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BSG 13 - 1365 Is there an Association between Parkinson’s Disease and IBD? M. W. Johnson, K. Lithgo, T. Price Gastroenterology Department, Luton & Dunstable University Hospital, Luton. LU40DZ. UK. Introduction Results Conclusions 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}. 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 proportion of PD patients having concomitant IBD is considerably higher than one would have expected by chance. This raises questions abount a possible shared aetiology. There are a variety of aetiological theories in IBD, that consider bacteria (or a change in the balance of mucosal adherent flora) to be a precipitating or aggrevating factor in the subsequent intra-mucosal inflammatory cascade. As the BRAAK theory states; it is possible that the initial insult in Parkinson’s disease may come from the translocation of bacteria (or pathogens) across the intestinal mucosal barrier. The breakdown in this barrier mechanism may be related to the two conditions having shared common genetic associations. Interestingly, those patients with more significant IBD also had more severe PD. Aims To assess whether there was a higher than expected association between inflammatory bowel disease (IBD) and Parkinson’s disease (PD). 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. 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 both 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-tomoderate IBD. Three of the PD patients were scored as having moderate-to-severe disease, and 2 of these also had moderate-to-severe IBD. Identifier A B C D E F PD Severity Moderate to serve Mild to moderate Moderate to serve Mild to moderate Mild to moderate Moderate to serve IBD Severity Moderate to severe Mild to moderate Mild to moderate Mild to moderate Mild to moderate Moderate to severe Table 1. Association between PK and IBD Disease Severity Scores References Lenardo, M. et al (2011) Autoimmune Diseases; Protein involved in Parkinson’s disease also regulates inflammatory bowel disease. Nature immunology (9). Parkinson’s disease foundation (2012) Common bacterium related to Parkinson’s disease. Parkinson’s disease foundation. Pierantozzi, M. et al (2006) Helicobacter pylori eradication and L-dopa absorption in patients PD and motor fluctuation. BMA Neurology: vol 66. 12 1824 – 1829. Rees, K et al (2011) Helicobacter pylori eradication for Parkinson’s disease. Wiley online library. [assess on: 09/2012] Schnabel, J. (2010) Does Parkinson’s disease start outside the brain? Schulz, J. et al (2006) Cycad toxins, helicobacter pylori and Parkinsonism: Cholesterol glucosides as the common denominator. Medline 66 (6) 1222-6.