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Coeliac disease (CD) is a gluten-induced enteropathy affecting 1% of the population and has extra intestinal manifestations. One such expression involves nervous system, and CD may present as gluten ataxia (GA), peripheral neuropathy and epileptiform disorder among others. Considerable controversy exists on the exact pathophysiological mechanism of gluten leading to ataxia. It is, however, clear that in intestinal axis tissue transglutaminase 2 (tTG2) is the primary target but in the nervous system, tTG6 may be the causative antigen although its exact role is not clear. Furthermore, it has also been postulated that anti-gangliodise antibodies may play a role in the emergence of central pathology if not the key contender. Moreover, the association of neurological injury with non-coeliac gluten sensitivity (NCGS), a related but pathologically different condition implies an independent mechanism of neuronal injury by gluten in the absence of CD. This review will touch on the salient features of CD and the nervous system and will highlight current controversies in relation to gluten and GA.

Oliver Bendall,1 Joel James,1 Katarzyna M Pawlak,2 Sauid Ishaq,3,4 J Andy Tau,5 Noriko Suzuki,6 Steven Bollipo,7,8 Keith Siau1 1Department of Gastroenterology, Royal Cornwall Hospitals NHS Trust, Truro, UK; 2Endoscopy Unit, Department of Gastroenterology, Ministry of Interior and Administration, Szczecin, Poland; 3Department of Gastroenterology, Dudley Group Hospitals NHS Foundation Trust, Dudley, UK; 4Medicine, Birmingham City Hospital, Birmingham, UK; 5Austin Gastroenterology, Austin, TX, USA; 6Wolfson Unit for Endoscopy, St. Mark’s Hospital, London, UK; 7School of Medicine & Public Health, The University of Newcastle, Callaghan, New South Wales, Australia; 8Department of Gastroenterology, John Hunter Hospital, New Lambton Heights, New South Wales, AustraliaCorrespondence: Keith SiauDepartment of Gastroenterology, Royal Cornwall Hospitals NHS Trust, Truro, TR1 3LJ, UKEmail keithsiau@nhs.netAbstract: Delayed post-polypectomy bleeding (DPPB) is a potentially severe complication of therapeutic colonoscopy which can result in hospital readmission and re-intervention. Over the last decade, rates of DPPB reported in the literature have fallen from over 2% to 0.3– 1.2%, largely due to improvements in resection technique, a shift towards cold snare polypectomy, better training, adherence to guidelines on periprocedural antithrombotic management, and the use of antithrombotics with more favourable bleeding profiles. However, as the complexity of polypectomy undertaken worldwide increases, so does the importance of identifying patients at increased risk of DPPB. Risk factors can be categorised according to patient, polyp and personnel related factors, and their integration together to provide an individualised risk score is an evolving field. Strategies to reduce DPPB include safe practices relevant to all patients undergoing colonoscopy, as well as specific considerations for patients identified to be high risk. This narrative review sets out an evidence-based summary of factors that contribute to the risk of DPPB before discussing pragmatic interventions to mitigate their risk and improve patient safety.Keywords: colonoscopy, polypectomy, haemorrhage, adverse event, complications

Background A pharyngeal pouch or Zenker’s diverticulum (ZD) is a mucosal out-pouching in the cervical oesophagus. It arises from the posterior oesophageal wall in a structural weakness between horizontal and oblique cricopharyngeus fibre known as Killian’s dehiscence located between the oblique and horizontal muscle fibre layers of the Cricopharyngeus (CP) muscle Killian.The aim of the treatment is to provide symptom relief and improve quality of life. Literature on ZD consisted of small series, retrospective studies. With wide variation in the procedure technique using different cutting Devices. Some experts would use general anaesthesia, some use Propofol, or midazolam. There was variation in use of clips, antibiotics to be used. Methods and results We looked at the deficiencies in the knowledge that that provided the justification to start our research on treatment of Zenker’s diverticulum. We carried out the first systematic review and meta-analysis (MA) of the literature focusing on Flexible Endoscopic Septum Division (FESD) for Zenker’s diverticulum including in-depth evaluation of its efficacy safety and limitation. WE introduced new comprehensive symptom scoring tool that we validated in prospective study. We explored the incidence and aetiology of intubation failure in endoscopy to assess the predictors of intubation failure and predictors of pathology in patient’s pharyngeal symptoms. We introduced concept of two stage sedation using HFNOT in a prospective observational study. We conducted the first study with large number of patient with longest follow up and looked at the predictors of recurrence. Conclusion Our studies on all aspects of ZD to address gaps in literature but also highlighted implication for future research

Background A pharyngeal pouch or Zenker’s diverticulum (ZD) is a mucosal out-pouching in the cervical oesophagus. It arises from the posterior oesophageal wall in a structural weakness between horizontal and oblique cricopharyngeus fibre known as Killian’s dehiscence located between the oblique and horizontal muscle fibre layers of the Cricopharyngeus (CP) muscle Killian.The aim of the treatment is to provide symptom relief and improve quality of life. Literature on ZD consisted of small series, retrospective studies. With wide variation in the procedure technique using different cutting Devices. Some experts would use general anaesthesia, some use Propofol, or midazolam. There was variation in use of clips, antibiotics to be used. Methods and results We looked at the deficiencies in the knowledge that that provided the justification to start our research on treatment of Zenker’s diverticulum. We carried out the first systematic review and meta-analysis (MA) of the literature focusing on Flexible Endoscopic Septum Division (FESD) for Zenker’s diverticulum including in-depth evaluation of its efficacy safety and limitation. WE introduced new comprehensive symptom scoring tool that we validated in prospective study. We explored the incidence and aetiology of intubation failure in endoscopy to assess the predictors of intubation failure and predictors of pathology in patient’s pharyngeal symptoms. We introduced concept of two stage sedation using HFNOT in a prospective observational study. We conducted the first study with large number of patient with longest follow up and looked at the predictors of recurrence. Conclusion Our studies on all aspects of ZD to address gaps in literature but also highlighted implication for future research

SCOPUS: er.j, info:eu-repo/semantics/published

In the above-mentioned article, the institution of Daniel Pohl has been corrected. This was corrected in the online version on June 19, 2020.

In the above-mentioned article, the institution of Daniel Pohl has been corrected. This was corrected in the online version on June 24, 2020., SCOPUS: er.j, info:eu-repo/semantics/published

Background Clostridium difficile infection (CDI) recurs after initial treatment in approximately one in four patients. A single-centre pilot study suggested that this could be reduced using ‘follow-on’ rifaximin treatment. We aimed to assess the efficacy of rifaximin treatment in preventing recurrence. Methods A multisite, parallel group, randomised, placebo controlled trial recruiting patients aged ≥18 years immediately after resolution of CDI through treatment with metronidazole or vancomycin. Participants received either rifaximin 400 mg three times a day for 2 weeks, reduced to 200 mg three times a day for a further 2 weeks or identical placebo. The primary endpoint was recurrence of CDI within 12 weeks of trial entry. Results Between December 2012 and March 2016, 151 participants were randomised to either rifaximin or placebo. Primary outcome data were available on 130. Mean age was 71.9 years (SD 15.3). Recurrence within 12 weeks was 29.5% (18/61) among participants allocated to placebo compared with 15.9% (11/69) among those allocated to rifaximin, a difference between groups of 13.7% (95% CI −28.1% to 0.7%, p=0.06). The risk ratio was 0.54 (95% CI 0.28 to 1.05, p=0.07). During 6-month safety follow-up, nine participants died in each group (12%). Adverse event rates were similar between groups. Conclusion While ‘follow-on’ rifaximin after CDI appeared to halve recurrence rate, we failed to reach our recruitment target in this group of frail elderly patients, so the estimated effect of rifaximin lacks precision. A meta-analysis including a previous trial suggests that rifaximin may be effective; however, further, larger confirmatory studies are needed.