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Association between diabetes and subsequent Parkinson disease: A record-linkage cohort study
Eduardo De Pablo-Fernandez1, Raph Goldacre1, Julia Pakpoor1
1From the Reta Lila Weston Institute of Neurological Studies, Department of Molecular Neurosciences (E.D.P.-F., A.J.N., T.T.W.), and Queen Square Brain Bank for Neurological Disorders (E.D.P.-F., T.T.W.), UCL Institute of Neurology, London; Unit of Health-Care Epidemiology (R.G., J.P.), Big Data Institute, Li Ka Shing Centre for Health Information and Discovery, Nuffield Department of Population Health, University of Oxford; and Preventive Neurology Unit (A.J.N.), Wolfson Institute of Preventive Medicine, Queen Mary University of London, UK.
Objective:
To investigate the association between type 2 diabetes mellitus (T2DM) and subsequent Parkinson disease (PD).
Methods:
Linked English national Hospital Episode Statistics and mortality data (1999-2011) were used to conduct a retrospective cohort study. A cohort of individuals admitted for hospital care with a coded diagnosis of T2DM was constructed, and compared to a reference cohort. Subsequent PD risk was estimated using Cox regression models. Individuals with a coded diagnosis of cerebrovascular disease, vascular parkinsonism, drug-induced parkinsonism, and normal pressure hydrocephalus were excluded from the analysis.
Results:
A total of 2,017,115 individuals entered the T2DM cohort and 6,173,208 entered the reference cohort. There were significantly elevated rates of PD following T2DM (hazard ratio [HR] 1.32, 95% confidence interval [CI] 1.29-1.35; p < 0.001). The relative increase was greater in those with complicated T2DM (HR 1.49, 95% CI 1.42-1.56) and when comparing younger individuals (HR 3.81, 95% CI 2.84-5.11 in age group 25-44 years).
Conclusions:
We report an increased rate of subsequent PD following T2DM in this large cohort study. These findings may reflect shared genetic predisposition and/or disrupted shared pathogenic pathways with potential clinical and therapeutic implications.
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