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PWE-096 Is there an Association Between Parkinson’S Disease and Inflammatory Bowel Disease ?
  1. M W Johnson1,
  2. K Lithgo1,
  3. T Price1
  1. 1Gastroenterology, Luton & Dunstable University Hospital, Luton, UK

Abstract

Introduction The BRAAK theory of Parkinson’s disease believes that the aetiology may all start in the bowel with a “slow virus” entering the central nervous system after passing through the intestinal mucosa {Hawkes C.H., 2007}. There is already work confirming an increased frequency of H. pylori infections (requiring treatment) in the 5 years prior to Parkinson’s disease being diagnosed {Nielsen H.H. 2012}. Recently a gene associated with the inherited form of Parkinson’s disease (leucine-rich repeat kinase 2 - LRRK2), has been shown to regulate the transcription factor NFAT1 (nuclear factor of activated T cells 1), which in turn appears to regulate cells in the immune system, including macrophages, dendritic cells and T cells. Higher quantities of NFAT1 activity are seen in the colonic mucosa of Crohn’s patients, where the total quantity directly correlates to the severity of the disease {Liu Z., 2011}. Objective: With these theories in mind, we aimed to assess whether a higher than expected association between inflammatory bowel disease (IBD) and Parkinson’s disease (PD) could be found.

Methods A cross correlation analysis was performed using the IBD and PD databases at the Luton & Dunstable University Hospital. A retrospective analysis was also performed using medical notes and the internal electronic results system to assess the disease severity of these two conditions.

Results The prevalence of IBD and PD within the UK population is said to be 225/100,000 (UC 150/100,000 + CrD 75/100,000) and 140/100,000, respectively. The L&D catchment area covers 330,000 and so one would have expected approximately 742 IBD and 462 PD patients, respectively. The databases had 2783 IBD patients (median age = 51) and 350 PD patients (median age = 79) listed. Probability analysis predicted that we would find just 1 patient with concomitant PK and IBD, however, we found 6 subjects with these conditions concomitantly. This translates into 0.2% of IBD patients having PD and 1.72% of PD patients having IBD. Mild-to-moderate PD was noted in 3 patients, and all 3 had mild-to-moderate IBD. Three of the PD patients were scored as having moderate-to-severe disease, and 2 of these also had moderate-to-severe IBD.

Conclusion The proportion of PD patients having concomitant IBD is considerably higher than one would have expected by chance. This raises possible issues around genetic association, but also lends some credence to theories that PD may owe its origins to the bowel and infective translocation across bowel mucosa. Those patients with more significant IBD also appeared to have more severe PD.

Disclosure of Interest None Declared.

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