Abstract

Inflammatory Bowel Disease and Parkinson's Disease: A Nationwide Swedish Cohort Study

Weimers P1, Halfvarson J2, Sachs MC3, Saunders-Pullman R4, Ludvigsson JF5,6, Peter I7, Burisch J1, Olén O8,9,10. Inflamm Bowel Dis. 2018 May 16. doi: 10.1093/ibd/izy190. [Epub ahead of print]
 
     

Author information

1 Department of Gastroenterology, North Zealand University Hospital, Frederikssund, Denmark.

2 Department of Gastroenterology, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.

3 Unit of Biostatistics, Institute of Environmental Medicine, Stockholm, Sweden.

4 Department of Neurology, New York, USA.

5 Department Medical Epidemiology and Biostatistics, Stockholm, Sweden.

6 Department of Pediatrics, Örebro University Hospital, Örebro, Sweden.

7 Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, USA.

8 Clinical Epidemiology Unit, Department of Medicine Solna, Stockholm, Sweden.

9 Department of Pediatric gastroenterology and nutrition, Sachs' Children and Youth Hospital, Stockholm, Sweden.

10 Department of Clinical Science and Education Södersjukhuset, Karolinska Institutet, Stockholm, Sweden.

Abstract

BACKGROUND: Few studies have examined the association between inflammatory bowel disease (IBD) and Parkinson's disease (PD).

METHODS: To estimate the incidence and relative risk of PD development in a cohort of adult IBD, we included all incident IBD patients (n = 39,652) in the Swedish National Patient Register (NPR) between 2002 and 2014 (ulcerative colitis [UC]: n = 24,422; Crohn's disease [CD]: n = 11,418; IBD-unclassified [IBD-U]: n = 3812). Each IBD patient was matched for sex, age, year, and place of residence with up to 10 reference individuals (n = 396,520). In a cohort design, all incident PD occurring after the index date was included from the NPR. In a case-control design, all incident PD occurring before the index date was included. The association between IBD and PD and vice versa was investigated by multivariable Cox and logistic regression.

RESULTS: In IBD, there were 103 cases of incident PD, resulting in hazard ratios (HRs) for PD of 1.3 (95% confidence interval [CI], 1.0-1.7; P = 0.04) in UC, 1.1 (95% CI, 0.7-1.7) in CD, and 1.7 (95% CI, 0.8-3.0) in IBD-U. However, these effects disappeared when adjusting for number of medical visits during follow-up to minimize potential surveillance bias. In a case-control analysis, IBD patients were more likely to have prevalent PD at the time of IBD diagnosis than matched controls, with odds ratios of 1.4 (95% CI, 1.2-1.8) in all IBD patients, 1.4 (95% CI, 1.1-1.9) for UC, and 1.6 (95% CI, 1.1-2.3) for CD patients alone.

CONCLUSIONS: IBD is associated with an increased risk of PD, but some of this association might be explained by surveillance bias.

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