Background: Human rhinoviruses (HRVs) infection is a common cause of exacerbations in pediatric patients with asthma. However, the effects of corticosteroids on HRV-induced exacerbations in pediatric asthma are unknown. We conducted a prospective observational study to determine the viral pathogens in school-age pediatric inpatients with asthma exacerbations. We assessed the effects of maintenance inhaled corticosteroids (ICS) on the detection rates of HRV species and treatment periods of systemic corticosteroids during exacerbations on pulmonary lung function after exacerbations.
Methods: Nasopharyngeal samples and clinical information were collected from 59 patients with asthma exacerbations between April 2018 and March 2020. Pulmonary function tests were carried out 3 months after exacerbations in 18 HRV-positive patients. Changes in forced expiratory volume in 1 second (FEV)% predicted from baseline in a stable state were compared according to the treatment periods of systemic corticosteroids.
Results: Fifty-four samples collected from hospitalized patients were analyzed, and viral pathogens were identified in 45 patients (83.3%) using multiplex PCR assay. HRV-A, -B, and -C were detected in 16 (29.6%), one (1.9%), and 16 (29.6%) patients, respectively. The detection rates of HRV-C were lower in the ICS-treated group compared with those in the ICS-untreated group (p = 0.01), whereas maintenance ICS treatment did not affect the detection rate for viral pathogens in total and HRV-A. Changes in FEV% predicted in patients treated with systemic corticosteroids for 6-8 days (n = 10; median, 4.90%) were higher than those in patients treated for 3-5 days (n = 8; median, - 10.25%) (p = 0.0085).
Conclusions: Maintenance ICS reduced the detection rates of HRV (mainly HRV-C) in school-age inpatients with asthma exacerbations, and the treatment periods of systemic corticosteroids during exacerbations affected lung function after HRV-induced exacerbations. The protective effects of corticosteroids on virus-induced asthma exacerbations may be dependent upon the types of viral pathogen.
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http://dx.doi.org/10.1186/s12890-023-02798-6 | DOI Listing |
Environ Pollut
January 2025
School of Medicine, Taizhou University, Taizhou 318000, China.
Allergic asthma is a significant international concern in respiratory health, which can be exacerbated by the increasing levels of non-allergenic pollutants. This rise in airborne pollutants is a primary driver behind the growing prevalence of asthma, posing a health emergency. Additionally, climatic risk factors can contribute to the onset and progression of asthma.
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January 2025
Personalized Medicine, Asthma and Allergy, IRCCS Humanitas Clinical and Research Hospital, Via Alessandro Manzoni 56, 20089, Rozzano, MI, Italy.
Introduction: The burden of severe asthma on patients, especially on those with concomitant chronic rhinosinusitis with nasal polyps (CRSwNP), is substantial. Treatment intensification with oral corticosteroids is a common strategy for managing severe asthma exacerbations; however, prolonged exposure to systemic corticosteroids is associated with multisystem toxicity. This study aimed to quantify the association between oral corticosteroid use and annual asthma-related costs in patients with severe asthma with or without CRSwNP.
View Article and Find Full Text PDFBMJ Open Respir Res
January 2025
Peking University, Beijing, China
Background: Chronic respiratory diseases (CRDs) have been shown to be associated with frailty, but these findings have not yet reached a consensus. The aim of this study was to investigate the association between CRDs and frailty in the elderly using a nationally representative data from China.
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Rev Alerg Mex
December 2024
Master's in economics, HS Pharmacoeconomic Research, Mexico City, Mexico.
Alzheimers Dement
December 2024
University of North Dakota, Grand Forks, ND, USA.
Background: Alzheimer's disease (AD) is an age-related neurodegenerative disorder affecting nearly 50 million individuals worldwide. Besides aging, various comorbidities can increase the risk of AD, such as asthma. However, the molecular mechanism(s) underlying this asthma-associated AD exacerbation is unknown.
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