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Gender-based differences in the use of professional titles during speaker introductions have been described in other medical specialties. Our primary aim was to assess gender-based differences in the formality of speaker introductions at the American College of Gastroenterology 2020 Virtual Annual Scientific Meeting. Our secondary aim was to assess gender-based differences in the formality of speaker self-introductions. Reviewed presentations from the American College of Gastroenterology Annual Meeting for gender-based differences in professional title use during speaker introductions and self-introductions. Speakers included 29 women (37.2%) and 49 men (62.8%). We found no significant gender differences in the use of professional titles by introducers (t(67) = − 0.775, p = 0.441) or in self-introductions (36.4% of women vs. 41.9% of men, t(63) = 0.422, p = 0.674). The lack of gender differences in professional title use may represent a novel advantage of virtual meeting formats or suggest increased attention to gender bias in introductions.

Because ADAM17 promotes colonic tumorigenesis, we investigated potential miRNAs regulating ADAM17; and examined effects of diet and tumorigenesis on these miRNAs. We also examined pre-miRNA processing and tumour suppressor roles of several of these miRNAs in experimental colon cancer. Using TargetScan, miR-145, miR-148a, and miR-152 were predicted to regulate ADAM17. miR-143 was also investigated as miR-143 and miR-145 are co-transcribed and associated with decreased tumour growth. HCT116 colon cancer cells (CCC) were co-transfected with predicted ADAM17-regulating miRNAs and luciferase reporters controlled by ADAM17-3’UTR. Separately, pre-miR-143 processing by colonic cells was measured. miRNAs were quantified by RT-PCR. Tumours were induced with AOM/DSS in WT and transgenic mice (Tg) expressing pre-miR-143/miR-145 under villin promoter. HCT116 transfection with miR-145, −148a or −152, but not scrambled miRNA inhibited ADAM17 expression and luciferase activity. The latter was suppressed by mutations in ADAM17-3’UTR. Lysates from colonocytes, but not CCC, processed pre-miR-143 and mixing experiments suggested CCC lacked a competency factor. Colonic miR-143, miR-145, miR-148a, and miR-152 were downregulated in tumours and more moderately by feeding mice a Western diet. Tg mice were resistant to DSS colitis and had significantly lower cancer incidence and tumour multiplicity. Tg expression blocked up-regulation of putative targets of miR-143 and miR-145, including ADAM17, K-Ras, XPO5, and SET. miR-145, miR-148a, and miR-152 directly suppress colonocyte ADAM17 and are down-regulated in colon cancer. This is the first direct demonstration of tumour suppressor roles for miR-143 and miR-145 in an in vivo model of colonic tumorigenesis.

Background Blocking of lymphocyte trafficking to bile ducts is a potential mechanism to alter the disease course of patients with primary sclerosing cholangitis (PSC). Aim To describe the effect of the α4 β7 integrin antibody, vedolizumab, on liver biochemistry and disease activity in patients with PSC and inflammatory bowel disease (IBD). Methods This is a retrospective multi-centre study of adult patients with a diagnosis of both IBD and PSC. The primary outcome was change in serum alkaline phosphatase level at weeks 14 and 30. Secondary outcomes included changes in other liver biochemistries and in clinical outcomes for the bowel disease. A safety analysis for adverse events was performed. Results Thirty-four patients (16 Crohn's disease, 18 ulcerative colitis) were included. Nine (26%) had a history of liver transplant. Median follow-up on vedolizumab was 9 months (IQR: 7-16). There was no overall change in serum alkaline phosphatase level with vedolizumab therapy (median 268 [IQR: 105-551] IU/L at baseline versus 249 [IQR: 183-634] IU/L, P = 0.99 at week 30). No significant changes in other liver biochemistries or the Mayo PSC Risk Score were demonstrated at week 30. Clinical remission was achieved at week 30 in 55% of Crohn's disease and 29% of ulcerative colitis patients. Seven (21%) patients ceased vedolizumab; six patients stopped therapy due to persistent IBD activity and one for worsening of liver biochemistries. Conclusion Vedolizumab treatment in patients with PSC and IBD did not improve liver biochemistry but was associated with improvement in bowel disease and a favourable safety profile.

IntroductionA small bowel source is suspected when evaluation of overt gastrointestinal (GI) bleeding with upper and lower endoscopy is negative. Video capsule endoscopy (VCE) is the recommended next diagnostic test for small bowel bleeding sources. However, clinical or endoscopic predictive factors for small bowel bleeding in the setting of an overt bleeding presentation are unknown. We aimed to define predictive factors for positive VCE among individuals presenting with overt bleeding and a suspected small bowel source.MethodsWe included consecutive inpatient VCE performed between September 1, 2012 to September 1, 2015 for melena or hematochezia at two tertiary centers. All patients had EGD and colonoscopy performed prior to VCE. Patient demographics, medication use, and endoscopic findings were retrospectively recorded. VCE findings were graded based on the P0-P2 grading system. The primary outcome of interest was a positive (P2) VCE. The secondary outcome of interest was the performance of a therapeutic intervention. Data were analyzed with the Fisher exact test for dichotomous variables and logistic regression.ResultsTwo hundred forty-three VCE were reviewed, and 117 were included in the final analysis. A positive VCE (P2) was identified in 35 (29.9%) cases. In univariate analysis, a positive VCE was inversely associated with presence of diverticula on preceding colonoscopy (OR: 0.44, 95% CI: 0.2-0.99), while identification of blood on terminal ileal examination was associated with a positive VCE (OR: 5.18, 95% CI: 1.51-17.76). In multivariate analysis, only blood identified on terminal ileal examination remained a significant risk factor for positive VCE (OR: 6.13, 95% CI: 1.57-23.81). Blood on terminal ileal examination was also predictive of therapeutic intervention in both univariate (OR: 4.46, 95% CI: 1.3-15.2) and multivariate analysis (OR: 5.04, 95% CI: 1.25-20.32).ConclusionAmong patients presenting with overt bleeding but negative upper and lower endoscopy, the presence of blood on examination of the terminal ileum is strongly associated with a small bowel bleeding source as well as with small bowel therapeutic intervention. Presence of diverticula on colonoscopy is inversely associated with a positive VCE and therapeutic intervention in univariate analysis.

The original version of the article unfortunately contained an error in a percentage value in Results section of Abstract.

Background: Blocking of lymphocyte trafficking is a potential mechanism to alter the disease course of primary sclerosing cholangitis (PSC). We studied the effect of the selective α4β7 integrin antibody, vedolizumab, on liver biochemistry and inflammatory bowel disease (IBD) activity in patients with IBD and PSC (IBD-PSC). Methods: We reviewed electronic medical records of adult patients who had an established diagnosis of IBD-PSC from five tertiary centers. We assessed baseline patient and disease characteristics and treatment exposures. The primary outcome was change in serum alkaline phosphatase at weeks 14 and 30. Secondary outcomes included changes in other liver biochemistries, the Mayo Risk Score for PSC and IBD clinical and endoscopic remission. We also performed a safety analysis for the development of adverse events including liver-related complications. Results: We identified 34 patients with IBD-PSC. Nine (26%) had a history of orthotopic liver transplant, 7 were on stable doses of ursodeoxycholic acid (UDCA) and 2 patients commenced UDCA during the study period. Median follow-up was 9 (IQR: 7–16) months; 28 (92%) had at least 6 months of clinical follow-up. Serum alkaline phosphatase activities did not significantly decrease with vedolizumab therapy (median 268 (IQR: 105–551) IU/L at baseline versus 249 (IQR: 183–634) IU/L, p=0.9899 at week 30). Of the 18 patients with an abnormal alkaline phosphatase at baseline (>120IU/L), 11 (61%) had improvement with treatment. In these patients, alkaline phosphatase trended down from 475 IU/L (IQR: 241–757) at baseline to 283 IU/L (IQR: 207–658), p=0.267 at week 30 but none of these normalized (Figure 1). Median alkaline phosphatase changes remained similar when patients exposed to UDCA were excluded. Of the 8 patients (31%) with normal alkaline phosphatase at baseline, 4 (50%) had a subsequent increase to abnormal levels by week 30, from a baseline median of 98 IU/L (IQR: 77–102) to 146 IU/L (IQR: 90–203), p=0.036 at week 30 (Figure 2). No significant changes in other liver biochemistries or the Mayo PSC Risk Score were demonstrated at week 30. 55% of Crohn's disease and 21% of ulcerative colitis patients achieved clinical remission at week 30. Seven patients (21%) ceased vedolizumab therapy; one for a deterioration in liver biochemistry thought to be a drug reaction and six for IBD primary non-response. Two patients developed ascending cholangitis but continued vedolizumab. Conclusions: Vedolizumab therapy in patients with IBD-PSC has little overall effect on liver biochemistry, but is safe and does improve IBD clinical activity. Treatment earlier in the disease course of PSC and assessment of longer-term exposure of lymphocyte trafficking blockade in IBD-PSC remains of interest.