4.7 Article

Autoimmune disease and risk for Parkinson disease A population-based case-control study

Journal

NEUROLOGY
Volume 73, Issue 18, Pages 1462-1468

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1212/WNL.0b013e3181c06635

Keywords

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Funding

  1. NIH [NINDS NS038367, NIEHS 5P01ES016732, NIEHS 1R01-ES013717, 1R03ES017139, R03 ES017119, R03 ES017314, ES013717]
  2. Department of Defense [X81XWH-071-0005]
  3. US EPA [R833629, 010003LA]
  4. HRSA [1R40MC08726]
  5. Danish Cancer Society
  6. EPA [R833629, 909253] Funding Source: Federal RePORTER

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Objective: Inflammatory mediators are increased in autoimmune diseases and may activate microglia and might cause an inflammatory state and degeneration of dopaminergic neurons in the brain. Thus, we evaluated whether having an autoimmune disease increases the risk for developing Parkinson disease (PD). Methods: A population based case-control study was conducted in Denmark of 13,695 patients with a primary diagnosis of PD recorded in the Danish National Hospital Register during the period 1986-2006. Each case was matched on year of birth and sex to 5 population controls selected at random from among inhabitants of Denmark who were alive at the date of the patient's diagnosis. The main exposure measure was a hospital diagnosis of 1 of 32 selected autoimmune diseases recorded 5 or more years before the index date in the files of the Danish Hospital Register. Results: We observed no overall association between a diagnosis of autoimmune disease and risk for subsequent PD (odds ratio 0.96, 95% confidence interval 0.85-1.08). In a subgroup of patients with autoimmune diseases with systemic involvement, primarily rheumatoid arthritis, we saw a decrease in risk for PD of 30%. Conclusions: Our results do not support the hypothesis that autoimmune diseases increase the risk for Parkinson disease. The decreased risk observed among patients with rheumatoid arthritis might be explained by underdiagnosis of movement disorders such as Parkinson disease in this patient group or by a protective effect of the treatment with anti-inflammatory drugs over prolonged periods. Neurology (R) 2009;73:1462-1468

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