Mercedes Ramas

Extracolonic Cancer in Inflammatory Bowel Disease: Data from the GETECCU Eneida Registry

Objectives:The objective of this study was (a) To know the prevalence and distribution of extracolonic cancer (EC) in patients with inflammatory bowel disease (IBD); (b) To estimate the incidence rate of EC; (c) To evaluate the association between EC and treatment with immunosuppressants and anti-tumor necrosis factor (TNF) agents.Methods:This was an observational cohort study. Inclusion criteria: IBD and inclusion in the ENEIDA Project (a prospectively maintained registry) from GETECCU. Exclusion criteria: Patients with EC before the diagnosis of IBD, lack of relevant data for this study, and previous treatment with immunosuppressants other than corticosteroids, thiopurines, methotrexate, or anti-TNF agents. The Kaplan–Meier method was used to evaluate the impact of several variables on the risk of EC, and any differences between survival curves were evaluated using the log-rank test. Stepwise multivariate Cox regression analysis was used to investigate factors potentially associated with the development of EC, including drugs for the treatment of IBD, during follow-up.Results:A total of 11,011 patients met the inclusion criteria and were followed for a median of 98 months. Forty-eight percent of patients (5,303) had been exposed to immunosuppressants or anti-TNF drugs, 45.8% had been exposed to thiopurines, 4.7% to methotrexate, and 21.6% to anti-TNF drugs. The prevalence of EC was 3.6%. In the multivariate analysis, age (HR=1.05, 95% CI=1.04–1.06) and having smoked (hazards ratio (HR)=1.47, 95% confidence interval (CI)=1.10–1.80) were the only variables associated with a higher risk of EC.Conclusions:Neither immunosuppressants nor anti-TNF drugs seem to increase the risk of EC. Older age and smoking were associated with a higher prevalence of EC.

Efficacy and safety of rifaximin associated with standard triple therapy (omeprazole, clarithromycin and amoxicillin) for H. pylori eradication: A phase IV pilot clinical trial

BACKGROUND A progressive decrease in Helicobacter pylori eradication rates has been described over the years, driving the need for new antibiotic treatments. AIM To evaluate the efficacy and safety of the addition of rifaximin (Spiraxin®) to standard triple therapy (omeprazole, amoxicillin and clarithromycin) for the eradication of H. pylori. METHODS Independent prospective clinical trial (EUDRACT no.: 2013-001080-23). Forty consecutive adult patients were included with H. pylori infection, dyspeptic symptoms and naive to eradication treatment. A full blood test was performed in the first five patients enrolled to evaluate the safety of the treatment. H. pylori eradication was confirmed with the 13C-urea breath test at least four weeks after the end of treatment with rifaximin 400mg/8h, clarithromycin 500mg/12h, amoxicillin 1g/12h and omeprazole 20mg/12h for 10 days. RESULTS Forty patients were consecutively enrolled, 53% woman, mean age 44 years. Indication for eradication: 60% non-investigated dyspepsia, 38% functional dyspepsia and 2% gastric ulcer. Four patients did not attend the eradication confirmatory breath test. The eradication rate was 61% (95% CI: 45-77%) for the protocol and 55% (40-70%) for intention-to-treat. About 76% of the patients experienced adverse events (35% diarrhea, 14% nausea and 24% metallic taste), none of which was serious. The blood tests did not show significant alterations. CONCLUSION Acceptable H. pylori eradication rates are not achieved with rifaximin associated with standard triple therapy for 10 days.

Probiotic supplementation with Lactobacillus plantarum and Pediococcus acidilactici for Helicobacter pylori therapy: A randomized, double-blind, placebo-controlled trial

To evaluate the safety, tolerability and efficacy of a probiotic supplementation for Helicobacter pylori (H. pylori) eradication therapy.

P372 Prospective, randomized clinical trial comparing the efficacy of two vaccines against hepatitis B virus (HBV) in inflammatory bowel disease (IBD) patients

Introduction and aim: Indoleamine 2,3-dioxygenase (IDO) is expressed in innate immune cells and acts as the first rate-limiting step in the tryptophan (TRP) catabolism along the kynurenine pathway. Decreased serum TRP levels have been associated with active inflammation in Crohns disease (CD) due to induction of IDO (Gupta, Inflamm Bowel Dis 2012). We studied the effect of infliximab-induced downregulation of inflammation on serum levels of TRP and kynurenine, as well as mucosal IDO expression in patients with inflammatory bowel disease (IBD). Methods: Serum samples and endoscopically-derived ileal or colonic mucosal biopsies were obtained from controls and patients with active IBD, and this before and after their first treatment with infliximab. Short-term clinical response and mucosal healing were assessed by experienced clinicians at 4 or 10 weeks after a single infusion or induction schedule, respectively (Ferrante, Inflamm Bowel Dis 2007; Schnitzler, GUT 2009). Serum TRP and kynurenine were measured by high performance liquid chromatography, and IDO mucosal gene expression was measured by Affymetrix Human Genome U133 Plus 2.0 Arrays. Data were analyzed with SPSS software using non-parametric tests and p-values of 9-fold increased in active IBD patients before infliximab therapy vs. controls (pileum=0.001 and pcolon<0.001). Although the IDOmucosal expression levels significantly decreased after infliximab therapy in IBD responders when compared to their baseline samples (pshort-term response and pmucosal healing<0.001), the colonic expression still remained significantly higher than controls (pshort-term response<0.001 and pmucosal healing=0.002). Serum TRP levels were significantly decreased (p<0.001) and the kynurenine/ tryptophan (K/T) ratio was significantly increased (p=0.001) in active IBD patients when compared to controls. However, we found no significant effect of infliximab therapy on both the TRP levels and K/T ratio. Conclusion: This study demonstrates that mucosal IDO expression levels are increased and serum TRP levels decreased in IBD patients with active disease. Of note, after controlling the inflammation with infliximab therapy, both levels remained impaired in IBD responders showing a complete mucosal healing. This persistent upregulation of IDO in patients with complete colonic healing may explain why mucosal ulcers recur very early if patients do not receive maintenance therapy with infliximab.

Mo1740 Prospective, Randomized Clinical Trial Comparing the Efficacy of Two Vaccines Against Hepatitis B Virus (HBV) in Inflammatory Bowel Disease (IBD) Patients

Introduction and aim: Indoleamine 2,3-dioxygenase (IDO) is expressed in innate immune cells and acts as the first rate-limiting step in the tryptophan (TRP) catabolism along the kynurenine pathway. Decreased serum TRP levels have been associated with active inflammation in Crohns disease (CD) due to induction of IDO (Gupta, Inflamm Bowel Dis 2012). We studied the effect of infliximab-induced downregulation of inflammation on serum levels of TRP and kynurenine, as well as mucosal IDO expression in patients with inflammatory bowel disease (IBD). Methods: Serum samples and endoscopically-derived ileal or colonic mucosal biopsies were obtained from controls and patients with active IBD, and this before and after their first treatment with infliximab. Short-term clinical response and mucosal healing were assessed by experienced clinicians at 4 or 10 weeks after a single infusion or induction schedule, respectively (Ferrante, Inflamm Bowel Dis 2007; Schnitzler, GUT 2009). Serum TRP and kynurenine were measured by high performance liquid chromatography, and IDO mucosal gene expression was measured by Affymetrix Human Genome U133 Plus 2.0 Arrays. Data were analyzed with SPSS software using non-parametric tests and p-values of 9-fold increased in active IBD patients before infliximab therapy vs. controls (pileum=0.001 and pcolon<0.001). Although the IDOmucosal expression levels significantly decreased after infliximab therapy in IBD responders when compared to their baseline samples (pshort-term response and pmucosal healing<0.001), the colonic expression still remained significantly higher than controls (pshort-term response<0.001 and pmucosal healing=0.002). Serum TRP levels were significantly decreased (p<0.001) and the kynurenine/ tryptophan (K/T) ratio was significantly increased (p=0.001) in active IBD patients when compared to controls. However, we found no significant effect of infliximab therapy on both the TRP levels and K/T ratio. Conclusion: This study demonstrates that mucosal IDO expression levels are increased and serum TRP levels decreased in IBD patients with active disease. Of note, after controlling the inflammation with infliximab therapy, both levels remained impaired in IBD responders showing a complete mucosal healing. This persistent upregulation of IDO in patients with complete colonic healing may explain why mucosal ulcers recur very early if patients do not receive maintenance therapy with infliximab.