147 Does Persistent Stress Impact Quality of Life and Disease Course in Patients With IBD? A 4 Year Prospective Study

147 Does Persistent Stress Impact Quality of Life and Disease Course in Patients With IBD? A 4 Year Prospective Study

IBD patients using the IBD-DI and to identify associated factors. Patients and Methods: From February 1st 2012 to 31st March 2014, the questionnaire w...

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IBD patients using the IBD-DI and to identify associated factors. Patients and Methods: From February 1st 2012 to 31st March 2014, the questionnaire was administered to a random sample of 200 adult patients with an established diagnosis of IBD for at least 3 months. This random sample was selected among a well-defined population-based registry in France. The IBD-DI consists of 28 items covering the 4 domains of Body Functions, Activity Participation, Body Structures and Environmental Factors. The steps of the quantitative validation included Item quality, factorial validity, internal and external consistency, inter and intra-observer reproducibility. Socio demographic and clinical associated factors were assessed using a multivariate regression. Clinical variables according to the Montreal classification and disease activity according to HBI and partial Mayo scores were recorded at the time of interview. Results: A total of 150 CD patients and 50 UC completed the validation phase of the IBD-DI. Intraclass correlation was 0.9 and Cronbach's alpha of internal consistency was 0.86. IBD-DI correlated with IBDQ (-0.82; p<10-3) and SF36 (0.61 for physical and -0.71 for Mental; p<0.05). IBD-DI score varied from 0 to 100 (higher is the IBD-DI higher is the disability) with a mean at 35.3±20.5 without any difference between CD and UC (33.9±19.5 in CD vs 39.2±23.1 in UC; p=0.12). The only factor independently associated with higher IBD-DI in both CD and UC was the female gender. The IBD-DI was associated with increased clinical disease activity (p<10-4) in CD, while a trend was observed in UC (p=0.06). Conclusions: The IBD-DI is reliable and reproducible for measuring disability status in IBD. It comprises 19 questions and it ranges from 0 to 100. The mean disability score was 35, it correlated with clinical disease activity and was associated with female gender in this population-based cohort. This validated index and its scoring system can now be used in cohort studies and clinical trials. (1) Peyrin-Biroulet et al. Gut 2012;61:241-7

147 Does Persistent Stress Impact Quality of Life and Disease Course in Patients With IBD? A 4 Year Prospective Study Claudia Ramos Rivers, Eva Szigethy, Kimberly Baker, Jana G. Hashash, Michael A. Dunn, Miguel Regueiro, Arthur Barrie, Marc Schwartz, Jason M. Swoger, Leonard Baidoo, David G. Binion Introduction: Inflammatory bowel diseases (IBD) are lifelong immunologic conditions with a waxing and waning clinical course. IBD flares can increase perceived stress and likewise, perceived stress from exogenous sources has been hypothesized to contribute to disease flares. We sought to characterize persistent stress over time in IBD patients and its association with quality of life (QoL) and disease course over a 4 year period. Methods: IBD patients followed over 4 consecutive years from a consented, prospective research registry were identified. QoL was measured using short inflammatory bowel disease questionnaire (SIBDQ) scores obtained at the time of clinic visits. The sub score from SIBDQ question #8 ( How often during the last 2 weeks have you felt relaxed and free of tension? ) was used to gauge selfperceived stress. This 7 point Likert scale was prospectively validated using the Perceived Stress Scale. A mean stress score for each calendar year was created. Mean scores 1-3 were considered positive for stress; while mean scores 4 - 7 defined the negative stress group. Patients were dichotomized into 2 categories based on annual patterns of mean stress score; sporadic stress (0- 1 year with stress) and persistent stress (3- 4 years with stress). We compared QoL scores (SIBDQ), disease activity scores (Harvey Bradshaw (HB) and UCAI) and presence of inflammation (any C reactive protein (CRP) elevation over the calendar year) for sporadic and persistent stress groups. Results: 260 IBD patients were analyzed (40.8% male; mean age 43.7±14.5y; 69% Crohn's disease, 31% UC). Persistent stress was identified in 53.8% of pts. There was no difference in age, gender and disease duration between patients with sporadic and persistent stress. CD was associated with more persistent stress 58.7% compared to UC 42.5%; p<0.02. In 2010, patients with persistent stress had lower QoL and higher disease activity compared with sporadic stress (mean SIBDQ 41.1±9.5 vs. 56.5±9.6; p=0.0001 and median HB 5.2 vs.7 and UCAI 1.3 vs.1.8; <0.0001/ 0.0001). Active inflammation was associated with further negative impact on quality of life in patients with persistent stress but not in patients with sporadic stress. Similar results were found for the other 3 years. During the 4 years, patients with persistent stress had significantly more clinic visits, phone call utilization, ED visits and hospitalization rates vs. patients with sporadic stress. Conclusions: Persistent stress over time negatively impacts QoL and disease course in IBD patients. Active inflammation has a greater negative impact on QoL in IBD patients with persistent stress compared to those with sporadic stress. These data suggest a need to help develop coping mechanisms for persistent stress in IBD patients in order to optimize clinical outcomes. Impact of inflammation on QoL and disease activity

Figure 1: Th2 predominant Balb/c but not Th1 predominant C57BL6 develop visceral hypersensitivity upon oral re-challenge with the bystander antigen OVA. {BR}Data are shown for both Balb/c (A) and C57BL6 (B) mice. Oral feeding with OVA at week 5 postinfection induces VHS in Balb/c but not in C57Bl6 mice. Uninfected control mice are shown in blue full lines, infected mice are shown in red dashed lines. The visceromotor response is expressed as area under the curve (relative to the maximum pain at baseline VMR recording) ± SEM. The X-axis shows the protocol in time. Statistical analysis was performed by 2-way ANOVA, ** p < 0.01, *** p < 0.001.

146 Validation of the Inflammatory Bowel Disease Disability Index in a Population-Based Cohort Corinne Gower-Rousseau, Hélène Sarter, Noemie Tavernier, Guillaume Savoye, Mathurin Fumery, Alain Duhamel, Nathalie Guillon, Alarcos Cieza, Jean-Frederic Colombel, Laurent Peyrin-Biroulet

Health care utilization over 4 years

Inflammatory bowel diseases (IBD) are chronic disabling conditions influencing physical, psychological, familial and social dimensions of life and may result in disability. Recently, an international collaborative effort led to the development of the first IBD Disability Index (IBD-DI) according to the WHO classification (1). The aims of this prospective study were: 1. To validate the IBD-DI in an independent cohort of IBD patients; 2. To develop a scoring system for the IBD-DI to be used in clinical trials and cohort studies; 3. To assess for the first time disability status among a well-defined population-based cohort of French

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in infected or control mice exposed to OVA 2 weeks before s.c. OVA immunization. To check for oral tolerance, footpad swelling to OVA challenge s.c and diarrhea development after oral OVA re-challenge were evaluated. RESULTS: Infection with C. rodentium induced VHS 2 weeks PI recovering to normal within 4 weeks PI in Balb/c mice. Of note however, VHS was re-installed by oral feeding of OVA (week 5) in infected Balb/c but not C57Bl6 mice compared to uninfected controls (Fig. 1), indicating loss of tolerance against OVA in infected Balb/c mice. In line, s.c. OVA resulted in footpad swelling in infected immunized mice while oral OVA re-challenge resulted in diarrhea in infected immunized Balb/c but not C57BL6 mice. CONCLUSION: Our data show that infection with C. rodentium prevents the induction of oral tolerance and triggers the induction of an immune response to the "innocent" bystander antigen OVA. Re-exposure to this antigen in the PI phase results in reactivation of this immune response leading to VHS in mice with a Th2 genetic background. Based on these data, we propose that this mechanism may contribute to the development of post-infectious IBS, especially in Th2 prone individuals.