Background: Polymorphisms of plasminogen activator inhibitor-1 (PAI-1) and angiotensin-converting enzyme (ACE) genes have been implicated in susceptibility to asthma. In this study, we aimed to investigate whether there was any association between childhood asthma and polymorphisms of the PAI-1 and ACE genes.
Methods: Two hundred and three Turkish children aged 5-15 years, including 102 asthmatic patients and 101 healthy control subjects were included in this study. The asthma group was divided into two groups as follows: Group I: Asthmatic children with positive family history for atopy (n=53), Group II: Asthmatic children without any family history for atopy (n=49). One hundred and twenty-eight atopic family members were also included in the study. The insertion/deletion (I/D) polymorphism of the ACE and PAI-1 4G/5G gene polymorphisms was carried out by polymerase chain reaction.
Results: The prevalence of the PAI-1 4G allele was significantly greater in asthmatic children compared to control group (p<0.05, OR: 1.64 (1.11-2.43)) but there was no significant relation between ACE I/D genotypes and childhood asthma. No significant difference was detected between Groups I and II in terms of these ACE and PAI-1 genotypes and allele frequencies. No significant relationship was found between both gene polymorphisms and total serum IgE and skin prick test results.
Conclusion: It has been established that PAI-1 4G allele may be a genetic risk factor for childhood asthma but ACE gene I/D polymorphisms do not play a role in the development of asthma in the sample of Turkish children.
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http://dx.doi.org/10.1016/j.aller.2011.12.003 | 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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