Background: Leukotriene (LT) E(4) and 8-isoprostane concentrations are elevated in exhaled breath condensate in children with asthma. The effects of leukotriene receptor antagonists (LTRAs) on exhaled leukotriene and prostanoids in children with asthma are unknown.
Objective: (1) To study the effect of montelukast, a LTRA, on exhaled LTE(4), 8-isoprostane, and prostaglandin E(2) in children with asthma and atopic children; (2) to measure exhaled nitric oxide.
Methods: An open-label study with oral montelukast (5 mg once daily for 4 weeks) was undertaken in 17 atopic children with asthma and 16 atopic children without asthma.
Results: Pretreatment exhaled LTE(4) (P < .0001) and 8-isoprostane (P < .0001) values were higher in atopic children with asthma than in atopic children without asthma. In atopic children with asthma, montelukast reduced exhaled LTE(4) by 33% (P < .001), and this reduction was correlated with pretreatment LTE(4) values (r = -0.90; P = .0001). Posttreatment exhaled LTE(4) levels in children with asthma were higher than pretreatment LTE(4) values in atopic children without asthma (P < .004). Montelukast had no effect on exhaled LTE(4) in atopic children without asthma (P = .74), or on exhaled 8-isoprostane (atopic children with asthma, P = .94; atopic children without asthma, P = .55) and PGE(2) (atopic children with asthma, P = .56; atopic children without asthma, P = .93) in both groups. In atopic children with asthma, exhaled nitric oxide concentrations were reduced by 27% (P < .05) after montelukast.
Conclusion: Leukotriene receptor antagonists decrease exhaled LTE(4) in atopic children with asthma. This reduction is dependent on baseline exhaled LTE(4) values.
Clinical Implications: Measurement of exhaled LTE(4) might help identify children with asthma most likely to benefit from LTRAs.
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http://dx.doi.org/10.1016/j.jaci.2006.04.010 | DOI Listing |
JAMA Pediatr
January 2025
Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
Importance: Spontaneous reports have indicated that montelukast increases the risk of neuropsychiatric adverse events, and the US Food and Drug Administration added a boxed warning about these risks in 2020. However, the potential mechanism is not well understood, and the observational evidence is scarce, particularly in children.
Objective: To assess the potential association between the use of montelukast and the risk of neuropsychiatric adverse events in children and adolescents.
Am J Respir Crit Care Med
January 2025
Beth Israel Deaconess Medical Center, Pulmonary, Critical Care and Sleep Medicine, Boston, Massachusetts, United States.
Am J Respir Cell Mol Biol
January 2025
University of Groningen, University Medical Center Groningen, Department of Pulmonology and Pediatric Allergy, Beatrix Children's Hospital, Groningen, Netherlands.
Asthma is a genetically complex inflammatory airway disease associated with over 200 Single nucleotide polymorphisms (SNPs). However, the functional effects of many asthma-associated SNPs in lung and airway epithelial samples are unknown. Here, we aimed to conduct expression quantitative trait loci (eQTL) analysis using a meta-analysis of nasal and lung samples.
View Article and Find Full Text PDFJ Asthma
January 2025
Department of Pharmacology and Toxicology, University of Antioquia, Medellín, Colombia.
Introduction: Asthma imposes a critical economic burden on health systems, especially with the incorporation of new drugs. Recently, mepolizumab has been approved to prevent exacerbations in patients with eosinophilic asthma, however their high cost constitutes a barrier for their use, especially in middle- and low-income countries. This study aimed to estimate the economically justifiable price of mepolizumab for preventing exacerbations in patients with severe asthma in Colombia.
View Article and Find Full Text PDFAm J Physiol Lung Cell Mol Physiol
January 2025
Division of Pulmonology, Asthma, Cystic Fibrosis, and Sleep, Emory University School of Medicine, Atlanta, GA, USA.
Secondhand smoke exposure (SHSe) is a public health threat for people with cystic fibrosis (CF) and other lung diseases. Primary smoking reduces CFTR channel function, the causative defect in CF. We reported that SHSe worsens respiratory and nutritional outcomes in CF by disrupting immune responses and metabolic signaling.
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