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Irritable Bowel Syndrome: HELP
Articles by Sander Van Wanrooy
Based on 3 articles published since 2009
(Why 3 articles?)
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Between 2009 and 2019, Sander Van Wanrooy wrote the following 3 articles about Irritable Bowel Syndrome.
 
+ Citations + Abstracts
1 Clinical Trial Psychological comorbidity increases the risk for postinfectious IBS partly by enhanced susceptibility to develop infectious gastroenteritis. 2016

Wouters, Mira M / Van Wanrooy, Sander / Nguyen, Anh / Dooley, James / Aguilera-Lizarraga, Javier / Van Brabant, Winde / Garcia-Perez, Josselyn E / Van Oudenhove, Lukas / Van Ranst, Marc / Verhaegen, Jan / Liston, Adrian / Boeckxstaens, Guy. ·Department of Clinical and Experimental Medicine, Translational Research Center for Gastrointestinal Disorders, University Hospital Leuven, KU Leuven, Leuven, Belgium. · Department of Microbiology and Immunology, KU Leuven, Leuven, Belgium Autoimmune Genetics Laboratory, VIB, Leuven, Belgium. · Laboratory of Clinical Virology, Rega Institute for Medical Research, University Hospital Leuven, Leuven, Belgium. · Department of Microbiology, University Hospital Leuven, KU Leuven, Leuven, Belgium. ·Gut · Pubmed #26071133.

ABSTRACT: OBJECTIVE: Psychological factors increase the risk to develop postinfectious IBS (PI-IBS), but the mechanisms involved are unclear. As stress affects the immune system, we investigated the potential interaction between psychological factors, the immune response against infectious gastroenteritis (IGE) and the development of IGE and PI-IBS in a large cohort exposed to contaminated drinking water. DESIGN: 18 620 people exposed to contaminated drinking water (norovirus, Giardia lamblia, Campylobacter jejuni) were invited to participate in a prospective controlled cohort study. They were asked to complete questionnaires assessing demographic, psychological and clinical data during the outbreak and 1 year later. At both time points, in-depth immune function (peripheral blood and rectal biopsies) was studied in a subgroup of subjects. RESULTS: 1379 subjects completed the questionnaires during the outbreak, of which 271 developed IGE. Risk factors for IGE included younger age, pre-existing dyspepsia-like symptoms, anxiety and drinking contaminated tap water. Anxiety scores before the outbreak inversely correlated with interleukin-2-expressing CD4+ T cells (r=0.6, p=0.01, n=23). At follow-up, 34 of 172 (20%) IGE subjects developed IBS compared with 24/366 exposed participants (7%, p<0.0001, χ(2) test). A Th2 cytokine phenotype at time of infection was associated with increased risk for PI-IBS 1 year later. Except for increased B cell numbers, no evidence for systemic or rectal mucosal immune activation in PI-IBS was demonstrated at follow-up. CONCLUSIONS: Our study shows that the increased risk of patients with psychological comorbidity to develop PI-IBS may partly result from an increased susceptibility to develop IGE, possibly resulting from a Th2-immune bias. TRIAL REGISTRATION NUMBER: (ClinicalTrials.gov NCT01497847).

2 Article Histamine Receptor H1-Mediated Sensitization of TRPV1 Mediates Visceral Hypersensitivity and Symptoms in Patients With Irritable Bowel Syndrome. 2016

Wouters, Mira M / Balemans, Dafne / Van Wanrooy, Sander / Dooley, James / Cibert-Goton, Vincent / Alpizar, Yeranddy A / Valdez-Morales, Eduardo E / Nasser, Yasmin / Van Veldhoven, Paul P / Vanbrabant, Winde / Van der Merwe, Schalk / Mols, Raf / Ghesquière, Bart / Cirillo, Carla / Kortekaas, Inge / Carmeliet, Peter / Peetermans, Willy E / Vermeire, Séverine / Rutgeerts, Paul / Augustijns, Patrick / Hellings, Peter W / Belmans, Ann / Vanner, Stephen / Bulmer, David C / Talavera, Karel / Vanden Berghe, Pieter / Liston, Adrian / Boeckxstaens, Guy E. ·Department of Clinical and Experimental Medicine, Translational Research Center for Gastrointestinal Disorders, University Hospital Leuven, KU Leuven, Leuven, Belgium. · Autoimmune Genetics Laboratory, Flemish Institute for Biotechnology (VIB) and Department of Microbiology and Immunology, KU Leuven, Leuven, Belgium. · National Centre for Bowel Research and Surgical Innovation, Centre for Neuroscience and Trauma, Blizard Institute, Bart's and the London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom. · Department of Cellular and Molecular Medicine, Laboratory of Ion Channel Research and Transient Receptor Potential (TRP) channel Research Platform, KU Leuven, Leuven, Belgium. · Gastrointestinal Diseases Research Unit, Kingston General Hospital, Queen's University, Kingston, Canada. · Department of Cellular and Molecular Medicine, Laboratory of Lipid Biochemistry and Protein-Interaction, KU Leuven, Leuven, Belgium. · Department of Clinical and Experimental Medicine, Hepatology, University Hospital Leuven, KU Leuven, Leuven, Belgium. · Department of Pharmaceutical and Pharmacological Sciences, Drug Delivery and Disposition, University Hospital Leuven, KU Leuven, Leuven, Belgium. · Laboratory of Angiogenesis and Neurovascular Link (Vesalius Research Center), KU Leuven, Leuven, Belgium. · Department of Microbiology and Immunology, Laboratory of Clinical Immunology, KU Leuven, Leuven, Belgium. · Department of Internal Medicine, Laboratory for Clinical Infectious and Inflammatory Disorders, University Hospital Leuven, KU Leuven, Leuven, Belgium. · Department of Microbiology and Immunology, Laboratory of Clinical Immunology, KU Leuven, Leuven, Belgium; Department of Otorhinolaryngology, Academic Medical Center Amsterdam, Amsterdam, The Netherlands; Department of Otorhinolaryngology, University of Ghent, Ghent, Belgium. · Department of Biostatistics and Centre of Statistical Bioinformatics, KU Leuven, Leuven, Belgium. · Department of Clinical and Experimental Medicine, Translational Research Center for Gastrointestinal Disorders, University Hospital Leuven, KU Leuven, Leuven, Belgium. Electronic address: guy.boeckxstaens@med.kuleuven.be. ·Gastroenterology · Pubmed #26752109.

ABSTRACT: BACKGROUND & AIMS: Histamine sensitizes the nociceptor transient reporter potential channel V1 (TRPV1) and has been shown to contribute to visceral hypersensitivity in animals. We investigated the role of TRPV1 in irritable bowel syndrome (IBS) and evaluated if an antagonist of histamine receptor H1 (HRH1) could reduce symptoms of patients in a randomized placebo-controlled trial. METHODS: By using live calcium imaging, we compared activation of submucosal neurons by the TRPV1 agonist capsaicin in rectal biopsy specimens collected from 9 patients with IBS (ROME 3 criteria) and 15 healthy subjects. The sensitization of TRPV1 by histamine, its metabolite imidazole acetaldehyde, and supernatants from biopsy specimens was assessed by calcium imaging of mouse dorsal root ganglion neurons. We then performed a double-blind trial of patients with IBS (mean age, 31 y; range, 18-65 y; 34 female). After a 2-week run-in period, subjects were assigned randomly to groups given either the HRH1 antagonist ebastine (20 mg/day; n = 28) or placebo (n = 27) for 12 weeks. Rectal biopsy specimens were collected, barostat studies were performed, and symptoms were assessed (using the validated gastrointestinal symptom rating scale) before and after the 12-week period. Patients were followed up for an additional 2 weeks. Abdominal pain, symptom relief, and health-related quality of life were assessed on a weekly basis. The primary end point of the study was the effect of ebastine on the symptom score evoked by rectal distension. RESULTS: TRPV1 responses of submucosal neurons from patients with IBS were potentiated compared with those of healthy volunteers. Moreover, TRPV1 responses of submucosal neurons from healthy volunteers could be potentiated by their pre-incubation with histamine; this effect was blocked by the HRH1 antagonist pyrilamine. Supernatants from rectal biopsy specimens from patients with IBS, but not from the healthy volunteers, sensitized TRPV1 in mouse nociceptive dorsal root ganglion neurons via HRH1; this effect could be reproduced by histamine and imidazole acetaldehyde. Compared with subjects given placebo, those given ebastine had reduced visceral hypersensitivity, increased symptom relief (ebastine 46% vs placebo 13%; P = .024), and reduced abdominal pain scores (ebastine 39 ± 23 vs placebo 62 ± 22; P = .0004). CONCLUSIONS: In studies of rectal biopsy specimens from patients, we found that HRH1-mediated sensitization of TRPV1 is involved in IBS. Ebastine, an antagonist of HRH1, reduced visceral hypersensitivity, symptoms, and abdominal pain in patients with IBS. Inhibitors of this pathway might be developed as a new treatment approach for IBS. ClinicalTrials.gov no: NCT01144832.

3 Article Genetic variants in CDC42 and NXPH1 as susceptibility factors for constipation and diarrhoea predominant irritable bowel syndrome. 2014

Wouters, Mira M / Lambrechts, Diether / Knapp, Michael / Cleynen, Isabelle / Whorwell, Peter / Agréus, Lars / Dlugosz, Aldona / Schmidt, Peter Thelin / Halfvarson, Jonas / Simrén, Magnus / Ohlsson, Bodil / Karling, Pontus / Van Wanrooy, Sander / Mondelaers, Stéphanie / Vermeire, Severine / Lindberg, Greger / Spiller, Robin / Dukes, George / D'Amato, Mauro / Boeckxstaens, Guy. ·Translational Research Center for Gastrointestinal Disorders, Leuven University, Leuven, Belgium. · Vesalius Research Center, VIB, Leuven University, Leuven, Belgium Laboratory for Translational Genetics, Department of Oncology, Leuven University, Leuven, Belgium. · Institute for Medical Biometry, Informatics and Epidemiology, University of Bonn, Bonn, Germany. · Department of Medicine, University of Manchester, Manchester, UK. · Centre for Family Medicine, Karolinska Institutet, Stockholm, Sweden. · Department of Medicine, Karolinska Institutet, Stockholm, Sweden. · Department of Internal Medicine, Örebro University Hospital, Örebro, Sweden. · Department of Internal Medicine, Gothenburg University, Gothenburg, Sweden. · Department of Clinical Sciences, Skånes University Hospital, Malmoe, Sweden. · Department of Medicine, Umeå University, Umeå, Sweden. · Queen's Medical Centre, Nottingham, UK. · Academic DPU, GlaxoSmithKline, Research Triangle Par, North Carolina, USA. · Department of Biosciences and Nutrition, Karolinska Institutet, Stockholm, Sweden. ·Gut · Pubmed #24041540.

ABSTRACT: OBJECTIVE: The complex genetic aetiology underlying irritable bowel syndrome (IBS) needs to be assessed in large-scale genetic studies. Two independent IBS cohorts were genotyped to assess whether genetic variability in immune, neuronal and barrier integrity genes is associated with IBS. DESIGN: 384 single nucleotide polymorphisms (SNPs) covering 270 genes were genotyped in an exploratory cohort (935 IBS patients, 639 controls). 33 SNPs with Puncorrected<0.05 were validated in an independent set of 497 patients and 887 controls. Genotype distributions of single SNPs were assessed using an additive genetic model in IBS and clinical subtypes, IBS-C and IBS-D, both in individual and combined cohorts. Trait anxiety (N=614 patients, 533 controls), lifetime depression (N=654 patients, 533 controls) and mRNA expression in rectal biopsies (N=22 patients, 29 controls) were correlated with SNP genotypes. RESULTS: Two SNPs associated independently in the exploratory and validation cohort: rs17837965-CDC42 with IBS-C (ORexploratory=1.59 (1.05 to 1.76); ORvalidation=1.76 (1.03 to 3.01)) and rs2349775-NXPH1 with IBS-D (ORexploratory=1.28 (1.06 to 1.56); ORvalidation=1.42 (1.08 to 1.88)). When combining both cohorts, the association of rs2349775 withstood post hoc correction for multiple testing in the IBS-D subgroup. Additionally, three SNPs in immune-related genes (rs1464510-LPP, rs1881457-IL13, rs2104286-IL2RA), one SNP in a neuronal gene (rs2349775-NXPH1) and two SNPs in epithelial genes (rs245051-SLC26A2, rs17837965-CDC42) were weakly associated with total-IBS (Puncorrected<0.05). At the functional level, rs1881457 increased IL13 mRNA levels, whereas anxiety and depression scores did not correlate with rs2349775-NXPH1. CONCLUSIONS: Rs2349775 (NXPH1) and rs17837965 (CDC42) were associated with IBS-D and IBS-C, respectively, in two independent cohorts. Further studies are warranted to validate our findings and to determine the mechanisms underlying IBS pathophysiology.