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Background Anti-TNF exposure has been linked to demyelination events. We sought to describe the clinical features of demyelination events following anti-TNF treatment and to test whether affected patients were genetically predisposed to multiple sclerosis [MS]. Methods We conducted a case-control study to describe the clinical features of demyelination events following anti-TNF exposure. We compared genetic risk scores [GRS], calculated using carriage of 43 susceptibility loci for MS, in 48 cases with 1219 patients exposed to anti-TNF who did not develop demyelination. Results Overall, 39 [74%] cases were female. The median age [range] of patients at time of demyelination was 41.5 years [20.7–63.2]. The median duration of anti-TNF treatment was 21.3 months [0.5-99.4] and 19 [36%] patients were receiving concomitant immunomodulators. Most patients had central demyelination affecting the brain, spinal cord, or both. Complete recovery was reported in 12 [23%] patients after a median time of 6.8 months [0.1–28.7]. After 33.0 months of follow-up, partial recovery was observed in 29 [55%] patients, relapsing and remitting episodes in nine [17%], progressive symptoms in three [6%]: two [4%] patients were diagnosed with MS. There was no significant difference between MS GRS scores in cases (mean -3.5 × 10–4, standard deviation [SD] 0.0039) and controls [mean -1.1 × 10–3, SD 0.0042] [p = 0.23]. Conclusions Patients who experienced demyelination events following anti-TNF exposure were more likely female, less frequently treated with an immunomodulator, and had a similar genetic risk to anti-TNF exposed controls who did not experience demyelination events. Large prospective studies with pre-treatment neuroimaging are required to identify genetic susceptibility loci.

Background Standardizing care through pathways has the potential to reduce emergency department (ED) utilization. We developed and evaluated inflammatory bowel disease (IBD) care pathways for that purpose. Methods Over 2014–2016, IBD patients were retrospectively stratified into those managed and not managed by pathways. Patient data were extracted, and negative binomial regression used to predict the annual number of ED visits. Results There was a difference of 30.7 ED visits/100 patients between managed and nonmanaged at 12 months (P < 0.001). The incidence rate ratio of total ED visits occurring annually was 0.750 (P = 0.008). Conclusions Management with IBD care pathways reduces ED utilization.

Background Variation in clinical practice exists in many aspects of inflammatory bowel disease (IBD) care. Our aim was to develop a comprehensive set of quality indicators (QIs) to be measured in view of improving the quality of IBD care provided in clinical practice. This initiative was part of a global Canadian quality initiative PACE (Promoting Access and Care through Centres of Excellence). Methods A modified RAND appropriateness method was used to identify and rate structure, process, outcome, and patient-derived QIs of IBD care. The process included a comprehensive literature search yielding a broad list of QIs, the online selection of QIs by a core expert panel, the selection of patient-derived QIs from 4 patient focus groups, and the subsequent selection of QIs by a multidisciplinary panel, followed by a moderated in-person multidisciplinary meeting during which each indicator was rated for importance and feasibility of measurement. Predetermined cutoffs for mean score and degree of disagreement were used to select the final list of QIs. Results Forty-five QIs, including 6 that were patient-derived, were selected. Nine structure QIs addressed aspects related to the services and specialist care offered at an IBD unit or clinic. Thirty process indicators included administrative and workflow processes, features related to IBD therapy, surveillance, vaccination, and risk management. Six outcome QIs included measures of healthcare utilization, steroid use, and patient satisfaction. Conclusions Forty-five QIs including patient-derived indicators were selected through an iterative process. These indicators can be used to measure and improve the quality of care provided to IBD patients. 10.1093/ibd/izy259_video1izy259.video15828250213001.

BACKGROUND: Primary sclerosing cholangitis (PSC) is a chronic cholestatic liver disease affecting bile ducts leading to cirrhosis and end-stage liver disease. Liver transplant is the only effective treatment however 6–59% of those transplanted develop recurrent PSC (rPSC). Many risk factors for recurrence have been proposed yet only the presence of ulcerative colitis has been validated in multiple studies. We hypothesized patients who develop rPSC have elevated liver tests within the first year following transplant, as previously observed with recurrent hepatitis C and recurrent autoimmune hepatitis. AIMS: To determine if elevated liver tests within 1 year of transplant predicts rPSC. METHODS: PSC patients who underwent liver transplant at the University of Alberta Hospital from 1991 to 2015 were included. Recurrent PSC was defined by cholangiography and/or histological findings. Recurrence free survival and graft loss was compared between patients with and without rPSC. Liver tests including alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and bilirubin were assessed at 3, 6, 9, and 12 months after liver transplant. Abnormal liver tests were defined as values above the ULN for ALT, AST and bilirubin or 1.5XULN for ALP. RESULTS: One hundred and thirty-one patients were included. Mean transplant age was 43 years with 98 (75%) males and rPSC occurred in 40/131 (30%) patients. Mean recurrence time was 70 months (4 to 172 months) with rPSC rates of 4% and 20%, at 1 and 5 years, respectively. Median survival time was similar between rPSC and non-rPSC (132 ± 11 vs 175 ± 13 months, P=0.28). Mean time to graft loss was lower in those with rPSC (109 ± 12 vs 180 ± 13 months, P=0.003). Recurrent PSC patients with AST and ALT≥ULN at 12 months had disease recurrence occur earlier than those with normal AST and ALT (19 ± 17 vs 78 ± 50 months, P=0.001) and rPSC developed sooner in patients with ALP≥1.5XULN and ALT≥ULN at 6, 9, and 12 months inclusive (13 ± 4 vs 66 ± 51months, P=0.001). Multiple liver test abnormalities were identified that predict the development of rPSC (see table). CONCLUSIONS: Post-transplant abnormal hepatocellular and cholestatic biochemical liver tests within the 1(st) year or transplant predicts rPSC. FUNDING AGENCIES: None