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Alpha-1 Antitrypsin Deficiency and Tobacco Smoking: Exploring Risk Factors and Smoking Cessation in a Registry Population.
Franciosi, Alessandro N; Alkhunaizi, Mansour A; Woodsmith, Andrew; Aldaihani, Layali; Alkandari, Hamad; Lee, Siobhán E; Fee, Laura T; McElvaney, Noel G; Carroll, Tomás P.
Afiliação
  • Franciosi AN; Department of Medicine, Beaumont Hospital, Dublin, Ireland.
  • Alkhunaizi MA; Irish Centre for Genetic Lung Disease, RCSI Education and Research Centre, Beaumont Hospital, Dublin, Ireland.
  • Woodsmith A; Royal College of Surgeons in Ireland, Dublin, Ireland.
  • Aldaihani L; Royal College of Surgeons in Ireland, Dublin, Ireland.
  • Alkandari H; Royal College of Surgeons in Ireland, Dublin, Ireland.
  • Lee SE; Royal College of Surgeons in Ireland, Dublin, Ireland.
  • Fee LT; Alpha-1 Foundation Ireland.
  • McElvaney NG; Irish Centre for Genetic Lung Disease, RCSI Education and Research Centre, Beaumont Hospital, Dublin, Ireland.
  • Carroll TP; Alpha-1 Foundation Ireland.
COPD ; 18(1): 76-82, 2021 02.
Article em En | MEDLINE | ID: mdl-33557645
The ZZ genotype of alpha-1 antitrypsin deficiency (AATD) is strongly associated with COPD, even in never-smokers. Moderate AATD genotypes (MZ and SZ) have been shown to increase the severity of COPD in smokers. In this comparative study, we examine the association between AATD, genotypes, and smoking cessation. Two hundred and ninety-three Irish people with AATD [MZ (n = 91), SZ (n = 72), and ZZ/rare (n = 130)] completed a custom questionnaire assessing their social and smoking histories. The primary outcomes analyzed were the predictors of ever-smoking and effect of genotype on awareness of AATD and maintained smoking cessation, using logistic regression analyses. Parental smoking exposure was associated with ever-smoking status (OR 1.84 vs. no parental smoking, p = 0.018), higher cumulative tobacco consumption (23.47 vs. 14.87 pack-years, p = 0.005) and more quit attempts required to achieve cessation among former-smokers (2.97 vs. 5.60, p = 0.007). Awareness of genotype was 67.7% versus 56.3% versus 33% for ZZ, SZ, and MZ, respectively (p < 0.001). Among ever-smokers, current-smoking was uncommon (2.5% vs. 17% vs. 16% for ZZ, SZ, and MZ, respectively, p = 0.009) with ZZs significantly less likely to be current-smokers (OR 0.15 relative to MZ, p = 0.025). These results suggest that the genetic risk of COPD in AATD families is compounded by transmission of social risk factors (via parental smoking). Increasing severity of genotype is associated with lower current-smoking rates among ever-smokers. Whether this is attributable to greater awareness of risk is an area of interest. Achieving a change in smoking habits may also result in positive health behavior in subsequent generations.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Abandono do Hábito de Fumar / Deficiência de alfa 1-Antitripsina Tipo de estudo: Etiology_studies / Prognostic_studies / Risk_factors_studies Limite: Humans Idioma: En Ano de publicação: 2021 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Abandono do Hábito de Fumar / Deficiência de alfa 1-Antitripsina Tipo de estudo: Etiology_studies / Prognostic_studies / Risk_factors_studies Limite: Humans Idioma: En Ano de publicação: 2021 Tipo de documento: Article