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Left ventricular (LV) thrombus formation remains a post-acute myocardial infarction (AMI) complication even in the modern era of early reperfusion. The optimal anticoagulation regimen in this clinical scenario is poorly defined. The present meta-analysis sought to investigate the efficacy and safety profile of direct oral anticoagulants (DOACs) compared with vitamin K antagonists (VKAs) for the management of LV thrombus after AMI. A systematic literature review was conducted in electronic databases to identify studies reporting efficacy and safety outcome data regarding the use of DOACs versus VKAs for patients with LV thrombus after AMI. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated, and random-effects meta-analyses were conducted to synthesize pooled ORs. Eight studies comprising a total of 605 patients were included. DOACs were associated with an almost twofold higher likelihood of thrombus resolution compared with VKAs (pooled OR 1.95 [1.25 to 3.04], p = 0.003, I 2 = 0%), and decreased the risk of systemic embolism by 70% (pooled OR 0.30 [0.12 to 0.75]; p = 0.01, I 2 = 0%). The use of DOACs was associated with a 54% lower risk of bleeding compared with VKAs (pooled OR 0.46 [0.26 to 0.84], p = 0.01, I 2 = 0%). Overall, patients receiving DOACs had a 63% lower risk of reaching the composite outcome of safety and efficacy compared with patients using VKAs (pooled OR 0.37 [0.23 to 0.60], p <0.0001, I 2 = 0%). In conclusion, DOACs appear to have a more favorable efficacy and safety profile compared with VKAs for the management of LV thrombus related to AMI., Competing Interests: Declaration of competing interest The authors have no competing interests to declare., (Copyright © 2024 Elsevier Inc. All rights reserved.)

The role of the gut microbiome (GM) and oral microbiome (OM) in cardiovascular disease (CVD) has been increasingly being understood in recent years. It is well known that GM is a risk factor for various CVD phenotypes, including hypertension, dyslipidemia, heart failure and atrial fibrillation. However, its role in valvular heart disease (VHD) is less well understood. Research shows that, direct, microbe-mediated and indirect, metabolite-mediated damage as a result of gut dysbiosis and environmental factors results in a subclinical, chronic, systemic inflammatory state, which promotes inflammatory cell infiltration in heart valves and subsequently, via pro-inflammatory molecules, initiates a cascade of reaction, resulting in valve calcification, fibrosis and dysfunction. This relationship between GM and VHD adds a pathophysiological link to the pathogenesis of VHD, which can be aimed therapeutically, in order to prevent or regress any risk for valvular pathologies. Therapeutic interventions include dietary modifications and lifestyle interventions, in order to influence environmental factors that can promote gut dysbiosis. Furthermore, the combination of probiotics and prebiotics, as well as fecal m transplantation and targeted treatment with inducers or inhibitors of microbial enzymes have showed promising results in animal and/or clinical studies, with the potential to reduce the inflammatory state and restore the normal gut flora in patients. This review, thus, is going to discuss the pathophysiological links behind the relationship of GM, CVD and VHD, as well as explore the recent data regarding the effect of GM-altering treatment in CVD, cardiac function and systemic inflammation., Competing Interests: The authors declare no conflicts of interest.

Ulcerative colitis (UC) is an autoimmune disease associated with both intestinal and extraintestinal manifestations. The latter may include heart complications, such as myopericarditis leading to life-threatening arrythmias. Nowadays, UC is commonly treated with biologic medications and infliximab is the first line therapy in an outpatient setting, while it is also used as rescue therapy in acute severe UC. However, it has been associated with severe immunosuppression, cytomegalovirus (CMV) reactivation and drug-induced hepatitis. We report a case of UC flare in a biologic naïve patient admitted with myopericarditis, which was further complicated by positive CMV biopsies and infliximab-induced transaminitis., Learning Points: In acute inflammatory bowel disease (IBD) flare presentation with tachycardia and chest pain, an underlying myocardial injury should be investigated.Mucosal healing should be evaluated endoscopically in cases of partial response to biologics.Both cytomegalovirus (CMV) infection and infliximab-induced liver injury may lead to acute hepatitis., Competing Interests: Conflicts of Interests: The Authors declare that there are no competing interests., (© EFIM 2024.)

Interleukins are potential therapeutic targets that can alter the prognosis and progression of inflammatory bowel disease (IBD). The roles of IL-6, IL-10, IL-17, and IL-23 have been extensively studied, setting the stage for the development of novel treatments for patients with IBD. Other cytokines have been less extensively studied. Members of the IL-20 family, mainly IL-19 and IL-24, are involved in the pathogenesis of IBD, but their exact role remains unclear. Similarly, IL-33, a newly identified cytokine, has been shown to control the Th1 effector response and the action of colonic Tregs in animal models of colitis and patients with IBD. IL-21 is involved in the Th1, Th2, and Th17 responses. Data support a promising future use of these interleukins as biomarkers of severe diseases and as potential therapeutic targets for novel monoclonal antibodies. This review aims to summarize the existing studies involving animal models of colitis and patients with IBD to clarify their role in the intestinal mucosa., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Pan-Arab Association of Gastroenterology. All rights reserved.)

Background: Data on the optimum positioning of biologics in the treatment of inflammatory bowel disease (IBD) are limited., Research Design and Methods: This was a longitudinal retrospective study of linked health-care data from northwest London, UK, for adults who started ustekinumab for IBD from 1 April 20161 April 2016 to 1 April 20211 April 2021. We compared outcomes by line of therapy (1 vs. 2 or 3+) and age group (18‒59 years or ≥ 60 years). In an analysis of CD patients, we calculated risks of IBD-related hospitalization, IBD-related abdominal surgery, ustekinumab persistence, and switching by line of therapy., Results: Of 163 patients screened, 149 were eligible. Age had no effect on outcomes. Elective all-cause hospital admissions were significantly higher when ustekinumab was used as second-line or third-line therapy compared with first-line treatment ( p  = 0.0048 and p  = 0.001, respectively). In CD patients the numbers of hospital admissions were also higher with second-line or third-line therapy ( p  = 0.040 and p  = 0.018, respectively). Use of ustekinumab as third-line therapy significantly increased the risk of IBD-related hospitalization (hazard ratio 2.5, 95% CI 1.1‒5.6, p  = 0.029), IBD-related abdominal surgery (9.45, 1.2‒75.7, p  = 0.03), and switching (14.6, 1.6‒131.0, p  = 0.02). Drug persistence risks did not differ., Conclusions: These findings support the use of ustekinumab as first-line therapy.

Purpose of Review: Small bowel dysmotility is common in the context of neurological disorders. Overlooking it can have an adverse impact on patient's quality of life and neurological outcomes. This review focuses on describing the mechanisms and effects of enteric dysmotility in neurological patients and providing treatment options., Recent Findings: Small bowel dysmotility is prevalent among neurological patients. The definition and diagnosis of small bowel dysmotility is a challenge; however, up to two-thirds of neurological patients may experience associated symptoms. Small bowel dysmotility can affect the absorption of nutrients and medication, impacts on social and professional function and can result in malnutrition and its associated morbidity and mortality., Summary: Small bowel dysmotility due to a neuropathy can result from acute or chronic disorders in the central and peripheral nervous system and includes the cerebral cortex, brain stem, spinal cord, parasympathetic (vagus) and sympathetic nerves and the myenteric and submucosal plexuses of the intestine. Generalized muscle disorders can also cause an enteral myopathy. Generally, the disorders may be degenerative or inflammatory. Both enteric neuropathy and myopathy may cause symptoms of abdominal pain, nausea/vomiting, bloating, constipation or diarrhoea and can cause malnutrition. The symptoms need to be addressed in order of importance to the patient and malnutrition prevented or treated., (Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.)

Therapeutic drug monitoring (TDM) has emerged as a useful tool for optimising the use of biologics, and in particular anti-tumour necrosis factor (anti-TNF) therapy, in inflammatory bowel disease (IBD). However, challenges remain and are hindering the widespread implementation of TDM in clinical practice. These barriers include identification of the optimal drug concentration to target, the lag time between sampling and results, and the proper interpretation of anti-drug antibody titres among different assays. Solutions to overcome these barriers include the harmonisation of TDM assays and the use of point-of-care testing. Other unmet needs include well designed prospective studies and randomised controlled trials focusing on proactive TDM, particularly during induction therapy. Future studies should also investigate the utility of TDM for biologics other than anti-TNF therapies in both IBD and other immune-mediated inflammatory diseases such as rheumatoid arthritis and psoriasis, and the use of pharmacokinetic modelling dashboards and pharmacogenetics towards individual personalised medicine., Competing Interests: Declaration of interests KP has received a lecture fee from Mitsubishi Tanabe Pharma and Physicians Education Resource; a consultancy fee from Prometheus Laboratories; and scientific advisory board fees from ProciseDx and Scipher Medicine Corporation. NVC has received research grants and personal fees from R-Biopharm, Takeda, and UCB; and personal fees from Alimentiv (formerly Robarts Clinical Trials), Celltrion, and Prometheus Laboratories. ASC has received consultancy fees from AbbVie, Janssen, Takeda, Bacainn, Arena Pharmaceuticals, Grifols, Prometheus Laboratories, Samsung, Bristol Myers Squibb, and Pfizer; and research support from Inform Diagnostics. SV has received grants from AbbVie, Johnson and Johnson, Pfizer, and Takeda; consultancy fees from AbbVie, Arena Pharmaceuticals, Avaxia, Boehringer Ingelheim, Celgene, Dr Falk Pharma, Ferring, Galapagos, Genentech (Roche), Gilead, Hospira, Janssen, Mundipharma, Merck Sharp & Dohme, Pfizer, Prodigest, Progenity, Prometheus Biosciences, Alimentiv, Second Genome, Shire, Takeda, Theravance, and Tillots Pharma; and speaker fees from AbbVie, Dr Falk Pharma, Ferring, Galapagos, Genentech-Roche, Janssen, Pfizer, Shire, Takeda, and Tillots Pharma. NA has received a grant from Pfizer and lecture fees from Janssen, Pfizer, and Takeda. TK reports personal fees from Alfresa Pharma, Covidien, Eli Lilly, Ferring Pharmaceuticals, Janssen, Kyorin Pharmaceutical, Mochida Pharmaceutical, Nippon Kyaku, Pfizer, Takeda Pharmaceutical, Thermo Fisher Scientific, AbbVie, Astellas, Celltrion, EA Pharma, Nippon Kyaku, Mochida Pharmaceutical, Mitsubishi Tanabe Pharma, Zeria Pharmaceutical, Gilead Sciences, Janssen, and JIMRO; and grants from AbbVie, EA Pharma, Otsuka Holdings, Zeria Pharmaceutical, Kyorin Pharmaceutical, Mochida Pharmaceutical, Thermo Fisher Scientific, Alfresa Pharma, and Nippon Kyaku. WJS reports research grants from AbbVie, Abivax, Arena Pharmaceuticals, Boehringer Ingelheim, Celgene, Genentech, Gilead Sciences, GlaxoSmithKline, Janssen, Lilly, Pfizer, Prometheus Biosciences, Seres Therapeutics, Shire, Takeda, and Theravance Biopharma; consultancy fees from AbbVie, Abivax, Admirx, Alfasigma, Alimentiv, Alivio Therapeutics, Allakos, Amgen, Applied Molecular Transport, Arena Pharmaceuticals, Salix (Bausch Health), Beigene, Bellatrix Pharmaceuticals, Boehringer Ingelheim, Boston Pharmaceuticals, Bristol Myers Squibb, Celgene, Celltrion, Cellularity, Cosmo Pharmaceuticals, Escalier Biosciences, Equillium, Forbion, Genentech (Roche), Gilead Sciences, Glenmark Pharmaceuticals, Gossamer Bio, Immunic, Index Pharmaceuticals, Intact Therapeutics, Janssen, Kyverna Therapeutics, Landos Biopharma, Lilly, Oppilan Pharma, Otsuka, Pandion Therapeutics, Pfizer, Progenity, Prometheus Biosciences, Prometheus Laboratories, Protagonists Therapeutics, Provention Bio, Reistone Biopharma, Seres Therapeutics, Shanghai Pharma Biotherapeutics, Shire, Shoreline Biosciences, Sublimity Therapeutics, Surrozen, Takeda, Theravance Biopharma, Thetis Pharmaceuticals, Tillotts Pharma, UCB, Vendata Biosciences, Ventyx Biosciences, Vimalan Biosciences, Vivelix Pharmaceuticals, Vivreon Biosciences, and Zealand Pharma; and stock or stock options from Allakos, BeiGene, Gossamer Bio, Oppilan Pharma, Prometheus Biosciences, Prometheus Laboratories, Progenity, Shoreline Biosciences, Ventyx Biosciences, Vimalan Biosciences, and Vivreon Biosciences. PMI reports lecture fees from AbbVie, Bristol Myers Squibb, Celgene, Falk Pharma, Ferring, Gilead, Merck Sharp & Dohme, Janssen, Pfizer, Takeda, Tillotts, Sapphire Medical, Sandoz, Shire, and Warner Chilcott; financial support for research from Merck Sharp & Dohme, Pfizer, and Takeda; and advisory fees from AbbVie, Arena Pharmaceuticals, Genentech, Gilead, Hospira, Janssen, Lilly, Merck Sharp & Dohme, Pfizer, Pharmacosmos, Procise, Prometheus Biosciences, Roche, Sandoz, Samsung Bioepis, Takeda, Topivert, VHsquared, Vifor Pharma, and Warner Chilcott. MF reports financial support for research from AbbVie, Amgen, Biogen, Janssen, Pfizer, and Takeda; consultancy fees from AbbVie, Boehringer-Ingelheim, Celltrion, Janssen, Lilly, Medtronic, Merck Sharp & Dohme, Pfizer, Sandoz, Takeda, and Thermo Fisher Scientific; and speaker fees from AbbVie, Amgen, Biogen, Boehringer-Ingelheim, Falk, Ferring, Janssen, Lamepro, Merck Sharp & Dohme, Mylan, Pfizer, Sandoz, Takeda, and Truvion Healthcare. PGK has received consultancy and speaker fees from AbbVie, Janssen, Pfizer, Takeda, Ferring, and Novartis; and scientific grants from Takeda and Pfizer. DD has served as a speaker, a consultant, and an advisory board member for Merck Sharp & Dohme, AbbVie, Takeda, Pfizer, Janssen, Amgen, Biogen, and Krka. JL has received unrestricted grants from AbbVie, Almirall, Celgene, Eli Lilly, Janssen-Cilag, LEO Pharma, Novartis, and UCB; speaker fees for AbbVie, Almirall, BMS, Janssen-Cilag, Pfizer, and UCB; and consultancy fees for AbbVie, Bristol Myers Squibb, Celgene, Eli Lilly, Janssen-Cilag, LEO Pharma, Novartis, and UCB. NK has received speaker fees from Janssen. WA has received consultancy fees from AbbVie, Amgen, Arena Pharmaceuticals, Dynacare, Janssen, Merck, Novartis, Pfizer, Sandoz, and Takeda. AJY has received consultant or advisory board fees from Prometheus Laboratories, Takeda, Arena Pharmaceuticals, and Bristol Myers Squibb. SD has served as a speaker, consultant, and advisory board member for Schering-Plough, AbbVie, Merck Sharp & Dohme, UCB, Ferring, Cellerix, Takeda, Nycomed, Pharmacosmos, Actelion, Alphawasserman, Genentech, Grunenthal, Pfizer, AstraZeneca, Novo Nordisk, Cosmo Pharmaceuticals, Vifor Pharma, Johnson and Johnson, Nikkiso Europe, and Theravance. MCD has received consultancy fees from Janssen, AbbVie, Pfizer, Takeda, UCB, Celgene, Bristol Myers Squibb, Prometheus Biosciences, Arena Pharmaceuticals, and Lilly; and grant support from AbbVie, Pfizer, and Janssen. LPB has received grant support from AbbVie, Merck Sharp & Dohme, and Takeda; consulting fees from AbbVie, Janssen, Genentech, Ferring, Tillots, Pharmacosmos, Celltrion, Takeda, Boerhinger-Ingelheim, Pfizer, Index Pharmaceuticals, Sandoz, Celgene, Biogen, Samsung Bioepis, Alma, Sterna, Nestle, Enterome, Allergan, Merck Sharp & Dohme, Roche, Arena Pharmaceuticals, Gilead, Hikma, Amgen, Bristol Myers Squibb, Vifor, Norgine, Mylan, Lilly, Fresenius, Oppilan Pharma, Sublimity Therapeutics, Applied Molecular Transport, OSE Immunotherapeutics, and Enthera; and stock or stock options from Clinical Trials Mobile Application. All other authors declare no competing interests., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

Objective: Delayed second dose SARS-CoV-2 vaccination trades maximal effectiveness for a lower level of immunity across more of the population. We investigated whether patients with inflammatory bowel disease treated with infliximab have attenuated serological responses to a single dose of a SARS-CoV-2 vaccine., Design: Antibody responses and seroconversion rates in infliximab-treated patients (n=865) were compared with a cohort treated with vedolizumab (n=428), a gut-selective anti-integrin α4β7 monoclonal antibody. Our primary outcome was anti-SARS-CoV-2 spike (S) antibody concentrations, measured using the Elecsys anti-SARS-CoV-2 spike (S) antibody assay 3-10 weeks after vaccination, in patients without evidence of prior infection. Secondary outcomes were seroconversion rates (defined by a cut-off of 15 U/mL), and antibody responses following past infection or a second dose of the BNT162b2 vaccine., Results: Geometric mean (SD) anti-SARS-CoV-2 antibody concentrations were lower in patients treated with infliximab than vedolizumab, following BNT162b2 (6.0 U/mL (5.9) vs 28.8 U/mL (5.4) p<0.0001) and ChAdOx1 nCoV-19 (4.7 U/mL (4.9)) vs 13.8 U/mL (5.9) p<0.0001) vaccines. In our multivariable models, antibody concentrations were lower in infliximab-treated compared with vedolizumab-treated patients who received the BNT162b2 (fold change (FC) 0.29 (95% CI 0.21 to 0.40), p<0.0001) and ChAdOx1 nCoV-19 (FC 0.39 (95% CI 0.30 to 0.51), p<0.0001) vaccines. In both models, age ≥60 years, immunomodulator use, Crohn's disease and smoking were associated with lower, while non-white ethnicity was associated with higher, anti-SARS-CoV-2 antibody concentrations. Seroconversion rates after a single dose of either vaccine were higher in patients with prior SARS-CoV-2 infection and after two doses of BNT162b2 vaccine., Conclusion: Infliximab is associated with attenuated immunogenicity to a single dose of the BNT162b2 and ChAdOx1 nCoV-19 SARS-CoV-2 vaccines. Vaccination after SARS-CoV-2 infection, or a second dose of vaccine, led to seroconversion in most patients. Delayed second dosing should be avoided in patients treated with infliximab., Trial Registration Number: ISRCTN45176516., Competing Interests: Competing interests: NAK reports grants from F. Hoffmann-La Roche AG, grants from Biogen Inc, grants from Celltrion Healthcare, grants from Galapagos NV, non-financial support from Immundiagnostik, during the conduct of the study; grants and non-financial support from AbbVie, grants and personal fees from Celltrion, personal fees and non-financial support from Janssen, personal fees from Takeda, personal fees and non-financial support from Dr Falk, outside the submitted work. SL reports non-financial support from Pfizer, non-financial support from Ferring, outside the submitted work. JRG reports grants from F. Hoffmann-La Roche AG, grants from Biogen, grants from Celltrion Healthcare, grants from Galapagos NV, non-financial support from Immundiagnostik, during the conduct of the study. DC reports non-financial support from Ferring, personal fees and non-financial support from Pfizer, outside the submitted work. JRFC reports grants and personal fees from Samsung, Pfizer & Biogen; personal fees and non-financial support from Janssen & Abbvie; grants, personal fees and non-financial support from Takeda; personal fees from MSD, Sandoz, Celltrion & NAPP, outside the submitted work. AF reports personal fees from Takeda UK Ltd, personal fees from Dr Falk Pharma, personal fees from Tillotts, personal fees from Abbvie Ltd, personal fees from Sheild, personal fees from Ferring, from Pharmacosmos, personal fees from Allergan, personal fees from Janssen, outside the submitted work. PMI reports grants and personal fees from Takeda, grants from MSD, grants and personal fees from Pfizer, personal fees from Galapagos, personal fees from Gilead, personal fees from Abbvie, personal fees from Janssen, personal fees from Boehringer Ingelheim, personal fees from Topivert, personal fees from VH2, personal fees from Celgene, personal fees from Arena, personal fees from Samsung Bioepis, personal fees from Sandoz, personal fees from Procise, personal fees from Prometheus, outside the submitted work. NK reports personal fees from Janssen, outside the submitted work. KBK reports personal fees from Janssen, personal fees from Takeda, personal fees from PredictImmune, personal fees from Amgen, outside the submitted work. CAL reports grants from Genentech, grants and personal fees from Janssen, grants and personal fees from Takeda, grants from AbbVie, personal fees from Ferring, grants from Eli Lilly, grants from Pfizer, grants from Roche, grants from UCB Biopharma, grants from Sanofi Aventis, grants from Biogen IDEC, grants from Orion OYJ, personal fees from Dr Falk Pharma, grants from AstraZeneca, outside the submitted work. JM reports grants and personal fees from Takeda Pharmaceuticals, grants and personal fees from Biogen, personal fees and non-financial support from AbbVie, personal fees from Grifols, personal fees from Sandoz, personal fees from Celltrion, personal fees and non-financial support from Janssen, personal fees from Vifor Pharmaceuticals, personal fees from Predictimmune, personal fees from Bristol Myers Squibb, non-financial support from Ferring Pharmaceuticals, outside the submitted work. RCGP reports acting as consultant, advisory board member, speaker or recipient of educational grant from Dr Falk, Ferring, Janssen, Pharmacosmos and Takeda. TR reports grants and personal fees from Abbvie, personal fees from BMS, personal fees from Celgene, personal fees from Ferring, personal fees from Gilead, personal fees from GSK, personal fees from LabGenius, personal fees from Janssen, personal fees from Mylan, personal fees from MSD, personal fees from Novartis, personal fees from Pfizer, personal fees from Sandoz, personal fees from Takeda, personal fees from Galapagos, personal fees from Arena, outside the submitted work. PJS reports speaker fees and advisory board sponsorship from Janssen, Celltrion and Takeda outside the submitted work. AMV reports personal fees and non-financial support from Takeda, personal fees and non-financial support from Celltrion, personal fees and non-financial support from Merck Sharp & Dohme, outside the submitted work. SJ is an employee of Roche Diagnostics and holds Roche shares. SS reports grants from Takeda, Abbvie, AMGEN, Tillots Pharma, personal fees from Jaansen, Takeda, Galapagos, Celltrion, Falk Pharma, Tillots pharma, Cellgene, Pfizer, Pharmacocosmos, outside the submitted work. CWL reports personal fees from Abbvie, personal fees from Janssen, personal fees from Pfizer, personal fees from Takeda, grants from Gilead, personal fees from Gilead, personal fees from Galapagos, personal fees from Iterative Scopes, personal fees from Trellus Health, personal fees from Celltion, personal fees from Ferring, personal fees from BMS, during the conduct of the study. NP reports personal fees from Takeda, personal fees from Janssen, personal fees from Pfizer, personal fees from Bristol-Myers Squibb, personal fees from Abbvie, personal fees from Roche, personal fees from Lilly, personal fees from Allergan, personal fees from Celgene, outside the submitted work; and NP has served as a speaker/advisory board member for Abbvie, Allergan, Bristol Myers Squibb, Celgene, Falk, Ferring, Janssen, Pfizer, Tillotts, Takeda and Vifor Pharma. TA reports grants and non-financial support from F. Hoffmann-La Roche AG, grants from Biogen Inc, grants from Celltrion Healthcare, grants from Galapagos NV, non-financial support from Immundiagnostik, during the conduct of the study; personal fees from Biogen, grants and personal fees from Celltrion Healthcare, personal fees and non-financial support from Immundiagnostik, personal fees from Takeda, personal fees from ARENA, personal fees from Gilead, personal fees from Adcock Ingram Healthcare, personal fees from Pfizer, personal fees from Genentech, non-financial support from Tillotts, outside the submitted work., (© Author(s) (or their employer(s)) 2021. No commercial re-use. See rights and permissions. Published by BMJ.)

Atherosclerosis and inflammatory bowel disease (IBD) are often regarded as 2 distinct entities. The commonest manifestation of atherosclerosis is ischemic heart disease (IHD), and an association between IHD and IBD has been reported. Atherosclerosis and IBD share common pathophysiological mechanisms in terms of their genetics, immunology, and contributing environmental factors. Factors associated with atherosclerosis are implicated in the development of IBD and vice versa. Therefore, treatments targeting the common pathophysiology pathways may be effective in both conditions. The current review considers the pathophysiological pathways that are shared between the 2 conditions and discusses the implications for treatment and research.

Background and Aims: Double balloon enteroscopy (DBE) has revolutionised the diagnosis and treatment of small bowel (SB) conditions. However, deep SB insertion can be challenging in patients with a history of abdominal surgery and a two-step procedure is required when findings are not amenable to endoscopic therapy. This case series reports the development of laparoscopically assisted DBE (LA-DBE) using single incision laparoscopic surgery (SILS)., Methods: Retrospective review of LA-DBE procedures performed in a single tertiary centre over 6 years., Results: Seventeen patients (median age: 40 years, male 41%) underwent 17 LA-DBE procedures. The approach was oral in 13 and rectal in 4. Laparoscopic approach was standard (multi-port) in the first four cases, SILS was then used in all subsequent patients (13/17). Indications for LA-DBE were previously failed standard DBE (n = 16) and need for a combined procedure (n = 1). Indications for DBE were Peutz-Jeghers syndrome (PJS) (n = 10), suspected submucosal/polypoid lesion at small bowel imaging (n = 5) and obscure gastrointestinal bleeding (OGIB) with vascular abnormalities seen at capsule endoscopy (n = 2). In 1/17 the suggested pathology on imaging was not identified. Therapy was applied in 15/17 (88%) cases. Diagnoses were PJS polyps (n = 8), neuroendocrine tumour (NET) (n = 2), PJS and NET (n = 1), transmural arteriovenous malformation (n = 1), angioectesia (n = 1), inflammatory polyp (n = 1), leiomyoma (n = 1) and Meckel's diverticulum (n = 1). The median (range) procedure time was 147 (84-210) mins. Median (range) length of stay post-procedure was 2 (1-19) days. Three patients developed complications. The 30-day mortality rate was 0%., Conclusions: LA-DBE is a safe, effective and minimally invasive procedure that can be applied for the management of selected patients with small bowel pathology. A SILS approach allows all therapeutic modalities to be available, including conversion to intraoperative enteroscopy (IOE), laparoscopic small bowel resection and laparotomy.

Background: Therapeutic drug monitoring (TDM) by measuring infliximab (IFX) trough levels and antibodies to infliximab (ATI) is used to optimise treatment in inflammatory bowel disease. We aimed to explore the clinical outcomes of TDM for patients with Crohn's disease on IFX in real life setting., Methods: This is a retrospective observational study. Primary outcomes were the clinicians' response to each TDM result and the rate of IFX discontinuation due to secondary loss of response or serious adverse event. Secondary outcomes included the intestinal surgery rate after IFX initiation and remission 6 months after TDM. Multivariate logistic regression was performed to identify factors associated with IFX discontinuation and abdominal surgery., Results: 291 patients were included. 238 (81.8%) patients were tested for TDM at least once during their follow-up with 672 TDM results. 95/238 patients (39.9%) had undetectable levels and 76 (31.9%) had positive ATI at least once. The median infliximab trough level was 3.4 µg/mL. IFX was discontinued in 109 patients (37.5%). 526/672 (78.3%) TDMs results were not followed by altered patient management. Treatment was discontinued in 40 (75.5%) patients never tested for TDM compared with 69 (29.0%) of those tested (p<0.01). Fewer TDM tested patients (29; 12.2%) required intestinal surgery post IFX initiation compared with TDM not-tested (15; 28.3%). Not being TDM tested was independently associated with IFX discontinuation and abdominal surgery., Conclusions: IFX discontinuation and intestinal surgery were significantly less frequent with TDM. TDM requested to investigate loss of response resulted in change in patient management., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2019. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: Inflammatory bowel disease (IBD) is a chronic relapsing-remitting condition affecting 600 000 people in the UK. Traditionally, patients attend outpatient clinics for monitoring regardless of their symptoms or risk of developing complications. This can lead to a mismatch between need and access: patients in remission given elective appointments displace those in need of urgent specialist attention. Novel initiatives implemented in the UK to improve outpatient monitoring have often required a well-maintained patient registry, empowered patients and significant information technology support., Design and Strategy: In this large-scale quality improvement project at St Mark's Hospital, a tertiary centre for IBD, we stratified over 1000 patients attending three non-complex IBD clinics over 12 months according to disease activity and risk profile. The aim was to offer a choice and subsequently transfer 50% of eligible patients to specialist nurse-led telephone clinics and demonstrate non-inferior satisfaction levels to existing outpatient follow-up. We also sought to ensure there was timely access to a newly established rapid access clinic for patients requiring urgent specialist attention.A core project team consisting of healthcare professionals, patients and quality improvement scientists met regularly. The team tested and scaled up interventions using 'Plan-Do-Study-Act' cycles within the 'Model for Improvement' framework and analysed data continuously using statistical process charts., Results: Over 12 months, the average number of eligible patients transferred to telephone clinics rose from 17.6% (42/239) using a questionnaire method to 59.3% (73/123) using active discussion in clinic. Patient satisfaction scores remained high and non-inferior to baseline scores in face-to-face clinics. The median waiting time to be seen in the rapid access clinic was 6.5 days., Conclusion: This is the first published study to report on the successful stratification of patients with IBD based on disease activity and risk of complications to create a more responsive, sustainable and patient-centred model for IBD monitoring., Competing Interests: Competing interests: None declared.

Background: Vedolizumab (VDZ) is effective for treatment of ulcerative colitis (UC) and Crohn's disease (CD). In GEMINI trials, anti-tumor necrosis factor (anti-TNF)-naïve patients had a superior response compared with anti-TNF-exposed patients. In real-world experience (RWE), the number of included anti-TNF-naïve patients was low. We aimed to evaluate the effectiveness and safety of VDZ in anti-TNF-naïve patients in an RWE setting., Methods: This retrospective multicenter European pooled cohort study included consecutive active anti-TNF-naïve IBD patients treated with VDZ. The primary end point was clinical response at week 14. Patients with follow-up beyond week 14 and those discontinuing VDZ at any time were included for maintenance outcomes analysis., Results: Since January 2015, 184 anti-TNF-naïve patients from 23 centers initiated VDZ treatment (Crohn's disease [CD], 50; ulcerative colitis [UC], 134). In CD, 42/50 (82%) patients responded by week 14 and 32 (64%) were in clinical remission; 26/50 (52%) achieved corticosteroid-free remission (CSFR). At last follow-up (44 weeks; interquartile range [IQR], 30-52 weeks), 27/35 (77.1%) patients with available data responded to treatment; 24/35 (68.6%) were in clinical remission, 21/35 (60%) were in CSFR. For UC, 116/134 (79.1%) responded to treatment by week 14, including 53 (39.5%) in clinical remission; 49/134 (36.6%) achieved CSFR. At last follow-up (42.5 weeks; IQR, 30-52 weeks), 79/103 (76.7%) patients responded to treatment, 69/103 (67.0%) were in remission, and 61/103 (59.2%) were in CSFR. Adverse effects were reported in 20 (11%) of the patients, leading to treatment discontinuation in 6 (3.3%)., Conclusions: VDZ is similarly effective in ant-TNF-naïve CD and UC patients. The efficacy is higher than reported in anti-TNF-experienced patients and is comparable to that of anti-TNF biologics in this population.

Background: Children and adolescents with inflammatory bowel disease (IBD) are more likely to have Crohn's disease (CD) than ulcerative colitis (UC) and their disease tends to be more extensive and severe than in adults. We hypothesized that the prevalence of anemia would therefore be greater in children and adolescents than in adults attending IBD outpatient clinics., Methods: Using the WHO age-adjusted definitions of anemia we assessed the prevalence, severity, type, and response to treatment of anemia in patients attending pediatric, adolescent, and adult IBD clinics at our hospital., Results: The prevalence of anemia was 70% (41/59) in children, 42% (24/54) in adolescents, and 40% (49/124) in adults (P < 0.01). Overall, children (88% [36/41]) and adolescents (83% [20/24]) were more often iron-deficient than adults (55% [27/49]) (P < 0.01). Multivariate logistic regression showed that both active disease (odds ratio [OR], 4.7 95% confidence interval [CI], 2.5, 8.8) and attending the pediatric clinic (OR 3.7; 95% CI, 1.6, 8.4) but not the adolescent clinic predicted iron deficiency anemia. Fewer iron-deficient children (13% [5/36]) than adolescents (30% [6/20]) or adults (48% [13/27]) had been given oral iron (P < 0.05); none had received intravenous iron compared with 30% (6/20) adolescents and 41% (11/27) adults (P < 0.0001)., Conclusions: Anemia is even more common in children than in older IBD patients. Oral iron was given to half of adolescents and adults but, despite similar tolerance and efficacy, only a quarter of children with iron-deficient anemia. Reasons for the apparent underutilization of iron therapy include a perceived lack of benefit and concerns about side effects, including worsening of IBD activity., (Copyright © 2011 Crohn's & Colitis Foundation of America, Inc.)