Introduction: Inflammatory bowel disease (IBD) and Parkinson’s disease (PD) are chronic progressive disorders that mainly affect different organs: the gut and brain, respectively. Increasing evidence supports reciprocal communication between the enteric and the central nervous system in disease, termed the 'gut-brain axis'. Biologics have been shown to decrease inflammation among IBD patients however the long-term neurological implications remain unclear. We sought to compare the prevalence of PD among individuals with or without IBD and to assess whether PD risk among patients with IBD is altered by biologics therapy. Methods: We used the IBM Explorys clinical database which includes over 74 million de-identified unique patients across 300 hospitals in the United States. Patient were identified using SNOMED and ICD codes. We identified all patients (age >18 years) who were diagnosed with either Crohn’s disease (CD) or ulcerative colitis (UC). We investigated the prevalence of PD in IBD patients compared to patients with no IBD. Also, we compared the prevalence of PD between IBD patients with and without anti-TNF therapy. Odds ratios with 95% confidence intervals were calculated to evaluate the risk of PD. Results: We identified 249,480 patients with CD and 209,030 patients with UC, of whom 7,180 (2.88%) and 2,700 (1.29%) developed PD, respectively compared to 0.37% in individuals without IBD, (Table) p< 0.0001 to all. Both CD [OR: 7.91; 95% CI: 7.73-8.10] and UC [OR: 3.44; 95%CI: 3.31-3.57] patients had a significantly higher risk of PD compared to patients without IBD. 45,030 (18.0%) patients with CD and 23,110 (11.1%) patients with UC received biologics therapy. Sub-group analysis of the biologics-treated cohort was associated with a significantly lower risk of developing PD in CD [OR: 0.13; 95%CI: 0.11-0.13] and UC [OR: 0.40; 95%CI: 0.34-0.49], respectively (Figure). Conclusion: In this large retrospective study, we found that the prevalence of PD in patients with IBD was significantly higher than the general population. Furthermore, we found that IBD patients treated with biologics were significantly less likely to be diagnosed with PD. These findings may support a role of systemic inflammation in the pathogenesis of both diseases. Further studies are required to determine whether biologics therapy may mitigate PD risk.Figure 1.: Logistic Regression of Parkinson’s disease Risk in IBD, IBD; inflammatory bowel disease. Immunomodulators included Azathioprine, Methotrexate and Mercaptopurine. Other biologics included Natalizumab, Ustekinumab and Vedolizumab. TNF-a Blockers; tumor necrosis factor-alpha blocker. Table 1. - Demographics of patients with IBD and PD Variable Patients with PD No PD With IBD Without IBD N 9050 259900 70129700 18-65 3310 (36.6%) 26610 (10.2%) 47,919,160 (68.3%) >65 5600 (61.9%) 226030 (87.0%) 21,034,720 (30.0%) Female 5210 (57.6%) 112100 (43.1%) 38,353,970 (54.7%) Caucasian 7710 (85.2%) 200420 (77.1%) 37,649,020 (53.7%) T2DM 3160 (34.9%) 74510 (28.7%) 5,575,570 (8.0%) Primary HTN 6200 (68.5%) 174330 (67.1%) 14,014,310 (20.0%) Hyperlipidemia 7700 (85.1%) 144590 (55.6%) 11,635,480 (16.6%) Obesity 2700 (29.8%) 36170 (13.9%) 5,404,010 (7.7%) Tobacco Abuse 3710 (41.0%) 22280 (8.6%) 3,789,760 (5.4%) Cannabis Abuse 280 (3.1%) 1540 (0.6%) 528,780 (0.75%) Alcohol Abuse 670 (7.4%) 6530 (2.5%) 1,083,540 (1.55%) Carbidopa-levodopa 2030 (22.4%) 130470 (50.2%) NA Dopamine agonists 2470 (27.3%) 145230 (55.9%) NA MAO-B inhibitors 310 (3.4%) 22630 (8.7%) NA IBD; inflammatory bowel disease, PD; Parkinson’s disease, T2DM; type 2 diabetes mellitus; HTN; hypertension, MAO-B inhibitors; mono-amine oxidase B inhibitors.
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