severe anaphylaxis-like reactions are uncommon, and a biphasic clinical course has not previously been reported. We describe the case of a 19-year-old woman who developed flushing, headache, generalized urticaria, facial edema, dyspnea, and hypotension approximately 30 minutes after ingesting raw amberjack tartare. Emergency treatment with adrenaline, antihistamines, corticosteroids, and intravenous fluids led to initial clinical improvement; however, three hours later, she experienced a recurrence of cutaneous, respiratory, and gastrointestinal symptoms, consistent with a biphasic reaction. The patient subsequently developed chest pain associated with transient electrocardiographic changes and mild troponin elevation, prompting further evaluation for suspected Kounis syndrome. Allergy assessment, including specific IgE testing and skin-prick testing with fresh fish, was negative, supporting a toxic rather than IgE-mediated mechanism. This case expands the clinical spectrum of scombroid syndrome by documenting a biphasic anaphylaxis-like presentation and underscores the importance of considering histamine fish poisoning in the differential diagnosis of severe food-related reactions. Careful evaluation is essential to prevent misdiagnosis and unnecessary long-term dietary restrictions.
DOI: https://doi.org/10.37349/eaa.2026.1009113
Peanut allergy (PA) is a significant public health problem in Western countries; however, while some previous work has been conducted in Mexico among specific subgroups, the national prevalence of PA in the Mexican population remains unknown. This ENRADAL-MEX study aimed to estimate the prevalence of PA among Mexican schoolchildren. A total of 4,269 children aged 6–12 years were included (mean age: 8.7 years; 51.7% male). The national prevalence of adverse food reactions was 9.5%; among these, 16 cases (0.37%) were associated with peanut consumption, but only 11 presented symptoms within the first hour after ingestion, yielding a PA prevalence of 0.26% (95% CI: 0.14–0.47%). Five cases corresponded to convincing non-severe reactions, and the other five to convincing severe reactions (prevalence of 0.12%; 95% CI: 0.06–0.28%, each). Oral symptoms occurred in 54.5% of cases, and 63.6% also had tree nut allergy, with no reactions to other legumes. Since this national study is the first of its kind and indicates that PA is not currently a public health problem among Mexican schoolchildren, further research is encouraged for more comprehensive results.
Peanut allergy (PA) is a significant public health problem in Western countries; however, while some previous work has been conducted in Mexico among specific subgroups, the national prevalence of PA in the Mexican population remains unknown. This ENRADAL-MEX study aimed to estimate the prevalence of PA among Mexican schoolchildren. A total of 4,269 children aged 6–12 years were included (mean age: 8.7 years; 51.7% male). The national prevalence of adverse food reactions was 9.5%; among these, 16 cases (0.37%) were associated with peanut consumption, but only 11 presented symptoms within the first hour after ingestion, yielding a PA prevalence of 0.26% (95% CI: 0.14–0.47%). Five cases corresponded to convincing non-severe reactions, and the other five to convincing severe reactions (prevalence of 0.12%; 95% CI: 0.06–0.28%, each). Oral symptoms occurred in 54.5% of cases, and 63.6% also had tree nut allergy, with no reactions to other legumes. Since this national study is the first of its kind and indicates that PA is not currently a public health problem among Mexican schoolchildren, further research is encouraged for more comprehensive results.
DOI: https://doi.org/10.37349/eaa.2026.1009110
This article belongs to the special issue Practical Issues in Pediatric Allergy
Aim:
This study aimed to assess the effectiveness of mepolizumab in enhancing asthma control, achieving clinical remission, and alleviating upper airway symptoms in patients with severe eosinophilic asthma (SEA) with comorbid nasal polyps and/or chronic rhinosinusitis (CRS). Additionally, it aimed to identify clinical and laboratory predictors of remission. The findings are based on real-world data from a single center.
Methods:
This retrospective, single-center, real-world study included 99 patients diagnosed with SEA. Patients were categorized into three groups based on the presence or absence of nasal polyps and CRS. Treatment response was evaluated using the asthma control test (ACT), spirometry, laboratory biomarkers, computed tomography (CT) scores, and nasal polyp scores. Remission was defined as the absence of asthma exacerbations and systemic corticosteroid use, along with improvements in both forced expiratory volume in 1 second (FEV1) and ACT scores.
Results:
After 12 months of mepolizumab therapy, there were significant improvements in FEV1 values, asthma exacerbation frequency, systemic corticosteroid requirements, and nasal symptom scores. The overall remission rate was 30.6%. Patients with higher baseline FEV1 and no prior exposure to omalizumab were more likely to achieve remission.
Conclusions:
This real-world evidence suggests that mepolizumab provides meaningful clinical, functional, and radiological improvements in patients with SEA, regardless of comorbid nasal polyps or CRS. Furthermore, the study highlights independent predictors associated with treatment-induced remission in this population.
Aim:
This study aimed to assess the effectiveness of mepolizumab in enhancing asthma control, achieving clinical remission, and alleviating upper airway symptoms in patients with severe eosinophilic asthma (SEA) with comorbid nasal polyps and/or chronic rhinosinusitis (CRS). Additionally, it aimed to identify clinical and laboratory predictors of remission. The findings are based on real-world data from a single center.
Methods:
This retrospective, single-center, real-world study included 99 patients diagnosed with SEA. Patients were categorized into three groups based on the presence or absence of nasal polyps and CRS. Treatment response was evaluated using the asthma control test (ACT), spirometry, laboratory biomarkers, computed tomography (CT) scores, and nasal polyp scores. Remission was defined as the absence of asthma exacerbations and systemic corticosteroid use, along with improvements in both forced expiratory volume in 1 second (FEV1) and ACT scores.
Results:
After 12 months of mepolizumab therapy, there were significant improvements in FEV1 values, asthma exacerbation frequency, systemic corticosteroid requirements, and nasal symptom scores. The overall remission rate was 30.6%. Patients with higher baseline FEV1 and no prior exposure to omalizumab were more likely to achieve remission.
Conclusions:
This real-world evidence suggests that mepolizumab provides meaningful clinical, functional, and radiological improvements in patients with SEA, regardless of comorbid nasal polyps or CRS. Furthermore, the study highlights independent predictors associated with treatment-induced remission in this population.
DOI: https://doi.org/10.37349/eaa.2026.1009109
This article belongs to the special issue Update on Chronic Rhinosinusitis
Aim:
Woodworking exposes carpenters to a higher risk of developing asthma or worsening pre-existing asthma. The objective of this study was to determine the prevalence of and factors associated with work-related asthma (WRA) among carpenters in Parakou in 2024.
Methods:
This was a cross-sectional, descriptive, and analytical study with prospective data collection conducted from June to September 2024. Following a voluntary survey, the included carpenters were interviewed using the Occupational Asthma Screening Questionnaire-11 (OASQ-11) to assess the relationship between asthma symptoms and the occupational environment. Peak expiratory flow (PEF) variability and spirometry were also measured. Data were analyzed using R software version 4.4.1. Factors associated with WRA were identified using simple and multiple logistic regression analyses.
Results:
Out of 153 carpenters/apprentices in 117 workshops, 144 (94.1%) were included, all of whom were male. The mean age was 35.9 ± 12.1 years. Among them, 15 (10.4%) had a WRA profile, including 10 (6.9%; 95% CI: 3.8–12.3) with occupational asthma and 5 (3.5%; 95% CI: 1.5–7.9) with work-aggravated asthma. Asthma was confirmed in 7 of the 15 carpenters suspected of having WRA through PEF variability measurement and spirometry. Simple and multiple logistic regression analyses identified a history of allergic rhinitis (aOR = 3.90; p = 0.033) and urticaria (aOR = 8.21; p = 0.002) as factors significantly associated with WRA.
Conclusions:
The prevalence of WRA among carpenters in Parakou is not negligible, particularly occupational asthma. Awareness campaigns, education for carpenters, regular monitoring of working conditions, and systematic medical follow-up of exposed workers could help preserve their respiratory health.
Aim:
Woodworking exposes carpenters to a higher risk of developing asthma or worsening pre-existing asthma. The objective of this study was to determine the prevalence of and factors associated with work-related asthma (WRA) among carpenters in Parakou in 2024.
Methods:
This was a cross-sectional, descriptive, and analytical study with prospective data collection conducted from June to September 2024. Following a voluntary survey, the included carpenters were interviewed using the Occupational Asthma Screening Questionnaire-11 (OASQ-11) to assess the relationship between asthma symptoms and the occupational environment. Peak expiratory flow (PEF) variability and spirometry were also measured. Data were analyzed using R software version 4.4.1. Factors associated with WRA were identified using simple and multiple logistic regression analyses.
Results:
Out of 153 carpenters/apprentices in 117 workshops, 144 (94.1%) were included, all of whom were male. The mean age was 35.9 ± 12.1 years. Among them, 15 (10.4%) had a WRA profile, including 10 (6.9%; 95% CI: 3.8–12.3) with occupational asthma and 5 (3.5%; 95% CI: 1.5–7.9) with work-aggravated asthma. Asthma was confirmed in 7 of the 15 carpenters suspected of having WRA through PEF variability measurement and spirometry. Simple and multiple logistic regression analyses identified a history of allergic rhinitis (aOR = 3.90; p = 0.033) and urticaria (aOR = 8.21; p = 0.002) as factors significantly associated with WRA.
Conclusions:
The prevalence of WRA among carpenters in Parakou is not negligible, particularly occupational asthma. Awareness campaigns, education for carpenters, regular monitoring of working conditions, and systematic medical follow-up of exposed workers could help preserve their respiratory health.
DOI: https://doi.org/10.37349/eaa.2026.1009108
There is unequivocal evidence that the climate is changing, and it is generally accepted that the trend will continue. Climate change is relevant to public health, as it can lead to alterations in the distribution and flowering phenology of plants and to changes in pollen exposure, with subsequent impacts on human health. The primary objective of this paper was to provide a quantitative synthesis of the available literature on the evolution of pollen season intensity and timing in plants with a higher allergenic potential. Six botanical families have been studied: Betulaceae (birch, hazel, alder), Cupressaceae, Oleaceae (olive, ash), Poaceae, Urticaceae, and Asteraceae (mugwort, ragweed). Three main indicators of the potential impact of climate change on pollination have been retained: the pollen integral, the start date of the pollen season, and the duration of the pollen season. The outcome is a dominant trend toward earlier and more abundant pollen seasons, particularly for trees that flower in winter and spring. In contrast, trends for grass or weeds that pollinate later are less consistent and often region-specific. The variations recorded are taxon-, site-, and period-dependent, with some species even showing opposing trends within the same botanical family, illustrating the complex interactions between biological adaptation and climatic variability. While the current influence of climate change on pollen production and phenology is well established, the magnitude of its future impact remains uncertain, and the diversity of methodologies and study durations limits the comparability of available data. Nevertheless, most projections support a continued, though possibly attenuated, increase in pollen intensity and season advancement. In any case, when combined with likely qualitative and quantitative changes in the concentration of allergens in pollen grains, the identified trends may already have, and will very likely continue to have, an impact on both allergic sensitizations, the prevalence of seasonal symptoms, and their severity, thus affecting their diagnosis, prevention, and treatment.
There is unequivocal evidence that the climate is changing, and it is generally accepted that the trend will continue. Climate change is relevant to public health, as it can lead to alterations in the distribution and flowering phenology of plants and to changes in pollen exposure, with subsequent impacts on human health. The primary objective of this paper was to provide a quantitative synthesis of the available literature on the evolution of pollen season intensity and timing in plants with a higher allergenic potential. Six botanical families have been studied: Betulaceae (birch, hazel, alder), Cupressaceae, Oleaceae (olive, ash), Poaceae, Urticaceae, and Asteraceae (mugwort, ragweed). Three main indicators of the potential impact of climate change on pollination have been retained: the pollen integral, the start date of the pollen season, and the duration of the pollen season. The outcome is a dominant trend toward earlier and more abundant pollen seasons, particularly for trees that flower in winter and spring. In contrast, trends for grass or weeds that pollinate later are less consistent and often region-specific. The variations recorded are taxon-, site-, and period-dependent, with some species even showing opposing trends within the same botanical family, illustrating the complex interactions between biological adaptation and climatic variability. While the current influence of climate change on pollen production and phenology is well established, the magnitude of its future impact remains uncertain, and the diversity of methodologies and study durations limits the comparability of available data. Nevertheless, most projections support a continued, though possibly attenuated, increase in pollen intensity and season advancement. In any case, when combined with likely qualitative and quantitative changes in the concentration of allergens in pollen grains, the identified trends may already have, and will very likely continue to have, an impact on both allergic sensitizations, the prevalence of seasonal symptoms, and their severity, thus affecting their diagnosis, prevention, and treatment.
DOI: https://doi.org/10.37349/eaa.2026.1009107
This article belongs to the special issue Climate Change, Allergy, and Immunotherapy
Cow’s milk allergy (CMA) is one of the most common food allergies in infancy, with a prevalence of up to 7.5%. However, accurate diagnosis in primary care remains difficult due to overlapping symptoms with common infant behaviours and limited access to specialist allergy testing. Consequently, CMA is frequently over diagnosed, leading to unnecessary elimination diets, nutritional deficiencies, and increased parental anxiety. This paper introduces the EATERS-X framework, an enhanced, structured approach to obtaining an allergy-focused clinical history (AFCH) that aims to improve diagnostic precision and clinical decision-making in CMA. The tool expands upon the traditional EATERS method—comprising Environment, Allergen, Timing, Exposure, Reproducibility, and Symptoms—by incorporating an additional element, X, denoting treatment and healthcare response. Through clinical scenarios, we demonstrate how EATERS-X can be applied to distinguish between IgE-mediated, non-IgE-mediated, and mixed-type CMA, including subtypes such as food protein-induced enterocolitis syndrome (FPIES). While EATERS-X provides a practical and systematic framework for history-taking, its effectiveness is dependent on clinician training and appropriate clinical interpretation. In addition, the framework has not yet undergone formal validation against gold-standard diagnostic tests such as oral food challenges. Future prospective studies should evaluate the diagnostic reliability, inter-observer consistency, and clinical impact of EATERS-X across different healthcare settings. Integration of the EATERS-X approach in primary care aligns with current BSACI and EAACI guidelines and promotes structured, evidence-based, and patient-centred care. Future research should focus on validating the framework’s diagnostic reliability and exploring its applicability across a wider spectrum of allergic conditions.
Cow’s milk allergy (CMA) is one of the most common food allergies in infancy, with a prevalence of up to 7.5%. However, accurate diagnosis in primary care remains difficult due to overlapping symptoms with common infant behaviours and limited access to specialist allergy testing. Consequently, CMA is frequently over diagnosed, leading to unnecessary elimination diets, nutritional deficiencies, and increased parental anxiety. This paper introduces the EATERS-X framework, an enhanced, structured approach to obtaining an allergy-focused clinical history (AFCH) that aims to improve diagnostic precision and clinical decision-making in CMA. The tool expands upon the traditional EATERS method—comprising Environment, Allergen, Timing, Exposure, Reproducibility, and Symptoms—by incorporating an additional element, X, denoting treatment and healthcare response. Through clinical scenarios, we demonstrate how EATERS-X can be applied to distinguish between IgE-mediated, non-IgE-mediated, and mixed-type CMA, including subtypes such as food protein-induced enterocolitis syndrome (FPIES). While EATERS-X provides a practical and systematic framework for history-taking, its effectiveness is dependent on clinician training and appropriate clinical interpretation. In addition, the framework has not yet undergone formal validation against gold-standard diagnostic tests such as oral food challenges. Future prospective studies should evaluate the diagnostic reliability, inter-observer consistency, and clinical impact of EATERS-X across different healthcare settings. Integration of the EATERS-X approach in primary care aligns with current BSACI and EAACI guidelines and promotes structured, evidence-based, and patient-centred care. Future research should focus on validating the framework’s diagnostic reliability and exploring its applicability across a wider spectrum of allergic conditions.
DOI: https://doi.org/10.37349/eaa.2026.1009106
This article belongs to the special issue Practical Issues in Pediatric Allergy
The symptoms of atopic dermatitis (AD), a chronic, recurrent inflammatory skin condition, include immunological dysregulation, severe pruritus, and malfunctioning of the epidermal barrier. Recent developments in our understanding of AD’s molecular and immunological pathways have shed light on the functions of cytokines, including interleukin (IL)-4, IL-13, IL-31, and IL-22, as well as the impact of genetic mutations in filaggrin and other barrier proteins. Inflammation and barrier dysfunction are further aggravated by microbial dysbiosis, especially colonisation of Staphylococcus aureus. Treatment options include topical corticosteroids, topical calcineurin inhibitors, targeted biologics, and small-molecule inhibitors that alter the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) and phosphodiesterase 4 (PDE4) pathways, as well as Mn- and Fe-porphyrin ring-based topical formulations. Even with these advancements, tailored treatment and long-term illness control are still challenging to achieve. New strategies that emphasise gene therapy and microbiome restoration can potentially improve the accuracy and comprehensiveness of AD treatment.
The symptoms of atopic dermatitis (AD), a chronic, recurrent inflammatory skin condition, include immunological dysregulation, severe pruritus, and malfunctioning of the epidermal barrier. Recent developments in our understanding of AD’s molecular and immunological pathways have shed light on the functions of cytokines, including interleukin (IL)-4, IL-13, IL-31, and IL-22, as well as the impact of genetic mutations in filaggrin and other barrier proteins. Inflammation and barrier dysfunction are further aggravated by microbial dysbiosis, especially colonisation of Staphylococcus aureus. Treatment options include topical corticosteroids, topical calcineurin inhibitors, targeted biologics, and small-molecule inhibitors that alter the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) and phosphodiesterase 4 (PDE4) pathways, as well as Mn- and Fe-porphyrin ring-based topical formulations. Even with these advancements, tailored treatment and long-term illness control are still challenging to achieve. New strategies that emphasise gene therapy and microbiome restoration can potentially improve the accuracy and comprehensiveness of AD treatment.
DOI: https://doi.org/10.37349/eaa.2026.1009105
This article belongs to the special issue Atopic Dermatitis – Pathology and Treatment Modalities
Background:
The diversity of physiological actions and pharmacological effects of glucocorticoids (GCs) allows their use in a large group of diseases and pathological conditions. However, this treatment can be accompanied by a multitude of more or less severe side effects. As the mainstay of treatment for asthma and chronic obstructive pulmonary disease (COPD), inhaled corticosteroids (ICS) dramatically reduce morbidity and mortality. This research aims to examine the safety considerations associated with glucocorticoid therapy in patients with COPD and asthma.
Methods:
The search was performed in PubMed, EBSCO, UpToDate, Medline, and Google Scholar for pertinent English-language articles published between 1990 and 2025, using the following keywords: glucocorticoids, asthma, COPD, management, and side effects.
Results:
GCs stand out as one of the most widely prescribed classes of drugs globally, with well-established effectiveness in addressing acute or chronic inflammation, allergic conditions, and acute pathological situations. The undeniable efficacy of GCs, however, comes with a range of reported side effects. These include but are not limited to immunosuppression, cardiovascular issues, manifestation of Cushingoid features, development of diabetes, osteoporosis, suppression of the hypothalamic-pituitary-adrenal (HPA) axis, and adverse effects on the gastrointestinal and dermatologic systems. However, the majority of these events are associated with systemic drug administration, which is less commonly indicated in the treatment of COPD and asthma. There are several factors and specific considerations when deciding on GC treatment in COPD. In the context of corticosteroid treatment for asthma, the overarching impact involves the suppression of inflammatory genes, leading to reduced transcription of genes responsible for cytokines, chemokines, adhesion molecules, inflammatory enzymes, and receptors.
Discussion:
GCs are associated with fewer side effects in both COPD and asthma treatment. It’s crucial to take into account factors such as the patient’s overall health, the severity of symptoms, the presence of comorbidities, and the responsiveness of specific features to GCs therapy.
Background:
The diversity of physiological actions and pharmacological effects of glucocorticoids (GCs) allows their use in a large group of diseases and pathological conditions. However, this treatment can be accompanied by a multitude of more or less severe side effects. As the mainstay of treatment for asthma and chronic obstructive pulmonary disease (COPD), inhaled corticosteroids (ICS) dramatically reduce morbidity and mortality. This research aims to examine the safety considerations associated with glucocorticoid therapy in patients with COPD and asthma.
Methods:
The search was performed in PubMed, EBSCO, UpToDate, Medline, and Google Scholar for pertinent English-language articles published between 1990 and 2025, using the following keywords: glucocorticoids, asthma, COPD, management, and side effects.
Results:
GCs stand out as one of the most widely prescribed classes of drugs globally, with well-established effectiveness in addressing acute or chronic inflammation, allergic conditions, and acute pathological situations. The undeniable efficacy of GCs, however, comes with a range of reported side effects. These include but are not limited to immunosuppression, cardiovascular issues, manifestation of Cushingoid features, development of diabetes, osteoporosis, suppression of the hypothalamic-pituitary-adrenal (HPA) axis, and adverse effects on the gastrointestinal and dermatologic systems. However, the majority of these events are associated with systemic drug administration, which is less commonly indicated in the treatment of COPD and asthma. There are several factors and specific considerations when deciding on GC treatment in COPD. In the context of corticosteroid treatment for asthma, the overarching impact involves the suppression of inflammatory genes, leading to reduced transcription of genes responsible for cytokines, chemokines, adhesion molecules, inflammatory enzymes, and receptors.
Discussion:
GCs are associated with fewer side effects in both COPD and asthma treatment. It’s crucial to take into account factors such as the patient’s overall health, the severity of symptoms, the presence of comorbidities, and the responsiveness of specific features to GCs therapy.
DOI: https://doi.org/10.37349/eaa.2025.1009104
This article belongs to the special issue The Era of Biologics in Allergy
Asthma is one of the most common chronic respiratory diseases worldwide, traditionally defined as airway inflammation, reversible obstruction, and hyperresponsiveness. While this framework has guided decades of research and treatment, it fails to capture asthma as a heterogeneous and systemic condition. This pathology is shaped by complex interactions among genetic, epigenetic, immunological, neuroendocrine, metabolic, and environmental factors. Its coexistence with chronic obstructive pulmonary disease (COPD) in overlapping syndromes further complicates diagnosis and therapeutic decision-making. Asthma etiology involves oxidative stress, genetic susceptibility, and epigenetic regulation, along with age- and sex-dependent hormonal influences that modulate immune responses. Emerging evidence shows that structural and functional changes in the respiratory epithelium, airway smooth muscle (ASM), and alveoli extend the pathology beyond acute inflammation, involving processes such as epithelial barrier dysfunction, airway remodeling, and impaired mucociliary clearance (MCC). Neuro-immune-endocrine interactions have emerged as central contributors to asthma pathogenesis. Endocrine regulation shapes inflammatory activity and treatment responsiveness. Metabolic factors such as obesity introduce additional complexity by generating low-grade systemic inflammation, oxidative stress, adipokine imbalance, and steroid resistance, resulting in a distinct and often more severe asthma phenotype. Parasympathetic and sensory neural pathways amplify bronchoconstriction and inflammation through reciprocal communication with eosinophils, mast cells, innate lymphoid cells, and pulmonary neuroendocrine cells (PNECs). Neurotrophins and neuropeptides further promote airway hyperreactivity and remodeling. Current management integrates inhaled corticosteroids, bronchodilators, and targeted biologics—such as thymic stromal lymphopoietin (TSLP) inhibitors—alongside emerging non-pharmacological strategies. Psychological interventions, particularly mindfulness-based approaches, have demonstrated improvements in quality of life, stress reduction, and patient-reported asthma control, supporting the relevance of addressing the psychosocial dimensions of chronic disease. Understanding asthma as a systemic disorder underscores the need for personalized, multidimensional treatment strategies that integrate pharmacological, behavioral, and lifestyle components. This paradigm provides a more comprehensive framework for improving long-term outcomes and reducing the global burden of asthma.
Asthma is one of the most common chronic respiratory diseases worldwide, traditionally defined as airway inflammation, reversible obstruction, and hyperresponsiveness. While this framework has guided decades of research and treatment, it fails to capture asthma as a heterogeneous and systemic condition. This pathology is shaped by complex interactions among genetic, epigenetic, immunological, neuroendocrine, metabolic, and environmental factors. Its coexistence with chronic obstructive pulmonary disease (COPD) in overlapping syndromes further complicates diagnosis and therapeutic decision-making. Asthma etiology involves oxidative stress, genetic susceptibility, and epigenetic regulation, along with age- and sex-dependent hormonal influences that modulate immune responses. Emerging evidence shows that structural and functional changes in the respiratory epithelium, airway smooth muscle (ASM), and alveoli extend the pathology beyond acute inflammation, involving processes such as epithelial barrier dysfunction, airway remodeling, and impaired mucociliary clearance (MCC). Neuro-immune-endocrine interactions have emerged as central contributors to asthma pathogenesis. Endocrine regulation shapes inflammatory activity and treatment responsiveness. Metabolic factors such as obesity introduce additional complexity by generating low-grade systemic inflammation, oxidative stress, adipokine imbalance, and steroid resistance, resulting in a distinct and often more severe asthma phenotype. Parasympathetic and sensory neural pathways amplify bronchoconstriction and inflammation through reciprocal communication with eosinophils, mast cells, innate lymphoid cells, and pulmonary neuroendocrine cells (PNECs). Neurotrophins and neuropeptides further promote airway hyperreactivity and remodeling. Current management integrates inhaled corticosteroids, bronchodilators, and targeted biologics—such as thymic stromal lymphopoietin (TSLP) inhibitors—alongside emerging non-pharmacological strategies. Psychological interventions, particularly mindfulness-based approaches, have demonstrated improvements in quality of life, stress reduction, and patient-reported asthma control, supporting the relevance of addressing the psychosocial dimensions of chronic disease. Understanding asthma as a systemic disorder underscores the need for personalized, multidimensional treatment strategies that integrate pharmacological, behavioral, and lifestyle components. This paradigm provides a more comprehensive framework for improving long-term outcomes and reducing the global burden of asthma.
DOI: https://doi.org/10.37349/eaa.2025.1009103
This article belongs to the special issue Asthma and its Relationship with Psychological and Psychopathological Factors
Aim:
Angioedema is a common but often underestimated manifestation of chronic spontaneous urticaria (CSU). Its presence may indicate higher disease severity, longer duration, and autoimmune involvement. This study aims to assess the clinical relevance and associations of angioedema in CSU patients with disease severity and duration, treatment response to H1-antihistamines, correlation with autoimmune status, and autologous serum skin test (ASST) positivity.
Methods:
A prospective study was conducted at the Dermatology Department, General Hospital 8th September, Skopje, North Macedonia, from December 2021 to November 2022, including 230 CSU patients. Disease activity was assessed using the Urticaria Activity Score over 7 days (UAS7), and severity was categorized accordingly. Response to H1-antihistamines was defined as achieving UAS7 < 7 for several months. Angioedema was recorded as a symptom regardless of localization. Autoimmune status was based on autoimmune disease history and/or autoantibody (AAb) detection. The ASST was performed, classifying patients as ASST-positive (ASST⁺) or ASST-negative (ASST⁻).
Results:
Angioedema was observed in 70% of CSU patients, all with accompanying wheals. It was significantly more common in severe CSU than in moderate (82.02% vs. 65.38%, p = 0.026), mild (82.02% vs. 65.96%, p = 0.036), and well-controlled disease (82.02% vs. 45.45%, p = 0.0004). Patients with a positive autoimmune status more often had angioedema than those with a negative status (75.17% vs. 61.18%, p = 0.025). CSU showed longer duration in patients with angioedema (p = 0.000012), with no association to good antihistamine response (p = 0.55).
Conclusions:
Angioedema in CSU is associated with higher disease activity, autoimmune status, and prolonged disease duration but not with differences in antihistamine response. Its presence marks a more severe phenotype, emphasizing the need for careful monitoring and individualized management.
Aim:
Angioedema is a common but often underestimated manifestation of chronic spontaneous urticaria (CSU). Its presence may indicate higher disease severity, longer duration, and autoimmune involvement. This study aims to assess the clinical relevance and associations of angioedema in CSU patients with disease severity and duration, treatment response to H1-antihistamines, correlation with autoimmune status, and autologous serum skin test (ASST) positivity.
Methods:
A prospective study was conducted at the Dermatology Department, General Hospital 8th September, Skopje, North Macedonia, from December 2021 to November 2022, including 230 CSU patients. Disease activity was assessed using the Urticaria Activity Score over 7 days (UAS7), and severity was categorized accordingly. Response to H1-antihistamines was defined as achieving UAS7 < 7 for several months. Angioedema was recorded as a symptom regardless of localization. Autoimmune status was based on autoimmune disease history and/or autoantibody (AAb) detection. The ASST was performed, classifying patients as ASST-positive (ASST⁺) or ASST-negative (ASST⁻).
Results:
Angioedema was observed in 70% of CSU patients, all with accompanying wheals. It was significantly more common in severe CSU than in moderate (82.02% vs. 65.38%, p = 0.026), mild (82.02% vs. 65.96%, p = 0.036), and well-controlled disease (82.02% vs. 45.45%, p = 0.0004). Patients with a positive autoimmune status more often had angioedema than those with a negative status (75.17% vs. 61.18%, p = 0.025). CSU showed longer duration in patients with angioedema (p = 0.000012), with no association to good antihistamine response (p = 0.55).
Conclusions:
Angioedema in CSU is associated with higher disease activity, autoimmune status, and prolonged disease duration but not with differences in antihistamine response. Its presence marks a more severe phenotype, emphasizing the need for careful monitoring and individualized management.
DOI: https://doi.org/10.37349/eaa.2025.1009101
This article belongs to the special issue Bridging Experimental and Translational Allergology
