Pedro Augusto Silva Dos Santos Rodrigues, Álvaro Augusto Souza da Cruz Filho, Helena Mariana Pitangueira Teixeira, Luciano Gama da Silva Gomes, Hatilla Dos Santos Silva, Juliana Lopes Rodrigues, Almirane Lima de Oliveira, Cinthia Vila Nova Santana, Gabriela Pimentel Pinheiro das Chagas, Camila Alexandrina Viana de Figueiredo, Ryan Dos Santos Costa
{"title":"Influence of ADRB2 variants on bronchodilator response and asthma control in a mixed population.","authors":"Pedro Augusto Silva Dos Santos Rodrigues, Álvaro Augusto Souza da Cruz Filho, Helena Mariana Pitangueira Teixeira, Luciano Gama da Silva Gomes, Hatilla Dos Santos Silva, Juliana Lopes Rodrigues, Almirane Lima de Oliveira, Cinthia Vila Nova Santana, Gabriela Pimentel Pinheiro das Chagas, Camila Alexandrina Viana de Figueiredo, Ryan Dos Santos Costa","doi":"10.36416/1806-3756/e20250066","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>Given that b2 agonists constitute the primary treatment for asthma and that treatment response varies as a result of polymorphisms in the ADRB2 gene, we sought to investigate the associations between ADRB2 gene variants and bronchodilator response (BDR) in asthma patients.</p><p><strong>Methods: </strong>A genetic database comprising 813 individuals was analyzed for variants in the ADRB2 gene. A longitudinal analysis of severe asthma patients was performed to evaluate changes in BDR over time.</p><p><strong>Results: </strong>The rs1042713, rs1042714, and rs1042717 variants were associated with age-related changes in BDR in patients with severe asthma. The G allele (rs1042714) and the A allele (rs1042717) were associated with uncontrolled asthma, with carriers of the G46/G79/A252 alleles showing a higher risk of difficult-to-control asthma. Notably, no association was found between these variants and ADRB2 expression levels.</p><p><strong>Conclusions: </strong>Our findings suggest that a genetic panel including ADRB2 variants, as well as age-related differences in BDR, is a useful complementary tool in asthma management.</p>","PeriodicalId":14845,"journal":{"name":"Jornal Brasileiro De Pneumologia","volume":"51 4","pages":"e20250066"},"PeriodicalIF":3.0000,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12401121/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Jornal Brasileiro De Pneumologia","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.36416/1806-3756/e20250066","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"RESPIRATORY SYSTEM","Score":null,"Total":0}
引用次数: 0
Abstract
Objective: Given that b2 agonists constitute the primary treatment for asthma and that treatment response varies as a result of polymorphisms in the ADRB2 gene, we sought to investigate the associations between ADRB2 gene variants and bronchodilator response (BDR) in asthma patients.
Methods: A genetic database comprising 813 individuals was analyzed for variants in the ADRB2 gene. A longitudinal analysis of severe asthma patients was performed to evaluate changes in BDR over time.
Results: The rs1042713, rs1042714, and rs1042717 variants were associated with age-related changes in BDR in patients with severe asthma. The G allele (rs1042714) and the A allele (rs1042717) were associated with uncontrolled asthma, with carriers of the G46/G79/A252 alleles showing a higher risk of difficult-to-control asthma. Notably, no association was found between these variants and ADRB2 expression levels.
Conclusions: Our findings suggest that a genetic panel including ADRB2 variants, as well as age-related differences in BDR, is a useful complementary tool in asthma management.
期刊介绍:
The Brazilian Journal of Pulmonology publishes scientific articles that contribute to the improvement of knowledge in the field of the lung diseases and related areas.