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Background Since the consensus-based diagnostic algorithm for intestinal Behcet’s disease (iBD) was proposed by the IBD Study Group of the Korean Association for the Study of Intestinal Diseases, there were few studies regarding the prognosis of iBD according to the diagnostic algorithm. Methods We reviewed the medical records of patients who had ileocecal ulcers with clinical impression of iBD from March 1986 to August 2019 in Seoul St. Mary’s Hospital and evaluated factors at the time of diagnosis which were related with adverse events (AEs, major operation or admission from iBD) and disease-free survival (DFS). Results Among 204 eligible patients, a total of 163 were included in the study after exclusion of 41 patients with ileocecal ulcers from other disorders. The male-to-female ratio was 1:1 and the mean age at the time of diagnosis was 48.9 ± 15.9. The number of definite, probable, suspected, and non-diagnostic iBD was 18 (11.0%), 64 (39.3%), 37 (22.7%), and 44 (27.0%), respectively. Patients with definite, probable, and suspected iBD developed more AEs compared with patients with non-diagnostic iBD (p = 0.026). After exclusion of patients with non-diagnostic iBD, univariate analysis showed accompanying haematologic disorders, haemoglobin Conclusion Patients with definite, probable, and suspected iBD have a poor prognosis compared with patients with non-diagnostic iBD. Accompanying with haematologic disorders, anaemia, fever, and colonic involvement at the time of diagnosis are poor prognostic factors in patients with iBD.

abate metastasis dissemination by maintaining lymphatic vessel junctions’ integrity. Methods: The azoxymethane (AOM)/dextran sulfate sodium (DSS) CAC model was used. In addition, colitic mice were orthotopically injected with CT26 colon cancer cells. Modulation of lymphangiogenesis was obtained by systemic inhibition of VEGFR3 or adenoviral overexpression of VEGFC. Tumor density and size were measured at the end of the AOM/DSS protocol by visual, endoscopic and histological inspection. In the xenotransplantation model, liver, lung and draining lymphnodes were processed for metastasis quantification by FACS analysis. Whole mounts of colons were stained to analyse area density and dimension of lymphatic vessels (LVs) within peritumoral and tumoral regions. Moreover, VE-cadherin distribution and expression were studied in vivo on LVs and in vitro on Human intestinal lymphatic endothelial cells (HILEC) stimulated with VEGFC or with a VEGFR3 inhibitor. Results: In both the AOM/DSS and the xenotransplantation models, systemic inhibition of VEGFR3 inhibited lymphangiogenesis in peritumoral and tumoral regions, reducing both area density and LVs dimension. In addition, it reduced tumor density and size, together with an abatement of metastatic dissemination, when compared to untreated animals. In contrast, tumor density and growth, including metastasis formation was enhanced by VEGFC, which in turn increased lymphangiogenesis within the same regions. Whole mount staining showed that VEGFC altered VE-cadherin expression both in vivo and in vitro, whereas VEGFR3 inhibitor kept endothelial junction integrity, thus linking the VEGFC/VEGFR3 pathway to VE-cadherin-dependent metastasis dissemination. Conclusions: Our findings demonstrate that VEGFC/VEGFR3dependent lymphangiogenesis plays a key role both in CAC growth and metastasis dissemination. Our study reveals a novel mechanism of control of lymphatic junction integrity which may be a promising target for the treatment of CAC and the associated metastatic process.

Methods: We reviewed magnifying colonoscopic findings in 30 patients with quiescent UC who achieved complete MH (Endoscopic subscore of Mayo 0) by conventional colonoscopy. All patients performed magnifying observation using spraying with 0.1% indigo carmine dye solution after conventional colonoscopy. According to the fine network and cryptal pit patterns of colonic mucosa, we classified magnifying colonoscopic findings into four types (magnifying subscore 0 3); 0, the surface structures similar to normal colonic mucosa; 1, the disarray of fine network or cryptal pit patterns were observed; 2, the abnormal surface structures, such as fusion or disruption of fine network patterns and loss of cryptal pit patterns were observed; 3, the fine network or cryptal pit patterns were completely disappeared. We examined: (1) the proportion of patients without clinical relapse (magnifying subscore 0 or 1 group vs subscore 2 or 3 group); (2) the patients’ characteristics (age, gender, disease phenotype, extent disease, and medications) between our magnifying colonoscopic classifications. Disease activity was evaluated using a clinical activity index of Rachmilewitz (CAI), and clinical remission was defined as CAI score of 4 or more. Results: The distribution of magnifying colonoscopic findings was as follows; 10 (subscore 0), 9 (subscore 1), 8 (subscore 2) and 3 (subscore 3). The proportion of patients with relapsefree in magnifying subscore 0 or 1 group was significantly higher than that in magnifying subscore 2 or 3 group (89.5% vs 36.4% at 12 months after magnifying chromoendoscopy, log-rank test p < 0.01). The patients in magnifying subscore 2 or 3 group significantly received more cumulative dose of prednisolone compared with those in magnifying subscore 0 or 1 group (485.0±104.9 vs 77.6±47.4mg/month), however, there was no significant correlation between magnifying subscore and other clinical parameters. Conclusions: Magnifying colonoscopy can provide additional benefits for evaluation of MH by conventional colonoscopy in quiescent UC.