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Dive into the research topics where Pieter Hindryckx is active.

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Featured researches published by Pieter Hindryckx.


Journal of Crohns & Colitis | 2017

Third European Evidence-based Consensus on Diagnosis and Management of Ulcerative Colitis. Part 1: Definitions, Diagnosis, Extra-intestinal Manifestations, Pregnancy, Cancer Surveillance, Surgery, and Ileo-anal Pouch Disorders

Fernando Magro; Paolo Gionchetti; Rami Eliakim; Alessandro Armuzzi; Manuel Barreiro-de Acosta; Johan Burisch; Krisztina B. Gecse; Ailsa Hart; Pieter Hindryckx; Cord Langner; Jimmy K. Limdi; Gianluca Pellino; Edyta Zagórowicz; Tim Raine; Marcus Harbord; Florian Rieder

aDepartment of Pharmacology and Therapeutics, University of Porto; MedInUP, Centre for Drug Discovery and Innovative Medicines; Centro Hospitalar São João, Porto, Portugal bIBD Unit, DIMEC, University of Bologna, Bologna, Italy cDepartment of Gastroenterology and Hepatology, Chaim Sheba Medical Center, Tel Hashomer, Israel dGastrointestinal Unit ASST Fatebenefratelli Sacco—University of Milan—Milan, Italy eIBD Unit Complesso Integrato Columbus, Gastroenterological and Endocrino-Metabolical Sciences Department, Fondazione Policlinico Universitario Gemelli Universita’ Cattolica del Sacro Cuore, Rome, Italy fDepartment of Gastroenterology, IBD Unit, University Hospital Santiago De Compostela (CHUS), A Coruña, Spain gDepartment of Gastroenterology, North Zealand University Hospital, Frederikssund, Denmark hFirst Department of Medicine, Semmelweis University, Budapest, Hungary iIBD Unit, St Mark’s Hospital, Middlesex, UK jDepartment of Gastroenterology, University Hospital of Ghent, Ghent, Belgium kInstitute of Pathology, Medical University of Graz, Graz, Austria lDepartment of Gastroenterology, Pennine Acute Hospitals NHS Trust; Institute of Inflammation and Repair, University of Manchester, Manchester, UK mUnit of General Surgery, Second University of Naples, Napoli, Italy nMaria Skłodowska-Curie Memorial Cancer Centre and Institute of Oncology, Department of Oncological Gastroenterology Warsaw; Medical Centre for Postgraduate Education, Department of Gastroenterology, Hepatology and Clinical Oncology, Warsaw, Poland oDepartment of Medicine, University of Cambridge, Cambridge, UK pImperial College London; Chelsea and Westminster Hospital, London, UK qDepartment of Pathobiology /NC22, Lerner Research Institute; Department of Gastroenterology, Hepatology and Nutrition/A3, Digestive Disease and Surgery Institute, Cleveland Clinic Foundation, Cleveland, OH, USA


Inflammatory Bowel Diseases | 2013

Consecutive fecal calprotectin measurements to predict relapse in patients with ulcerative colitis receiving infliximab maintenance therapy

Martine De Vos; Edouard Louis; Jørgen Jahnsen; Jo G P Vandervoort; Maja Noman; Olivier Dewit; Geert DʼHaens; Denis Franchimont; Filip Baert; Roald Torp; Magne Henriksen; Philippe M R Potvin; Philippe Van Hootegem; Pieter Hindryckx; Tom G. Moreels; Arnaud Collard; Lars Karlsen; Eirik Kittang; Guy Lambrecht; Tore Grimstad; Jonas Koch; Idar Lygren; Jean-Claude R J Coche; Fazia Mana; André Van Gossum; Jacques Belaiche; Mike R Cool; Fernand Fontaine; Jean-Marc Maisin; Vinciane Muls

Background: This study examined whether fecal calprotectin can be used in daily practice as a marker to monitor patients with ulcerative colitis (UC) receiving infliximab maintenance therapy. Methods: This prospective multicenter study enrolled adult patients with UC in clinical remission under infliximab maintenance therapy. Fecal calprotectin levels were measured every 4 weeks. Sigmoidoscopies were performed at inclusion and at study end. Relapse was defined as a clinical need for change in treatment or an endoscopic Mayo subscore of ≥2 at week 52. Sustained deep remission was defined as a partial Mayo score <3 at all points and an endoscopic Mayo score 0 at week 52. Results: Full analysis was possible for 87 of 113 included patients with UC (77%). Of these patients, 30 (34.4%) were considered to be in sustained deep remission and 13 (14.9%) to have relapsed. Calprotectin levels in patients with sustained deep remission remained very low (median < 40 mg/kg at all time points). Patients who flared had significantly higher calprotectin levels (median > 300 mg/kg) already 3 months before the flare. Further receiver operator curve analysis suggested that a calprotectin level >300 mg/kg had a reasonable sensitivity (58.3%) and specificity (93.3%) to model flare. Two consecutive calprotectin measurements of >300 mg/kg with 1-month interval were identified as the best predictor of flare (61.5% sensitivity and 100% specificity). Conclusions: Fecal calprotectin can be used in daily practice to monitor patients with UC receiving infliximab maintenance therapy. Two consecutive measurements >300 mg/kg is more specific than a single measurement for predicting relapse.


Gastrointestinal Endoscopy | 2008

Clinical impact of capsule endoscopy on further strategy and long-term clinical outcome in patients with obscure bleeding

Pieter Hindryckx; Thomas Botelberge; Martine De Vos; Danny De Looze

BACKGROUND Capsule endoscopy (CE) is highly effective in detecting small-bowel lesions in patients with obscure GI bleeding (OGIB). Little is known about the impact of CE on further management and outcomes in patients with OGIB. OBJECTIVE To evaluate the impact of CE on the management and outcomes of patients with OGIB. DESIGN Retrospective cohort study. SETTING Tertiary-referral center. PATIENTS A total of 92 patients referred for obscure-overt bleeding (N = 36) or obscure-occult bleeding (N = 56). INTERVENTIONS CE was performed after a negative endoscopic examination of the upper-GI and lower-GI tract. Follow-up was performed by collecting information from the referring physicians. MAIN OUTCOME MEASUREMENTS Need for transfusion, overt bleeding, anemia. RESULTS Ninety-two patients (52 men, 40 women), with a mean age of 66.5 years (range 22-90 years) and a mean follow-up time of 635.5 days (range 81-1348 days) were studied. Relevant lesions were found in 55 of 92 patients (59.8%). After a CE, invasive small-bowel investigations were more often done in patients with a positive CE result (P = .01). Invasive endoscopic or surgical therapy was far more often performed in patients with a positive CE finding (P < .001). The outcome after a CE was favorable in 61 of 92 patients (66.3%) and was defined by the absence of overt bleeding and a normal Hb value on the latest available laboratory result. In the younger age category, a 100% resolution of OGIB was observed after long-term follow-up. On the contrary, angiodysplasia was a predictor for a less favorable clinical outcome (P = .04). LIMITATIONS Retrospective analysis. CONCLUSIONS A CE has an important impact on a further diagnostic workup, therapeutic strategy, and long-term clinical evolution in patients with OGIB, with a favorable outcome in 66.3% of patients after CE-guided therapy.


Journal of Immunology | 2010

Hydroxylase Inhibition Abrogates TNF-α–Induced Intestinal Epithelial Damage by Hypoxia-Inducible Factor-1–Dependent Repression of FADD

Pieter Hindryckx; Martine De Vos; Peggy Jacques; Liesbeth Ferdinande; Harald Peeters; Kim Olievier; Sara Bogaert; Brigitta M. Brinkman; Peter Vandenabeele; Dirk Elewaut; Debby Laukens

Hydroxylase inhibitors stabilize hypoxia-inducible factor-1 (HIF-1), which has barrier-protective activity in the gut. Because the inflammatory cytokine TNF-α contributes to inflammatory bowel disease in part by compromising intestinal epithelial barrier integrity, hydroxylase inhibition may have beneficial effects in TNF-α–induced intestinal epithelial damage. The hydroxylase inhibitor dimethyloxalylglycin (DMOG) was tested in a murine model of TNF-α–driven chronic terminal ileitis. DMOG-treated mice experienced clinical benefit and showed clear attenuation of chronic intestinal inflammation compared with that of vehicle-treated littermates. Additional in vivo and in vitro experiments revealed that DMOG rapidly restored terminal ileal barrier function, at least in part through prevention of TNF-α–induced intestinal epithelial cell apoptosis. Subsequent transcriptional studies indicated that DMOG repressed Fas-associated death domain protein (FADD), a critical adaptor molecule in TNFR-1-mediated apoptosis, in an HIF-1α–dependent manner. Loss of this FADD repression by HIF-1α-targeting small interfering RNA significantly diminished the antiapoptotic action of DMOG. Additional molecular studies led to the discovery of a previously unappreciated HIF-1 binding site in the FADD promoter, which controls repression of FADD during hypoxia. As such, the results reported in this study allowed the identification of an innate mechanism that protects intestinal epithelial cells during (inflammatory) hypoxia, by direct modulation of death receptor signaling. Hydroxylase inhibition could represent a promising alternative treatment strategy for hypoxic inflammatory diseases, including inflammatory bowel disease.


Annals of the Rheumatic Diseases | 2017

An induction or flare of arthritis and/or sacroiliitis by vedolizumab in inflammatory bowel disease: a case series

Gaëlle Varkas; Kristof Thevissen; G. De Brabanter; L. Van Praet; F Czul-gurdian; H. Cypers; J De Kock; Philippe Carron; M. De Vos; Pieter Hindryckx; J Arts; I Vanneuville; P Schoenaers; Barbara Claerhout; M Abreu; F. van den Bosch; Dirk Elewaut

Background In inflammatory bowel disease (IBD), a new biological therapy has recently been approved. Vedolizumab is a humanised IgG1 monoclonal antibody to α4β7 integrin that modulates gut lymphocyte trafficking. Although an exclusively local effect of vedolizumab could be expected based on the restricted presence of the α4β7–mucosal vascular addressin cell adhesion molecule 1 complex in the gut, past combined success with anti-tumour necrosis factor, and previous demonstration of α4β7 integrin in the joint, led to the expectation of a therapeutic efficacy in spondyloarthritis. Nonetheless, the effect of vedolizumab on extraintestinal manifestations—and especially the joint—has not been reported so far. Case report A series of five patients with IBD who were treated with vedolizumab and promptly developed new onset or exacerbation of sacroiliitis or arthritis are reported. Conclusions Vedolizumab therapy does not seem to show any efficacy in and might even induce arthritis and/or sacroiliitis. However, larger cohort studies are needed to provide information on the prevalence, the evolution and underlying mechanism.


World Journal of Gastrointestinal Endoscopy | 2015

Small bowel capsule endoscopy: Where are we after almost 15 years of use?

Cedric Van de Bruaene; Danny De Looze; Pieter Hindryckx

The development of capsule endoscopy (CE) in 2001 has given gastroenterologists the opportunity to investigate the small bowel in a non-invasive way. CE is most commonly performed for obscure gastrointestinal bleeding, but other indications include diagnosis or follow-up of Crohns disease, suspicion of a small bowel tumor, diagnosis and surveillance of hereditary polyposis syndromes, Nonsteroidal anti-inflammatory drug-induced small bowel lesions and celiac disease. Almost fifteen years have passed since the release of the small bowel capsule. The purpose of this review is to offer the reader a brief but complete overview on small bowel CE anno 2014, including the technical and procedural aspects, the possible complications and the most important indications. We will end with some future perspectives of CE.


Laboratory Investigation | 2010

Absence of placental growth factor blocks dextran sodium sulfate-induced colonic mucosal angiogenesis, increases mucosal hypoxia and aggravates acute colonic injury

Pieter Hindryckx; Anouk Waeytens; Debby Laukens; Harald Peeters; Jacques Van Huysse; Liesbeth Ferdinande; Peter Carmeliet; Martine De Vos

Angiogenesis has recently been described as a component of inflammatory bowel disease. Placental growth factor (PlGF), a vascular endothelial growth factor (VEGF) homologue, establishes its angiogenic capacity under pathophysiological conditions. We investigated the function of PlGF in experimental models of acute colitis. Acute colonic damage was induced in PlGF knock-out (−/−) mice and PlGF wild-type (+/+) mice by dextran sodium sulfate (DSS) and trinitrobenzenesulfonic acid (TNBS). The concentrations of PlGF and VEGF were measured in distal colonic lysates using an enzyme-linked immunosorbent assay. Colonic injury was evaluated by assessing colon length, colonocyte apoptosis (by terminal dUTP nick-end labeling), colonic cytokine production and histological score. Infiltration of polymorphonuclear cells was determined by assaying myeloperoxidase (MPO) activity. In a separate experiment, recombinant PlGF was administered to PlGF−/− mice by adenoviral transfer before DSS administration. Mucosal vascularization was quantified by computerized morphometric analysis of CD31-stained distal colonic sections. Colonic mucosal hypoxia was visualized by pimonidazole staining. Both VEGF and PlGF were upregulated during acute colitis. In addition, compared with PlGF+/+ controls, PlGF−/− mice showed a significant increase in weight loss and colonic shortening during both DSS and TNBS colitis. This correlated with enhanced colonocyte apoptosis, elevated colonic cytokine levels and increased histological damage score, but not with enhanced inflammatory cell infiltration (MPO activity). The increased morbidity of PlGF−/− mice during DSS colitis was preventable by adenovirus (Ad)-mediated overexpression of PlGF. After the administration of DSS, strongly reduced mucosal angiogenesis was observed in PlGF−/− mice compared with PlGF+/+ mice. This was associated with an early increase in intestinal epithelial pimonidazole accumulation in PlGF−/− mice, suggesting a function of enhanced epithelial hypoxia in the observed differences between the two groups. In summary, our data show that the absence of PlGF strongly inhibits mucosal intestinal angiogenesis in acute colitis, which is associated with an early increase in intestinal epithelial hypoxia and aggravation of the course of the disease.


Laboratory Investigation | 2014

Tauroursodeoxycholic acid inhibits experimental colitis by preventing early intestinal epithelial cell death

Debby Laukens; Lindsey Devisscher; Lien Van den Bossche; Pieter Hindryckx; Roosmarijn E. Vandenbroucke; Yves-Paul Vandewynckel; Claude Cuvelier; Brigitta M. Brinkman; Claude Libert; Peter Vandenabeele; Martine De Vos

Ulcerative colitis (UC) is characterized by increased epithelial cell death and subsequent breakdown of the intestinal epithelial barrier, which perpetuates chronic intestinal inflammation. Since fecal bile acid dysmetabolism is associated with UC and tauroursodeoxycholic acid (TUDCA) has been shown to improve murine colitis, we evaluated the effect of TUDCA on intestinal epithelial cell death in a mouse model of UC-like barrier dysfunction elicited by dextran sulfate sodium (DSS). We identified the prevention of colonic caspase-3 induction, a key proapoptotic marker which was also over-activated in UC, as the earliest event resulting in a clear clinical benefit. Whereas vehicle-treated mice showed a cumulative mortality of 40%, all TUDCA-treated mice survived the DSS experiment during a 14-day follow-up period. In line with a barrier protective effect, TUDCA decreased bacterial translocation to the spleen and stimulated mucin production. Similarly, TUDCA inhibited lipopolysaccharide-induced intestinal permeability and associated enterocyte apoptosis. The anti-apoptotic effect was confirmed in vitro by a dose-dependent inhibition of both receptor-dependent (using tumor necrosis factor and Fas ligand) and receptor-independent (staurosporine) caspase-3 induction in HT29 colonic epithelial cells. These data imply that caspase-3 activation is an early marker of colitis that is prevented by TUDCA treatment. These data, together with the previously reported beneficial effect in colitis, suggest that TUDCA could be an add-on strategy to current immunosuppressive treatment of UC patients.


Inflammatory Bowel Diseases | 2011

Longitudinal quantification of inflammation in the murine dextran sodium sulfate-induced colitis model using μPET/CT†

Pieter Hindryckx; Steven Staelens; Lindsey Devisscher; Steven Deleye; F. De Vos; L. Delrue; H Peeters; Debby Laukens; M. De Vos

Background: This study investigates whether deoxy‐2‐[18F]fluoro‐d‐glucose (FDG) micro‐positron emission tomography (&mgr;PET)/computed tomography (CT) can serve as a tool for monitoring of the commonly used dextran sodium sulfate (DSS)‐induced murine model of inflammatory bowel disease (IBD). Methods: DSS‐colitis was induced in Sv129 mice. In a first experiment, four animals were serially scanned with CT and FDG‐&mgr;PET on days 0, 3, 7, 11, and 14. The ratio of the mean voxel count of the PET images in the colon and the brain was compared with the histological inflammation score and the colonic myeloperoxidase levels. A second experiment was performed to investigate whether FDG‐&mgr;PET was able to detect differences in inflammation between two DSS‐treated groups, one receiving placebo (n = 4) and one receiving dimethyloxalylglycine (DMOG) (n = 4), a compound that protects against DSS‐induced colitis. Results: The progression of the colonic/brain FDG‐signal ratio (over days 0–14) agreed with the predicted histological inflammation score, obtained from a parallel DSS‐experiment. Moreover, the quantification of normalized colonic FDG‐activity at the final timepoint (day 14) showed an excellent correlation with both the MPO levels (Spearmans rho = 1) and the histological inflammation score (Spearmans rho = 0.949) of the scanned mice. The protective action of DMOG in DSS colitis was clearly demonstrated with FDG‐&mgr;PET/CT (normalized colonic FDG‐activity DMOG versus placebo: P < 0.05). Conclusions: FDG‐&mgr;PET‐CT is a feasible and reliable noninvasive method to monitor murine DSS‐induced colitis. The implementation of this technique in this widely used IBD model opens a new window for pathophysiological research and high‐throughput screening of potential therapeutic compounds in preclinical IBD research. (Inflamm Bowel Dis 2010;)


Sexually Transmitted Infections | 2006

Prevalence of high risk human papillomavirus types among Nicaraguan women with histological proved pre-neoplastic and neoplastic lesions of the cervix

Pieter Hindryckx; A Garcia; Patricia Claeys; C Gonzalez; R Velasquez; John-Paul Bogers; L Van Renterghem; Claude Cuvelier

Objectives: To determine the prevalence of high risk human papillomavirus (HPV) types in Nicaraguan women with histological proved pre-neoplastic and neoplastic cervical lesions, and to assess its potential impact on preventive strategies. Methods: 206 women with histopathological confirmed cervical lesions (CIN I or worse) were screened for HPV DNA on a liquid based cytology sample, using an HPV short fragment polymerase chain reaction based assay. HPV positive samples were genotyped with a reverse hybridisation line probe assay (Lipa). HPV negative samples were re-analysed using type specific real time polymerase chain reaction. Results: Of all lesions CIN II or worse, 12% tested negative. Prevalence of high risk HPV increased from 48.1% in cervical intraepithelial neoplasia I (CIN I) to 94.7% in invasive squamous cervical carcinoma (SCC). The most prevalent high risk HPV types were, in order of prevalence rate, HPV 16, 58, 31 and 52. HPV 16 and/or HPV 31 were present in 63.2% of SCC cases. Conclusion: Targeting HPV 16 and 31 with prophylactic vaccines could possibly have an important impact on the incidence of invasive cervical carcinoma in Nicaragua. Further research is needed to define the oncogenic potential of other high prevalent HPV genotypes. Meanwhile, primary prevention and cervical cancer screening programmes should be optimised.

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Martine De Vos

Ghent University Hospital

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Harald Peeters

Ghent University Hospital

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M. De Vos

Ghent University Hospital

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Danny De Looze

Ghent University Hospital

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Reena Khanna

University of Western Ontario

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Vipul Jairath

University of Western Ontario

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Brian G. Feagan

University of Western Ontario

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