AG

AA

bst

ract

swas identified in an additional 43.3% of patients at year 0 and 31.5% at year 5. Majorpolypharmacy at year 0 was associated with increasing age (44.3 versus 37.3, p <0.001),disability (14.3% versus 5.1%, p = 0.016), functional GI disorders (15. 0% versus 6.0 %,p = 0.021) and psychiatric disease (44.4% versus 12.1%, p<0.001). Major polypharmacywas associated with significantly higher use rates of certain drug classes, including vitaminsand minerals (74.2% versus 47.0%, p < 0.001), GI symptomatic drugs (63.6% versus 35.9%,p < 0.001), neuropsychiatric medications (44.7% versus 13.7%, p < 0.001), cardiovascularmedications (38.6% versus 8.5%, p < 0.001), and narcotic analgesics (22.1% versus 6.8%,p < 0.001). Over 5 years of follow up, major polypharmacy was not associated with significantdifferences in the risk of disease flares (61.7 versus 58.9%, p=0.78), therapy escalation (27.8versus 34.0%, p=0.22), IBD-related hospitalization (39.7 versus 41.4%, p = 0.79), or IBD-related surgery (25.0% versus 28.2%, p = 0.57). CONCLUSIONS: In this cohort, polyphar-macy was present in a substantial proportion of patients with Crohn's disease. Major polyphar-macy was associated with increasing age, disability, functional GI disorders, and concomitantpsychiatric disease. Over 5 years of follow up, patients with major polypharmacy did nothave significant differences in the risk of disease flares, therapy escalation, IBD-relatedhospitalization, or IBD-related surgery.

Su1357

Non-Surgical Porto-Mesenteric Vein Thrombosis Is Associated With WorseOutcomes in Inflammatory Bowel DiseasesZubin Arora, Xianrui Wu, Udayakumar Navaneethan, Bo Shen

Introduction: Porto-mesenteric vein thrombosis (PVT) is a well recognized complication ininflammatory bowel disease (IBD) patients after intra-abdominal/pelvic surgery, which wasnot shown to be associated with a worse clinical outcome. However, the impact of non-surgery-related PVT on the outcome of IBD has not been systematically studied. Aim: Toevaluate risk factors for non-surgery-related PVT in IBD patients and the impact of PVT onthe outcome of IBD. Methods: In this case-control study, we searched and identified IBDpatients with one or more abdominal imaging indicative of PVT and no history of intra-abdominal surgery in the preceding 3 months (n=20) from January 2004 to October 2013.The patients were matched for age, sex, and phenotype with IBD controls who had no PVTon abdominal imaging and no prior history of PVT (n=60). Patients with cirrhosis, primarysclerosing cholangitis, and malignancy were excluded. Subsequent IBD-related ER visit,hospital admission or surgery within 12 months after diagnosis of PVT was the primaryoutcome. Univariate and multivariate analyses were performed. Results: Of the 20 patientsin the study group, 6 (30%) had ulcerative colitis and 14 (70%) had Crohn's disease and11 (55%) were male. There were no significant differences in IBD duration, body massindex, smoking, oral contraceptive use, NSAID use, extra-intestinal manifestations, diseaseactivity or symptomatology between the study and control groups. The risk factors associatedwith the development of PVT are listed in Table 1. Hypercoagulability workup was availablein 11 patients in the study group out of which 5 (45.4%) tested positive. 13 (65%) patientswere treated with anticoagulation therapy. Warfarin was used for anticoagulation in 10(76.9%) and subcutaneous low molecular weight heparin was used in 3 (23.1%) patients.When treated, the duration of anticoagulation was 6 months in 10 (76.9%) patients, 12months in 2 (15.4%) patients, and lifelong therapy was initiated in 1 (7.7%) patient. At 1-year follow-up, PVT patients were more likely to require corticosteroids (47.4% vs. 23.3%,p=0.04), have an IBD-related emergency room visit (26.3% vs. 1.7%, p=0.003), requirehospitalization for medical management (60.0% vs. 20.0%, p=0.001) or undergo IBD relatedsurgery (65.0% vs. 26.7%, p=0.003), than the non-PVT controls. There was no statisticaldifference in rate of poor outcomes between patients who received anticoagulation and thosewho did not (92.3% vs. 71.4%, p=0.27). The risk factors associated with poor diseaseoutcome (requirement of corticosteroids, ER visit, hospitalization, and surgery) are listed inTable 2. Conclusions: Corticosteroid use in the last 6 months and hospital admission areassociated with the development of PVT. The presence of PVT, in addition to other traditionalfactors, is associated with poor clinical outcome in IBD.Table 1. Multivariate analysis: Risk factors associated with PVT development.

Table 2. Multivariate analysis: Risk factors associated with 1-yr poor outcomes (IBD-relatedER visit, hospitalization or surgery)

Su1358

IBD Is an Independent Risk Factor for Major Infectious Complications inElderly PatientsChristina Tofani, Teresa Valentin, Ann Tierney, Gary R. Lichtenstein

Background: Infections cause increased morbidity and mortality in elderly patients. Infectiousdiseases also lead to more hospitalizations in the elderly. Patients with IBD are at an increasedrisk for infectious complications. Current literature suggests that the increased risk of infectionobserved in IBD patients, is in part due to their use of immunosuppressive agents. No recent

S-446AGA Abstracts

studies have adequately assessed whether IBD is an independent risk factor for infectiouscomplications in elderly patients Our aim is to critically analyze the effect of IBD on infectiouscomplications in elderly patients. Methods: A retrospective cohort study was conducted ofpts aged 65 yrs and older at a tertiary care center, between 1/1/2007- 11/1/2012, comparinginfectious risk in pts with IBD and without IBD. The control group, who were consecutivepatients seen in outpatient clinic, were pts aged 65 yrs and older, that were immunocompe-tent. Pts with diabetes mellitus, rheumatologic diseases, or malignancy were excluded. Theuse of steroids, TNF inhibitors and immunomodulators were assessed in all pts. All infectiouscomplications were assessed in pts with IBD. Major infections were defined as systemicinfections, infections requiring hospitalization, or infections that directly led to the deathof the pt. The electronic medical records were reviewed to collect data on demographicinformation, diagnosis of IBD, and presence of infection. Populations were compared usingchi-square and logistic regression analyses. Results: 292 records of pts aged 65 yrs and olderwere reviewed, of which 146 had IBD and 146 did not have IBD (controls). Of the totalpts, 134 (45.9%) had an infection. 66 (45.2%) pts with IBD and 68 (46.6%) pts withoutIBD had an infection. 39 (29.1%) of the total pts had a major infection, 28 of which werein the IBD cohort. After adjusting for age, the OR for infections in IBD pts was 1.38 (CI0.82, 2.33). After adjusting for age, the OR for major infections in IBD pts was 7.00 (CI2.60, 18.85). Conclusion: Although IBD is not a significant independent risk factor foroverall infectious complications in elderly pts, it is an independent risk factor for majorinfections in this population. Major infectious complications, in general, have the potentialto cause profound impacts on pts. These findings reinforce the importance of diagnosingand managing infectious complications in elderly IBD pts, given their increased propensityto develop severe infectious complications.

Su1359

Aberrant DNA Methylation of Colonic Serrated Lesions and SubsequentColorectal Neoplasia in Ulcerative Colitis and Crohn's ColitisDavid H. Johnson, Mohammed M. Aboelsoud, Tracy C. Yab, Xiaoming Cao, Thomas C.Smyrk, Edward V. Loftus, Douglas W. Mahoney, David A. Ahlquist, John B. Kisiel

Background: Serrated epithelial changes (SEC) and sessile serrated adenoma (SSA) in chroniculcerative colitis (CUC) and Crohn's colitis (CD) are potentially pre-malignant. The molecularphenotype of these lesions is unknown and may influence neoplastic risk. Aim: Measure 1)aberrant DNA methylation and mutation in SEC and SSA in inflammatory bowel disease(IBD) patients (pts) and 2) rate of subsequent adenomatous colorectal neoplasia (CRN)Methods: A cohort of CUC and CD pts with SEC and SSA were identified in tissue archives.DNA was extracted from paraffin-embedded SEC and SSA (serrated-IBD) tissues and agematched frozen colorectal cancers (IBD-CRC) and IBD controls. Quantitative allele-specificreal time target and signal amplification (QuARTS) assays measured β-actin, methylatedNDRG4 (mNDRG4) and BMP3 (mBMP3). Where sufficient DNA was available, mutantKRAS (7 alleles) was assayed by QuARTS; BRAF and p53 mutations by Sanger sequencing.Serrated IBD pts were followed for development of subsequent CRN, measured by Kaplan-Meier method (with 95% confidence intervals [CI]). Pts with CRN events or colectomy <3mos from SEC/SSA diagnosis, or no subsequent colonoscopy, were excluded from time toevent analysis. Results: A total of 74 samples were assayed for mBMP3 and mNDRG4 (44serrated-IBD [34 SEC + 10 SSA], 17 IBD-CRC and 13 IBD-controls). Median age was 55years (yrs) (interquartile range [IQR] 46-62) and not significantly different among groups.Disease duration was similar for serrated-IBD and for CRC with 18 yrs (12-32) and 20 yrs(9-27), respectively (p=0.8), but was significantly less (2 yrs [0.5-12]) in IBD-controls (p=0.008, Wilcoxon). KRAS was assayed from 28 serrated lesions (18/34 SEC + 10 SSA) andall IBD-CRC and IBD-controls. Of serrated-IBD samples assayed, BRAF (1/35) and p53 (1/20) mutations were too rare for further study. Median β-actin corrected copy number ofmBMP3 was 14 (0.3-58) for IBD-CRC, 1.3 (0.02-12) for serrated-IBD, and 0 (0-0) for IBD-controls (p=0.0003); copies of mNDRG4 were 35 (7-55) for IBD-CRC, 9 (4-18) for serrated-IBD and 0 (0-0) for IBD-controls (p<0.0001); mutant KRAS copies were 0.07 (0-12) forIBD-CRC, 0.35 (0.02-8) for serrated IBD and 0 (0-0) for IBD-controls (p<0.001). Sensitivityat >90% specificity among IBD controls was calculated for each marker (table). Of 21serrated-IBD pts with at least 1 subsequent colonoscopy, all were positive for mNDRG4;the cumulative incidence of subsequent CRN was 19% (95% CI 6-43%) at 1 yr and 38%(95% CI 19-61%) at 2 yrs. Institutional IBD CRN rate was previously estimated at 6%/yr.Conclusions: Serrated IBD lesions are aberrantly methylated and contain frequent KRASmutations. Although caution is warranted from small sample size, the high rate of subsequentadenomatous dysplasia observed in these pts may be of potential relevance for use insurveillance algorithms.Tissue detection rate of IBD-associated neoplasms at >90% specificity

IBD, inflammatory bowel disease; CRC, colorectal cancer *Sufficient DNA was not availablefor KRAS assay on 16 samples ** β-actin did not amplify on a single KRAS assay

Su1360

Effect of a Low-Complex Carbohydrate Diet on Inflammatory Bowel DiseaseRobynne K. Chutkan, Eugenia R. Hamshaw, Farah Ashraf

BACKGROUND & AIMS: The relationship between diet and the activity and symptomatologyof inflammatory bowel disease (IBD) is unclear. The aim of this study was to assess theeffectiveness of the Specific Carbohydrate Diet (SCD), a low-complex carbohydrate diet that