544 32nd World Congress of Internal Medicine (October 24-28, 2014) The Korean Society of Gastroenterology & SIDDS 2014
PS 0880 Lower GI Tract
Clinical Factors and Disease Course Associated with Diagnostic Delay in Korean Patients with Crohn’s Disease; Results from the Connect Study
Chang Mo Moon1, Sung-Ae Jung1, Seong-Eun Kim1, Byong Duk Ye2, Jae Hee Cheon3, You Sun Kim4, Young-Ho Kim5, Joo Sung Kim6, Dong Soo Han7
Ewha Womans University School of Medicine, Korea1, University of Ulsan College of Medicine, Korea2, Yonsei University College of Medicine, Korea3, Inje University College of Medicine, Korea4, Sungkyunk- wan University School of Medicine, Korea5, Seoul National University College of Medicine, Korea6, Hanyang University College of Medicine, Korea7
Background: Crohn’s disease (CD) is the chronic and disabling infl ammatory disorder of the gastrointestinal tract over time. Diagnostic delay frequently occurs in CD pa- tients due to its unspecifi c clinical symptoms and inappropriate diagnostic accuracies.
However, Diagnostic delay and its related clinical factors remain elusive. Thus, this study aimed to identify clinical factors associated with diagnostic delay and to evalu- ate the impact of diagnostic delay on clinical course in a Korean CD cohort.
Methods: We conducted a retrospective multicenter analysis of a total of 1,306 CD patients registered in the Crohn’s disease clinical network and cohort (CONNECT) study in Korea. Diagnostic delay was defi ned as the time period from consulting a physician for specifi c symptoms to establishment of CD diagnosis.
Results: The mean period of diagnostic delay was 16.1 ± 32.3 months. In multivariate analysis, female gender, concomitant upper gastrointestinal (UGI) disease, penetrating disease behavior at diagnosis were signifi cantly associated with long diagnostic delay (>
12 months) (p < 0.05). When analyzed the association of clinical variables with the risk of CD-related abdominal surgery, there was no signifi cant difference among diagnostic delay groups. In contrast, diagnostic delay (> 18 months) was independently predictive of further development of intestinal stenosis (hazard ratio [HR], 1.42; 95% confi dence interval [CI], 1.11 to 1.83; p = 0.006) and internal fi stula (HR, 1.39; 95% CI, 1.03 to 1.89;
p = 0.033).
Conclusions: Diagnostic delay occurs in a considerable number of Korean CD patients and female gender, UGI involvement, and penetrating disease behavior are related to the diagnostic delay. Diagnostic delay is signifi cantly associated with an increased risk of CD-related complications such as intestinal stenosis and internal fi stula.
PS 0881 Lower GI Tract
Alcoholic Liver Disease is Associated with the Increased Risk of Advanced Colonic Neoplasm.
Da Yeon Oh1, Seong Joon Koh1, Hwi Young Kim1, Won Kim1, Yong Jin Jung1, Ji Won Kim1, Byeong Gwan Kim1, Kook Lae Lee1
Department of Internal Medicine, Seoul National University Boramae Hospital, Seoul National University College of Medicine, Korea1
Background: The aim of this study is to investigate whether alcoholic liver disease (ALD) is associated with the increased risk of advanced colonic neoplasm in patients with ALD.
Methods: We analyzed 118 consecutive patients with ALD who performed colonos- copy between January 2000 and December 2013. For each case, age- (±5 years) and sex- matched controls were identifi ed from patients with non-alcoholic fatty liver disease (NAFLD) and healthy controls. Clinical characteristics were reviewed through medical records, colonoscopic fi nding, pathologic fi nding, images.
Results: The prevalence of colorectal cancer was 6 (5.1%) in ALD patients, 5 (2.5%) in NAFLD patients, 0 (0.0%) healthy control (P =0.007). In addition, the prevalence of advanced colonic adenoma was 18(15.3%) in ALD patients, 17(8.6%) in NAFLD, in 6 (2.8%) healthy control (P<0.001). A case-control study showed that odds for detecting a colorectal advanced neoplasm among ALD patients without decompensated liver cirrhosis were approximately 10.1 times greater than in healthy controls [OR,10.095;
95% Confi dential interval(CI), 3.638-28.014; P<0.001) ]. There was no signifi cant dif- ference in the prevalence of colorectal cancer (P=0.428) and advanced colonic adeno- ma (P=0.876) according to the presence of decompensated liver cirrhosis (LC) in ALD patients. Age is an independent risk factor for detecting advanced colonic neoplasm in patients with ALD [OR, 1.091; 95% CI, 1.025-1.162; P= 0.007].
Conclusions: The yield for detecting advanced neoplasm was signifi cantly higher in patients with ALD than in healthy control. Screening for colorectal neoplasm using colonoscopy is warranted in ALD patients without decompensated LC.
PS 0882 Lower GI Tract
The Clinical Outcome of Surveillance Colonoscopy after Negative Index Colonoscopy in People with Average Risk of Colorectal Cancer
Byung Ik Jang1, Sung Bum Kim1, Kook Hyun Kim1, Kyeong Ok Kim1, Si Hyung Lee1, Tae Nyeun Kim1
Yeungnam University College of Medicine, Korea1
Background: Guidelines recommend to perform surveillance colonoscopy at 5 years after normal index colonoscopy. The present study aimed to evaluate the characteris- tics and fi ndings of surveillance colonoscopy performed after normal index colonosco- py in subjects with average risk of colorectal cancer.
Methods: Subjects who underwent surveillance colonoscopy following negative index colonoscopy in Yeungnam University Hospital health promotion center from Jan 2010 to Dec 2013 were included. The clinical characteristics and endoscopic fi ndings were compared and analyzed retrospectively.
Results: Among 4165 subjects who performed colonoscopy, 205 subjects had previous history of negative index colonoscopy. Adenoma was detected in 58 (28.3%) subjects during surveillance colonoscopy. Mean interval between surveillance and index colo- noscopy in subjects with or without colorectal adenoma on surveillance colonoscopy was not signifi cantly different (48.4 ± 26.3 vs 50.2± 24.7 months, p=0.285). Total 76 adenoma were found and 43 adenoma (56.6%) were located at proximal colon. Mean size of adenoma was 4.6 ± 2.3 mm and 51 (67.1%) were diminutive polyp. Advanced adenoma was diagnosed in 3 (3.9%) and all were located at distal colon. No colorectal cancer was found on surveillance colonoscopy. Mean withdrawal time (min, mean ± SD) was signifi cantly different in subjects with or without colorectal adenoma (7.9
± 3.9, 5.8 ± 3.6) (p=<0.001). By multivariate analysis, only withdrawal time above 6 minutes and colonoscopy performed by experienced endoscopist was associated with detection of colorectal adenoma (p=0.001 and 0.033).
Conclusions: The risk of colorectal cancer did not increase for at least 4 years after normal index colonoscopy. Meticulous examination with suffi cient withdrawal time for more than 6 minutes is needed in both inexperienced and experienced endoscopist not to miss the colorectal polyp.
PS 0883 Lower GI Tract
Isoliquiritigenin Inhibits TNF-a-Induced HMGB1 Release and HMGB1-Dependent Infl ammation in Ht-29 Cells
Jin-Hua Chi1, Hao Jin1, Wen-Yi Jiang1, Sung Hee Lee1, In Tae Hwang2, Suck Chei Choi2, Geom Seog Seo2
Department of Pharmacy, BK21 Plus Program & Department of Smart Life-Care Convergence, Wonk- wang University, Graduate School, Korea1, Digestive Disease Research Institute, Wonkwang University College of Medicine, Korea2
Background: High Mobility Group Box 1 protein (HMGB1) is a chromatin binding nucleus protein and has proinfl ammatory cytokine potential when released by dam- aged or necrosis cells during Infl ammatory bowel dieases(IBD). This study is aimed to explore the association between ISQ and HMGB1 release in human intestinal cell.
Methods: The protein expression of COX-2, fracnation of NF-κB and HMGB1, con- centration of culture medium were analyzed by Western blot. Translocation of NF-κ B and HMGB1 were assessed by Fluorescence staining. Co-Immunoprecipitation assay for demonstrated acetyled HMGB1 in medium. HMGB1 and COX-2 mRNA level was analyzed by RT-PCR.
Results: ISQ reduce TNF-a induced release of HMGB1 in extracellular and inhibit nucleus/cytosol translocation. ISQ also regulates NF-κB p65 translocation and in- hibit the COX-2 expression which is the downstream of the NF-κB. Moreover ISQ suppressed the release of HMGB1 through reduction of the mRNA level and inhibit HMGB1 acetylation.
Conclusions: In this study, all data evidence that released HMGB1 is a proinfl amma- tory cytokine and leads to signaling cascades in infl ammatory responses in human intestinal cell. These fi ndings highlight the potential of ISQ for clinical applications in the treatment of intestinal infl ammation including IBD.
