TY - JOUR
T1 - Association between use of ß2-adrenergic receptor agonists and incidence of Parkinson’s disease
T2 - Retrospective cohort analysis
AU - Nadeem, Hasan
AU - Zhou, Bo
AU - Goldman, Dana
AU - Romley, John
N1 - Funding Information:
Research reported in this publication was supported by a grant from the National Institute on Aging of the National Institutes of Health under Award number P30AG024968 (DG). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Publisher Copyright:
Copyright: © 2022 Nadeem et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
PY - 2022/11
Y1 - 2022/11
N2 - Introduction Previous observational studies assessing β2-agonist/-antagonist use on PD risk have yielded conflicting results. We evaluated the relationship between β2-agonist use and the incidence of Parkinson’s disease in patients with chronic lung disease. Methods We performed a retrospective cohort analysis on a 20% random sample abstracted from a traditional (fee-for-service) Medicare program in the United States. Inclusion criteria were individuals over 65 years old diagnosed with asthma, COPD, and/or bronchiectasis who were enrolled in a prescription drug (standalone Part D) plan over 2007–2010 and alive through 2014. The main outcome measure was a diagnosis of Parkinson’s disease over the period 2011–2014, in relation to the number of 30-day-equivalent drug claims over 2007–2010. Logistic regression analysis was performed on a sample including 236,201 Medicare beneficiaries. Results The sample was 68% female, 80% white, and on average 77 years old as of 2010. Compared to non-users, β2-agonist users were more likely to be younger (76.3y versus 78.0y), smokers (40.4% versus 31.1%) and asthmatic (62.4% versus 28.3%). The odds ratio for a β2-agonist claim on PD development was 0.986 (95% CI 0.977–0.995) after adjusting for demographics, smoking history, respiratory exacerbations, comorbidities, and other drug use. Risk reductions were larger for males than females (0.974 versus 0.994, P = 0.032), and for individuals with COPD compared to those with asthma (0.968 versus 0.998, P = 0.049). Reverse causality was addressed with a Cox analysis that allowed β2-agonist use to vary from medication initiation to disease onset. By the end of the follow-up period, β2-agonist use was shown to be associated with a true protective effect against PD onset. Discussion β2-agonist use is associated with decreased risk of PD incidence. Further investigation, possibly including clinical trials, is warranted to strengthen the evidence base supporting clinical decision-makers looking to repurpose pharmaceuticals to prevent neurodegenerative disease onset.
AB - Introduction Previous observational studies assessing β2-agonist/-antagonist use on PD risk have yielded conflicting results. We evaluated the relationship between β2-agonist use and the incidence of Parkinson’s disease in patients with chronic lung disease. Methods We performed a retrospective cohort analysis on a 20% random sample abstracted from a traditional (fee-for-service) Medicare program in the United States. Inclusion criteria were individuals over 65 years old diagnosed with asthma, COPD, and/or bronchiectasis who were enrolled in a prescription drug (standalone Part D) plan over 2007–2010 and alive through 2014. The main outcome measure was a diagnosis of Parkinson’s disease over the period 2011–2014, in relation to the number of 30-day-equivalent drug claims over 2007–2010. Logistic regression analysis was performed on a sample including 236,201 Medicare beneficiaries. Results The sample was 68% female, 80% white, and on average 77 years old as of 2010. Compared to non-users, β2-agonist users were more likely to be younger (76.3y versus 78.0y), smokers (40.4% versus 31.1%) and asthmatic (62.4% versus 28.3%). The odds ratio for a β2-agonist claim on PD development was 0.986 (95% CI 0.977–0.995) after adjusting for demographics, smoking history, respiratory exacerbations, comorbidities, and other drug use. Risk reductions were larger for males than females (0.974 versus 0.994, P = 0.032), and for individuals with COPD compared to those with asthma (0.968 versus 0.998, P = 0.049). Reverse causality was addressed with a Cox analysis that allowed β2-agonist use to vary from medication initiation to disease onset. By the end of the follow-up period, β2-agonist use was shown to be associated with a true protective effect against PD onset. Discussion β2-agonist use is associated with decreased risk of PD incidence. Further investigation, possibly including clinical trials, is warranted to strengthen the evidence base supporting clinical decision-makers looking to repurpose pharmaceuticals to prevent neurodegenerative disease onset.
UR - http://www.scopus.com/inward/record.url?scp=85142939928&partnerID=8YFLogxK
U2 - 10.1371/journal.pone.0276368
DO - 10.1371/journal.pone.0276368
M3 - Article
C2 - 36441791
AN - SCOPUS:85142939928
SN - 1932-6203
VL - 17
JO - PLoS ONE
JF - PLoS ONE
IS - 11 November
M1 - e0276368
ER -