Our early experience with vedolizumab demonstrates a clear benefit in terms of disease control as well as a steroid-sparing effect in a cohort, which included patients with complex and previously refractory disease.

Concomitant therapy led to statistically significant higher eradication rates over sequential therapy. Both therapies showed excellent compliance and an acceptable safety profile. The 10-day quadruple concomitant scheme should be the adopted for first-line H. pylori eradication in Greece.

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The significantly increased risk of colorectal cancer (CRC) in longstanding colonic inflammatory bowel disease (IBD) justifies the need for endoscopic surveillance. Unlike sporadic CRC, IBD-related CRC does not always follow the predictable sequence of low-grade to high-grade dysplasia and finally to invasive carcinoma, probably because the genetic events shared by both diseases occur in different sequences and frequencies. Surveillance is recommended for patients who have had colonic disease for at least 8-10 years either annually, every 3 years or every 5 years with the interval dependant on the presence of additional risk factors. Currently, the recommended endoscopic strategy is high-definition chromoendoscopy with targeted biopsies, although the associated lengthier procedure time and need for experienced endoscopists has limited its uniform uptake in daily practice. There is no clear consensus on the management of dysplasia, which continues to be a challenging area particularly when endoscopically invisible. Management options include complete resection (and/or referral to a tertiary centre), close surveillance or proctocolectomy. Technical advances in endoscopic imaging such as confocal laser endomicroscopy, show exciting potential in increasing dysplasia detection rates but are still far from being routinely used in clinical practice.

Our experience mirrors previously reported real-world cohorts and demonstrates similar outcomes to those observed in randomised controlled trials. These data demonstrate a meaningful reduction in clinical, biochemical and endoscopic disease activity as well as a steroid-sparing effect in patients with previously refractory disease.

Prebiotics may promote immune homeostasis and reduce sub-clinical inflammation in humans. This study investigated the effect of prebiotic galactooligosaccharide (GOS) supplementation in colonic inflammation. Seventeen patients with active ulcerative colitis (UC) consumed 2.8 g/d GOS for 6 weeks. At baseline and 6 weeks, gene expression (microarray), fecal calprotectin (ELISA), microbiota (16S rRNA), short-chain fatty acids (SCFAs; gas-liquid chromatography), and clinical outcomes (simple clinical colitis activity index (SCCAI), gastrointestinal symptom rating scale (GSRS), and Bristol stool form scale (BSFS)) were measured. Following prebiotics, clinical scores (SCCAI), fecal calprotectin, SCFAs, and pH were unchanged. Five genes were upregulated and two downregulated. Normal stool proportion (BSFS) increased (49% vs. 70%, p = 0.024), and the incidence (46% vs. 23%, p = 0.016) and severity (0.7 vs. 0.5, p = 0.048) of loose stool (GSRS), along with urgency (SCCAI) scores (1.0 vs. 0.5, p = 0.011), were reduced. In patients with a baseline SCCAI ≤2, prebiotics increased the relative abundance of Bifidobacterium from 1.65% (1.97) to 3.99% (5.37) (p = 0.046) and Christensenellaceae from 0.13% (0.33) to 0.31% (0.76) (p = 0.043). Prebiotics did not lower clinical scores or inflammation but normalized stools. Bifidobacterium and Christensenellaceae proportions only increased in patients with less active diseases, indicating that the prebiotic effect may depend on disease activity. A controlled study is required to validate these observations.

BackgroundDespite the proven efficacy of vedolizumab (VDZ) for ulcerative colitis (UC) and Crohn’s disease (CD), suboptimal response is commonly encountered. However, data regarding the effectiveness of dose intensification (by interval shortening) to achieve response are limited.ObjectivesWe evaluated the effectiveness of dose intensification at achieving response in patients with a previously suboptimal response to VDZ. Additionally, we aimed to identify predictors of response to this strategy.MethodsWe performed a retrospective cohort study of patients who underwent VDZ dose intensification for suboptimal response. Clinical disease activity was evaluated at the point of dose intensification (baseline) and at weeks 12 and 24. Response was defined as Harvey-Bradshaw Index (HBI) or Simple Clinical Colitis Activity Index (SCCAI) reduction of ≥3, and remission as HBI <5 or SCCAI <3.ResultsA total of 36 patients received dose intensification to 4-weekly infusions: 18 CD, 14 UC and 4 inflammatory bowel disease-unclassified (analysed in the UC group). Median SCCAI scores fell from 6 (range 0–11) at baseline to 4 (0–6, p=0.008) at week 24, while HBI scores did not change significantly (4 (0–27) and 3 (0–8), p=0.092). Overall median C reactive protein (CRP) fell from 6 mg/L (1–23) to 2 mg/L (1–17, p=0.011). Of 20 patients with clinically active disease at baseline, 10 (50%) responded, of whom 4 (20%) achieved remission at week 24. Univariate analysis demonstrated low baseline CRP (p=0.045) and response at week 12 (0.020) were associated with week 24 response.ConclusionsOur findings demonstrate VDZ dose intensification to be effective at achieving clinical response in half of patients. Low baseline CRP and response at week 12 are potential predictors of week 24 response.

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