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Sleep apnea and the subsequent risk of Parkinson’s disease: a 3-year nationwide population-based study

Authors Chou PS, Lai CL, Chou YH, Chang WP

Received 9 February 2017

Accepted for publication 10 March 2017

Published 30 March 2017 Volume 2017:13 Pages 959—965

DOI https://doi.org/10.2147/NDT.S134311

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Amy Norman

Peer reviewer comments 2

Editor who approved publication: Professor Wai Kwong Tang


Ping-Song Chou,1 Chiou-Lian Lai,1–3 Yii-Her Chou,4,5,* Wei-Pin Chang6,*

1Department of Neurology, Kaohsiung Medical University Hospital, 2Department of Neurology, Faculty of Medicine, College of Medicine, 3Department of Neurology, Kaohsiung Municipal Hsiao-Kang Hospital, 4Department of Urology, Faculty of Medicine, College of Medicine, 5Department of Urology, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, 6School of Health Care Administration, Taipei Medical University, Taipei City, Taiwan

*These authors contributed equally to this work

Purpose: Sleep apnea (SA)-induced chronic intermittent hypoxia increases oxidative stress and inflammation, which may contribute to the pathophysiology of Parkinson’s disease (PD). This study evaluated the risk of PD following SA diagnosis.
Patients and methods: This was a 3-year nationwide population-based matched cohort study using claims data from the National Health Insurance Research Database (NHIRD), Taiwan. We analyzed 1,944 patients diagnosed as having SA between 1997 and 2005 and a matched cohort of 9,720 non-SA patients from the NHIRD. Patients with a history of PD were excluded. Each patient was followed up for 3 years to evaluate subsequent PD development.
Results: Of the 11,664 patients, 17 (0.9%) and 38 (0.4%) from the SA and matched non-SA cohorts, respectively, were subsequently diagnosed as having PD during follow-up. After adjustments for potential confounders, the SA cohort had a 1.85-fold higher risk of PD than the non-SA cohort (95% confidence interval [CI] =1.02–3.35; P=0.042). After age and sex stratification, PD development was independently associated with SA only in men (adjusted hazard ratio [HR], 2.26; 95% CI =1.11–4.63; P<0.05) and in patients aged ≥60 years (adjusted HR, 1.93; 95% CI =1.01–3.71; P<0.05).
Conclusion: Our study suggests that patients with SA are at an increased longitudinal risk of PD. Furthermore, age and male sex are independently associated with the risk of PD.

Keywords: cohort study, intermittent hypoxia, National Health Insurance Research Database, population-based study
 
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