Allergic Rhinitis and Asthma Co-Morbidity

Sukhan, Victoria S

doi:10.36740/wlek201904122

Cited by 7 publications

(5 citation statements)

References 9 publications

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“…Patients with AR have poorer asthma control, frequent exacerbations and emergency visits, higher healthcare costs and lower Health Related Quality of Life (HRQoL) (25)(26)(27)(28)(29)(30)(31)(32).…”

Section: Allergic Rhinitis (Ar) and Asthmamentioning

confidence: 99%

Manifesto on united airways diseases (UAD): an Interasma (global asthma association – GAA) document

et al. 2021

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The large amount of evidence and the renewed interest on upper and lower airways involvement in infectious and inflammatory diseases has led Interasma (Global Asthma Association) to take a position on United Airways Diseases (UAD). Starting from an extensive literature review, Interasma excecutive committee discussed and approved this Manifesto developed by Interasma scientific network (INES) members. The manifesto describes the evidence gathered to date and defines, states, advocates, and proposes issues on UAD (rhinitis, rhinosinusitis and nasal polyposis), and concomitant/comorbid lower airways disorders (asthma, chronic obstructive pulmonary disease, bronchiectasis, cystic fibrosis, obstructive sleep apnoea) with the aim of challenging assumptions, fostering commitment, and bringing about change.UAD refer to clinical pictures characterized by the coexistence of upper and lower airways involvement, driven by a common pathophysiological mechanism, leading to a greater burden on patient's health status and requiring an integrated diagnostic and therapeutic plan.The high prevalence of UAD must be taken into account. Upper and lower airways diseases influence disease control and patient's quality of life. Patients with UAD need to have a timely and adequate diagnosis, treatment, and, when recommended, referral for management in a specialized center. Diagnostic testing including skin prick or serum specific IgE, lung function, fractional exhaled nitric oxide (FeNO), polysomnography, allergen-specific immunotherapies, biological therapies and homebased continuous positive airway pressure (CPAP) whenever these are recommended, should be part of the management plan for UAD.Education of medical students, physicians, health professionals, patients and caregivers on the UAD is needed.

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Section: Allergic Rhinitis (Ar) and Asthmamentioning

confidence: 99%

Manifesto on united airways diseases (UAD): an Interasma (global asthma association – GAA) document

et al. 2021

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“…At present, it is found that obesity-related asthma mainly includes two simple phenotypes: one is caused by obesity and has a delayed onset, which is late-onset asthma; the other is early-onset. Late-onset asthma has a low inflammatory response, and airway hyperresponsiveness gradually improves with weight loss; the other one has an earlier onset and a higher allergic inflammatory response, and the condition can be aggravated by obesity ( Sukhan, 2018 ). Microbes are an important part of maintaining homeostasis in the body, and obesity-related alterations in the gut and/or airway microbial diversity enlarge the risk of asthma in obese individuals ( Dupont et al., 2020 ).…”

Section: Introductionmentioning

confidence: 99%

Obesity-related asthma and its relationship with microbiota

Huang,

Zhou,

Dong

et al. 2024

Front. Cell. Infect. Microbiol.

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Obesity and asthma are global public health problems. Obesity-related asthma is a special phenotype of asthma with a complex pathogenesis. Its occurrence and development are related to mechanical compression, inflammatory response, metabolic regulation, gene regulation, and vitamin D deficiency. Different treatment strategies used in the process of weight loss have a beneficial impact on asthma. Alterations in gut and airway microbial community structure and their metabolites may also contribute to obesity-related asthma. The role of the Th17/Treg balance in the gut microbiota regulating the immune responses and host metabolism is important. Therapeutic measures associated with the gut microbiota variety may contribute to improving chronic inflammation associated with obesity by regulating the Th17/Treg balance. An early reduction in microbial diversity can predict the development of asthma and lead to allergy through an imbalance of Th2/Th1 responses. Short-chain fatty acids (SCFAs) regulate the differentiation and activation of regulatory T cells, thereby regulating immune homeostasis in the lung to suppress allergic inflammation and weight gain. Therefore, clarifying the microbial mechanism of obesity-related asthma has important guiding significance for clinical treatment. In this review, we used the following terms: “asthma and obesity” and “obesity-related asthma”, combining “phenotype”, “airway inflammation” and “lung function”, and reviewed the characteristics and pathogenesis of obesity-related asthma, the relationship between the gut and airway microbiota and obesity-related asthma, and the current treatment measures for the disease.

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“…As an upper respiratory allergic disease, allergic rhinitis (AR) is often co-morbid with bronchial asthma, and can aggravate the symptoms of bronchial asthma and promote its progression. [ 3 , 4 ] Asthma’s prevalence varies worldwide, ranging from 1% to 18%, with the highest rates observed in Western countries. [ 5 ] AR affects 10% to 20% of the population in Europe and the US.…”

Section: Introductionmentioning

confidence: 99%

Risk prediction model construction for asthma after allergic rhinitis by blood immune T effector cells

Wang,

Jiang,

2024

Medicine

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Background: Allergic rhinitis (AR) and asthma (AS) are prevalent and frequently co-occurring respiratory diseases, with mutual influence on each other. They share similar etiology, pathogenesis, and pathological changes. Due to the anatomical continuity between the upper and lower respiratory tracts, allergic inflammation in the nasal cavity can readily propagate downwards, leading to bronchial inflammation and asthma. AR serves as a significant risk factor for AS by potentially inducing airway hyperresponsiveness in patients. Currently, there is a lack of reliable predictors for the progression from AR to AS. Methods: In this exhaustive investigation, we reexamined peripheral blood single cell RNA sequencing datasets from patients with AS following AR and healthy individuals. In addition, we used the bulk RNA sequencing dataset as a validation lineup, which included AS, AR, and healthy controls. Using marker genes of related cell subtype, signatures predicting the progression of AR to AS were generated. Results: We identified a subtype of immune-activating effector T cells that can distinguish patients with AS after AR. By combining specific marker genes of effector T cell subtype, we established prediction models of 16 markers. The model holds great promise for assessing AS risk in individuals with AR, providing innovative avenues for clinical diagnosis and treatment strategies. Conclusion: Subcluster T effector cells may play a key role in post-AR AS. Notably, ACTR3 and HSPA8 genes were significantly upregulated in the blood of AS patients compared to healthy patients.

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Allergic Rhinitis and Asthma Co-Morbidity

Cited by 7 publications

References 9 publications

Manifesto on united airways diseases (UAD): an Interasma (global asthma association – GAA) document

Manifesto on united airways diseases (UAD): an Interasma (global asthma association – GAA) document

Obesity-related asthma and its relationship with microbiota

Risk prediction model construction for asthma after allergic rhinitis by blood immune T effector cells

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