Yueh-Feng Sung1, Feng-Cheng Liu2, Chun-Chieh Lin1, Jiunn-Tay Lee1, Fu-Chi Yang1, Yu-Ching Chou3, Cheng-Li Lin4, Chia-Hung Kao5, Hsin-Yi Lo6, Tse-Yen Yang7. 1. Department of Neurology, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan. 2. Rheumatology/Immunology and Allergy, Department of Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan. 3. School of Public Health, National Defense Medical Center, Taipei, Taiwan. 4. School of Medicine, Graduate Institute of Clinical Medical Science and School of Medicine, College of Medicine, China Medical University, Taichung, Taiwan; Department of Nuclear Medicine and PET Center, China Medical University, Taichung, Taiwan; Department of Bioinformatics and Medical Engineering, Asia University, Taichung, Taiwan; Management Office for Health Data, China Medical University Hospital, Taichung, Taiwan. 5. Department of Nuclear Medicine and PET Center, China Medical University Hospital, Taichung, Taiwan; Graduate Institute of Clinical Medicine Science and School of Medicine, College of Medicine, China Medical University, Taichung, Taiwan. 6. Graduate Institute of Chinese Medicine, China Medical University, Taichung, Taiwan. 7. Molecular and Genomic Epidemiology Center, and Department of Medical Laboratory Science and Biotechnology, China Medical University, Taichung, Taiwan. Electronic address: yang_t_y@yahoo.com.tw.
Abstract
OBJECTIVE: To investigate the association between rheumatoid arthritis (RA) and the risk of developing Parkinson disease (PD). PATIENTS AND METHODS: This retrospective cohort study was conducted from January 1, 1998, through December 31, 2010, using data from the Taiwan National Health Insurance Research Database. We identified 33,221 patients with newly diagnosed RA and 132,884 randomly selected age- and sex-matched patients without RA. A multivariable Cox proportional hazards regression model was used to evaluate the risk of developing PD in the RA cohort. RESULTS: The multivariable Cox proportional hazards regression analysis revealed an adjusted hazard ratio of 0.65 (95% CI, 0.58-0.73) for the development of PD in the RA cohort relative to the non-RA cohort. The cumulative incidence of PD was 2.42% lower in the RA cohort than in the non-RA cohort. The risk reduction of PD development in patients affected with RA was independent of treatment with disease-modifying antirheumatic drugs (DMARDs); subgroup analysis of patients treated with biologic DMARDs revealed further risk reduction (adjusted hazard ratio, 0.57; 95% CI, 0.41-0.79). CONCLUSION: Patients with RA have a reduced risk of developing PD. This risk reduction was independent of treatment with DMARDs; however, biologic DMARDs appear to further reduce this risk. Further research is necessary to explore the underlying mechanism.
OBJECTIVE: To investigate the association between rheumatoid arthritis (RA) and the risk of developing Parkinson disease (PD). PATIENTS AND METHODS: This retrospective cohort study was conducted from January 1, 1998, through December 31, 2010, using data from the Taiwan National Health Insurance Research Database. We identified 33,221 patients with newly diagnosed RA and 132,884 randomly selected age- and sex-matched patients without RA. A multivariable Cox proportional hazards regression model was used to evaluate the risk of developing PD in the RA cohort. RESULTS: The multivariable Cox proportional hazards regression analysis revealed an adjusted hazard ratio of 0.65 (95% CI, 0.58-0.73) for the development of PD in the RA cohort relative to the non-RA cohort. The cumulative incidence of PD was 2.42% lower in the RA cohort than in the non-RA cohort. The risk reduction of PD development in patients affected with RA was independent of treatment with disease-modifying antirheumatic drugs (DMARDs); subgroup analysis of patients treated with biologic DMARDs revealed further risk reduction (adjusted hazard ratio, 0.57; 95% CI, 0.41-0.79). CONCLUSION:Patients with RA have a reduced risk of developing PD. This risk reduction was independent of treatment with DMARDs; however, biologic DMARDs appear to further reduce this risk. Further research is necessary to explore the underlying mechanism.
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