oru.sePublications
Change search
Refine search result
1 - 29 of 29
CiteExportLink to result list
Permanent link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Rows per page
  • 5
  • 10
  • 20
  • 50
  • 100
  • 250
Sort
  • Standard (Relevance)
  • Author A-Ö
  • Author Ö-A
  • Title A-Ö
  • Title Ö-A
  • Publication type A-Ö
  • Publication type Ö-A
  • Issued (Oldest first)
  • Issued (Newest first)
  • Created (Oldest first)
  • Created (Newest first)
  • Last updated (Oldest first)
  • Last updated (Newest first)
  • Disputation date (earliest first)
  • Disputation date (latest first)
  • Standard (Relevance)
  • Author A-Ö
  • Author Ö-A
  • Title A-Ö
  • Title Ö-A
  • Publication type A-Ö
  • Publication type Ö-A
  • Issued (Oldest first)
  • Issued (Newest first)
  • Created (Oldest first)
  • Created (Newest first)
  • Last updated (Oldest first)
  • Last updated (Newest first)
  • Disputation date (earliest first)
  • Disputation date (latest first)
Select
The maximal number of hits you can export is 250. When you want to export more records please use the Create feeds function.
  • 1. Amcoff, Karin
    et al.
    Joossens, Marie
    Pierik, Marie J.
    Jonkers, Daisy
    Bohr, Johan
    Joossens, Sofie
    Romberg-Camps, Marielle
    Nyhlin, Nils
    Wickbom, Anna K.
    Rutgeerts, Paul J.
    Tysk, Curt
    Bodin, Lennart
    Colombel, Jean-Frederic
    Vermeire, Severine
    Halfvarson, Jonas
    Örebro University, School of Medicine, Örebro University, Sweden.
    Influence of genetics in the expression of serological markers in twins with IBD2012In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 142, no 5, p. S881-S881Article in journal (Other academic)
  • 2. Burisch, Johan
    et al.
    Pedersen, Natalia
    Cukovic-Cavka, Silvija
    Kaimakliotis, John
    Duricova, Dana.
    Shonova, Olga
    Vind, Ida
    Thorsgaard, Niels
    Andersen, Vibeke
    Dahlerup, Jens F.
    Salupere, Riina
    Nielsen, Kári R.
    Manninen, Pia
    Tsianos, Epameinondas V.
    Ladefoged, Karin
    Bailey, Yvonne
    D'Inca, Renata
    Kupcinskas, Limas
    Turcan, Svetlana
    Magro, Fernando
    Goldis, Adrian
    Belousova, Elena
    Hernandez, Vicent
    Almer, Sven
    Halfvarson, Jonas
    Sebastian, Shaji
    Lakatos, Peter L.
    Langholz, Ebbe
    Odes, Selwyn H.
    Munkholm, Pia
    The Cost of Medical Management, Surgery and Clinical Investigations in a European Population-Based Inception Cohort From the Biological Era: An ECCO-Epicom Study2014In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 146, no 5, Supplement 1, p. S203-S203Article in journal (Refereed)
  • 3. Burisch, Johan
    et al.
    Xia, Bing
    Cukovic-Cavka, Silvija
    Kaimakliotis, John
    Duricova, Dana
    Shonova, Olga
    Vind, Ida
    Pedersen, Natalia
    Langholz, Ebbe
    Thorsgaard, Niels
    Andersen, Vibeke
    Dahlerup, Jens F.
    Salupere, Riina
    Nielsen, Kari R.
    Manninen, Pia
    Tsianos, Epameinondas V.
    Ladefoged, Karin
    Bjornsson, Einar
    Bailey, Yvonne
    Odes, Selwyn H.
    Martinato, Matteo
    Kupcinskas, Limas
    Turcan, Svetlana I.
    Magro, Fernando
    Goldis, Adrian
    Belousova, Elena
    Hernandez, Vicent
    Almer, Sven
    Halfvarson, Jonas
    Arebi, Naila
    Sebastian, Shaji
    Lakatos, Peter L.
    Munkholm, Pia S.
    Is there an east-west gradient in the incidence of IBD in Europe?: and further far east in China? First results from the epicom study2012In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 142, no 5, p. S569-S570Article in journal (Other academic)
  • 4.
    Burke, Kristin E.
    et al.
    Gastroenterology Unit, Massachusetts General Hospital, Boston Massachusetts, USA; Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Boston Massachusetts, USA; Harvard Medical School, Boston Massachusetts, USA.
    Ananthakrishnan, Ashwin N.
    Gastroenterology Unit, Massachusetts General Hospital, Boston Massachusetts, USA; Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Boston Massachusetts, USA; Harvard Medical School, Boston Massachusetts, USA.
    Lochhead, Paul
    Gastroenterology Unit, Massachusetts General Hospital, Boston Massachusetts, USA; Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Boston Massachusetts, USA; Harvard Medical School, Boston Massachusetts, USA.
    Liu, Po-Hong
    Gastroenterology Unit, Massachusetts General Hospital, Boston Massachusetts, USA; Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Boston Massachusetts, USA; Harvard Medical School, Boston Massachusetts, USA.
    Olen, Ola
    Pediatric Gastroenterology and Nutrition Unit, Sachs’ Children’s Hospital, Stockholm, Sweden; Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro University, Örebro, Sweden.
    Richter, James M.
    Gastroenterology Unit, Massachusetts General Hospital, Boston Massachusetts, USA; Harvard Medical School, Boston Massachusetts, USA.
    Tworoger, Shelley S.
    Moffit Cancer Center, Tampa Florida, USA; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston Massachusetts, USA.
    Chan, Andrew T.
    Gastroenterology Unit, Massachusetts General Hospital, Boston Massachusetts, USA; Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Boston Massachusetts, USA; Harvard Medical School, Boston Massachusetts, USA; Channing Division of Network Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston Massachusetts, USA; Broad Institute, Cambridge Massachusetts, USA; Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston Massachusetts, USA.
    Khalili, Hamed
    Gastroenterology Unit, Massachusetts General Hospital, Boston Massachusetts, USA; Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Boston Massachusetts, USA; Harvard Medical School, Boston Massachusetts, USA; Karolinska Clinical Epidemiology Unit, Karolinska Institutet, Solna, Sweden.
    Identification of Menopausal and Reproductive Risk Factors for Microscopic Colitis-Results From the Nurses' Health Study2018In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 155, no 6, p. 1764-1775Article in journal (Refereed)
    Abstract [en]

    BACKGROUND & AIMS: Microscopic colitis is a chronic inflammatory disorder of the colon primarily affecting postmenopausal women. However, the relation between hormonal determinants, including reproductive and menopausal factors, and risk of microscopic colitis has yet to be characterized.

    METHODS: We collected data from 227,766 women who participated in the Nurses' Health Study (NHS) and the NHSII without a baseline history of microscopic colitis. Reproductive and menopausal factors were assessed in 1988 in the NHS and 1989 in the NHSII and updated biennially. Cases of microscopic colitis were confirmed through review of pathology records. We used Cox proportional hazards modeling to estimate hazard ratios and 95% confidence intervals.

    RESULTS: Through 2014 in the NHS and 2015 in the NHSII, we confirmed 275 incident cases of microscopic colitis over 5,147,282 person-years. Compared with never use, current use of menopausal hormone therapy was associated with increased risk of microscopic colitis (multivariable-adjusted hazard ratio 2.64; 95% confidence interval 1.78-3.90). The risk increased with longer duration of use (P for trend < .0001) and decreased after discontinuation (P for trend = .002). The association did not differ according to disease subtype (P for heterogeneity = .34). Similarly, ever use of oral contraceptives was associated with increased risk of microscopic colitis (multivariable-adjusted hazard ratio 1.57; 95% confidence interval 1.16-2.13). There were no associations between age at menarche, parity, age at first birth, age at menopause, or menopause type and incident microscopic colitis.

    CONCLUSIONS: In 2 large prospective cohort studies, we observed an association between exogenous hormone use and incident microscopic colitis. Further studies are needed to determine the mechanisms underlying these associations.

  • 5. Ellinghaus, David
    et al.
    Zhang, Hu
    Zeissig, Sebastian
    Lipinski, Simone
    Till, Andreas
    Jiang, Tao
    Stade, Bjoern
    Bromberg, Yana
    Ellinghaus, Eva
    Keller, Andreas
    Rivas, Manuel A.
    Skieceviciene, Jurgita
    Doncheva, Nadezhda T.
    Liu, Xiao
    Liu, Qing
    Jiang, Fuman
    Forster, Michael
    Mayr, Gabriele
    Albrecht, Mario
    Haesler, Robert
    Boehm, Bernhard O.
    Goodall, Jane
    Berzuini, Carlo R.
    Lee, James
    Andersen, Vibeke
    Vogel, Ulla
    Kupcinskas, Limas
    Kayser, Manfred
    Krawczak, Michael
    Nikolaus, Susanna
    Weersma, Rinse K.
    Ponsioen, Cyriel Y.
    Sans, Miquel
    Wijmenga, Cisca
    Strachan, David P.
    McAardle, Wendy L.
    Vermeire, Severine
    Rutgeerts, Paul
    Sanderson, Jeremy D.
    Mathew, Christopher G.
    Vatn, Morten H.
    Wang, Jun
    Noethen, Markus M.
    Duerr, Richard H.
    Buening, Carsten
    Brand, Stephan
    Glas, Juergen
    Winkelmann, Juliane
    Illig, Thomas
    Latiano, Anna
    Annese, Vito
    Halfvarson, Jonas
    Örebro University, School of Medicine, Örebro University, Sweden. Örebro University Hospital.
    D'Amato, Mauro
    Daly, Mark J.
    Nothnagel, Michael
    Karlsen, Tom H.
    Subramani, Suresh
    Rosenstiel, Philip
    Schreiber, Stefan
    Parkes, Miles
    Franke, Andre
    Association between variants of PRDM1 and NDP52 and Crohn's disease, based on exome sequencing and functional studies2013In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 145, no 2, p. 339-347Article in journal (Refereed)
    Abstract [en]

    BACKGROUND & AIMS: Genome-wide association studies (GWAS) have identified 140 Crohn's disease (CD) susceptibility loci. For most loci, the variants that cause disease are not known and the genes affected by these variants have not been identified. We aimed to identify variants that cause CD through detailed sequencing, genetic association, expression, and functional studies.

    METHODS: We sequenced whole exomes of 42 unrelated subjects with CD and 5 healthy subjects (controls) and then filtered single nucleotide variants by incorporating association results from meta-analyses of CD GWAS and in silico mutation effect prediction algorithms. We then genotyped 9348 subjects with CD, 2868 subjects with ulcerative colitis, and 14,567 control subjects and associated variants analyzed in functional studies using materials from subjects and controls and in vitro model systems.

    RESULTS: We identified rare missense mutations in PR domain-containing 1 (PRDM1) and associated these with CD. These mutations increased proliferation of T cells and secretion of cytokines on activation and increased expression of the adhesion molecule L-selectin. A common CD risk allele, identified in GWAS, correlated with reduced expression of PRDM1 in ileal biopsy specimens and peripheral blood mononuclear cells (combined P = 1.6 x 10(-8)). We identified an association between CD and a common missense variant, Val248Ala, in nuclear domain 10 protein 52 (NDP52) (P = 4.83 x 10(-9)). We found that this variant impairs the regulatory functions of NDP52 to inhibit nuclear factor kappa B activation of genes that regulate inflammation and affect the stability of proteins in Toll-like receptor pathways.

    CONCLUSIONS: We have extended the results of GWAS and provide evidence that variants in PRDM1 and NDP52 determine susceptibility to CD. PRDM1 maps adjacent to a CD interval identified in GWAS and encodes a transcription factor expressed by T and B cells. NDP52 is an adaptor protein that functions in selective autophagy of intracellular bacteria and signaling molecules, supporting the role of autophagy in the pathogenesis of CD.

  • 6.
    Everhov, Åsa H.
    et al.
    Department of Clinical Science and Education, Södersjukhuset, Karolinska Institutet, Stockholm, Sweden; Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Halfvarson, Jonas
    Örebro University, School of Medical Sciences. Department of Gastroenterology.
    Myrelid, Pär
    Division of surgery, Department of Clinical and Experimental Medicine, Faulty of Health Sciences, Linköping University, Linköping, Sweden; Department of Surgery, County Council of Östergötland, Linköping, Sweden.
    Sachs, Michael C.
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Nordenvall, Caroline
    Dept. of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden; Center for Digestive Disease, Div. of Coloproctology, Karolinska University Hospital, Stockholm, Sweden.
    Söderling, Jonas
    Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Ekbom, Anders
    Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Neovius, Martin
    Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Department Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, , Örebro University Hospital, Örebro, Sweden; Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham, UK; Department of Medicine, Columbia University College of Physicians and Surgeons, New York, USA.
    Askling, Johan
    Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Olén, Ola
    Department of Clinical Science and Education, Södersjukhuset, Karolinska Institutet, Stockholm, Sweden; Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden; Department of pediatric gastroenterology and nutrition, Sachs' Children and Youth Hospital, Stockholm, Sweden.
    Incidence and Treatment of Patients Diagnosed With Inflammatory Bowel Diseases at 60 Years or Older in Sweden2018In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 154, no 3, p. 518-528Article in journal (Refereed)
    Abstract [en]

    BACKGROUND & AIMS: Diagnosis of inflammatory bowel diseases (IBD) is increasing among elderly persons (60 years or older). We performed a nationwide population-based study to estimate incidence and treatment.

    METHODS: We identified all incident IBD cases in Sweden, from 2006 through 2013, using national registers, and up to 10 matched population comparator subjects. We collected data on the patients' health care contacts and estimated incidence rates, health service burden, pharmacologic treatments, extra-intestinal manifestations, and surgeries in relation to age of IBD onset (pediatric, less than 18 years; adults, 18-59 years; elderly, 60 years or older).

    RESULTS: Of 27,834 persons diagnosed with incident IBD, 6443 (23%) had a first diagnosis of IBD at 60 years or older, corresponding to an incidence rate of 35/100,000 person-years (10/100,000 person-years for Crohn's disease, 19 /100,000 person-years for ulcerative colitis, and 5/100,000 person-years for IBD unclassified). During a median follow-up period of 4.2 years (range 0-9 years), elderly patients had less IBD-specific outpatient health care but more IBD-related hospitalizations and overall health care use than adult patients with IBD. Compared to patients with pediatric or adult onset, elderly patients used fewer biologics and immunomodulators, but more systemic corticosteroids. Occurrence of extra-intestinal manifestations was similar in elderly and adult patients, but bowel surgery was more common in the elderly (13% after 5 years vs 10% in adults) (P<.001). The absolute risk of bowel surgery was higher in the elderly than in the general population, but in relative terms, the risk increase was larger in younger age groups.

    CONCLUSIONS: In a nationwide cohort study in Sweden, we associated diagnosis of IBD at age 60 years or older with a lower use of biologics and immunomodulators but higher absolute risk of bowel surgery, compared to diagnosis at a younger age. The large differences in pharmacological treatment of adults and elderly patients are not necessarily due to a milder course of disease and warrant further investigation.

  • 7. Gustavsson, Anders
    et al.
    Jaenerot, Gunnar
    Hertervig, Erik
    Friis-Iiby, Ingalill
    Blomquist, Lars
    Karlen, Per
    Granno, Christer
    Vilien, Mogens
    Strom, Magnus
    Damelsson, Ake
    Verbaan, Hans
    Hellstrom, Per M.
    Halfvarson, Jonas
    Örebro University, School of Medicine, Örebro University, Sweden.
    Magnuson, Anders
    Tysk, Curt
    A 2-year follow-up of the swedish-danish Infliximab/Placebo trial in steroid resistant acute ulcerative colitis2007In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 132, no 4, p. A146-A147Article in journal (Other academic)
  • 8. Gustavsson, Anders
    et al.
    Magnuson, Anders
    Blomberg, Björn
    Andersson, Magnus V.
    Halfvarson, Jonas
    Örebro University, School of Medicine, Örebro University, Sweden.
    Tysk, Curt
    Endoscopic Balloon Dilation of Intestinal Strictures in Crohn's Disease2011In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 140, no 5, p. S140-S140Article in journal (Other academic)
  • 9. Halfvarson, Jonas
    et al.
    Bodin, Lennart
    Tysk, Curt
    Lindberg, Eva
    Järnerot, Gunnar
    Inflammatory bowel disease in a Swedish twin cohort: a long-term follow-up of concordance and clinical characteristics2003In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 124, no 7, p. 1767-1773Article in journal (Refereed)
    Abstract [en]

    BACKGROUND & AIMS: In 1988, we reported the first twin study in inflammatory bowel disease. The aim of the current study was to follow up these twins regarding new cases of inflammatory bowel disease and Crohn's disease characteristics using the Vienna classification.

    METHODS: The official Swedish population register and the cause of death register were used to search for the twins. All living patients were interviewed.

    RESULTS: Three monozygotic twins earlier classified as healthy had been diagnosed with inflammatory bowel disease (ulcerative colitis, n = 2; Crohn's disease, n = 1). Retrospectively, all 3 were symptomatic at the original survey. This changed the pair concordance in monozygotic twins from 6.3% to 18.8% in ulcerative colitis and from 44.4% to 50.0% in Crohn's disease. A high degree of concordance regarding age at diagnosis, disease location at diagnosis and during the course, and disease behavior was found in concordant monozygotic twin pairs with Crohn's disease. Seven of 9 pairs were identical in 3 or more of these disease characteristics compared with an expected number of 1.5 (P = 0.000076).

    CONCLUSIONS: This study confirms that the genetic influence is stronger in Crohn's disease than in ulcerative colitis. A remarkable phenotype similarity within concordant pairs with Crohn's disease was found using the Vienna classification.

  • 10. Halfvarson, Jonas
    et al.
    Bresso, F
    Tysk, C
    Pettersson, S
    Jarnerot, G
    Genetic Crohn's disease: A different entity than sporadic. A study in monozygotic twins2004In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 126, no 4, p. A359-A360Article in journal (Other academic)
  • 11. Halfvarson, Jonas
    et al.
    Dicksved, Johan
    Rosenquist, Magnus
    Järnerot, Gunnar
    Tysk, Curt
    Örebro University, School of Health and Medical Sciences.
    Engstrand, Lars
    Jansson, Janet K.
    W1182 molecular fingerprinting of the gut microbiota of twins reveals differences according to Crohn's disease2008In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 134, no 4, Supplement 1, p. A-650-A-650Article in journal (Refereed)
  • 12. Halfvarson, Jonas
    et al.
    Jess, T
    Bodin, L
    Tysk, C
    Binder, V
    Jarnerot, G
    Phenotypic concordance in monozygotic twin pairs with ulcerative colitis2004In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 126, no 4, p. A356-A356Article in journal (Other academic)
  • 13. Halfvarson, Jonas
    et al.
    Tysk, C
    Jarnerot, G
    Decreasing pair concordance in monozygotic twins with Crohn's disease2004In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 126, no 4, p. A45-A45Article in journal (Other academic)
  • 14. Heap, Graham A.
    et al.
    Singh, Abhey
    Bewshea, Claire M.
    Weedon, Michael
    Dubois, Patrick
    Andrews, Jane M.
    Annese, Vito
    Bampton, Peter A.
    Bell, Sally
    Cole, Andy
    Connor, Susan J.
    Creed, Tom
    D'Amato, Mauro
    Fedorak, Richard N.
    Florin, Timothy H.
    Gaya, Daniel R.
    Greig, Emma
    Halfvarson, Jonas
    Örebro University, School of Medicine, Örebro University, Sweden.
    Irving, Peter M.
    Karban, Amir
    Lawrance, Ian C.
    Lev-Tzion, Raffi
    Lindsay, James O.
    Mawsley, Joel
    Mazher, Zia
    Orchard, Timothy R.
    Radford-Smith, Graham L.
    Reffitt, David
    Silverberg, Mark S.
    Sturniolo, Giacomo C.
    Tsianos, Epameinondas V.
    Walsh, Alissa
    Zeissig, Sebastian
    Holden, Arthur L.
    Ahmad, Tariq
    Thiopurine induced pancreatitis in inflammatory bowel disease: clinical features and genetic determinants2014In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 146, no 5, Supplement 1, p. S2-S2Article in journal (Refereed)
  • 15. Jess, T
    et al.
    Halfvarson, Jonas
    Bodin, L
    Tysk, C
    Jarnerot, G
    Binder, V
    Strong genetic influence on longitudinal changes in Vienna Classification characteristics: a Danish-Swedish cohort study of IBD twins2004In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 126, no 4, p. A469-A469Article in journal (Other academic)
  • 16. Jess, Tine
    et al.
    Halfvarson, Jonas
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Tysk, Curt
    Binder, Vibeke
    Jarnerot, Gunnar
    Smoking as a possible explanation for the low concordance among twins with ulcerative colitis: a population based study of environmental factors in a Danish-Swedish twin cohort2003In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 124, no 4, p. A205-A205Article in journal (Other academic)
  • 17.
    Li, Dalin
    et al.
    F. Widjaja Foundation Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, USA.
    Achkar, Jean-Paul
    Department of Gastroenterology and Hepatology, Cleveland Clinic, Cleveland OH, USA.
    Haritunians, Talin
    F. Widjaja Foundation Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, USA.
    Jacobs, Jonathan P.
    Division of Digestive Diseases, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, USA.
    Hui, Ken Y.
    Division of Gastroenterology, Department of Medicine, Yale University, New Haven CT, USA.
    D'Amato, Mauro
    Department of Biosciences and Nutrition, Karolinska Institutet, Stockholm, Sweden; Biocruces Health Research Institute, Barakaldo, Spain.
    Brand, Stephan
    Department of Medicine II, University Hospital Munich-Grosshadern, Munich, Germany.
    Radford-Smith, Graham
    Inflammatory Bowel Diseases, Genetics and Computational Biology, QIMR Berghofer Medical Research Institute, Brisbane, Australia; Department of Gastroenterology, Royal Brisbane and Women’s Hospital, Brisbane, Australia; School of Medicine, University of Queensland, Brisbane, Australia.
    Halfvarson, Jonas
    Örebro University, School of Medical Sciences. Department of Gastroenterology, Örebro University Hospital, Örebro, Sweden.
    Niess, Jan-Hendrik
    Department of Internal Medicine I, University of Ulm, Ulm, Germany; Division of Visceral Surgery and Medicine, Department of Gastroenterology, Inselspital Bern, Bern, Switzerland; Gastroenterology and Hepatology, University Hospital, Basel, Switzerland.
    Kugathasan, Subra
    Department of Pediatrics, Emory University School of Medicine and Children's Health Care of Atlanta, Atlanta Ga, USA.
    Büning, Carsten
    Internal Medicine, Krankenhaus Waldfriede, Berlin, Germany.
    Schumm, L. Philip
    Department of Public Health Sciences, Biostatistical Laboratory, University of Chicago, Chicago ILL, USA.
    Klei, Lambertus
    Department of Psychiatry, School of Medicine, University of Pittsburgh, Pittsburgh PA, USA.
    Ananthakrishnan, Ashwin
    Gastroenterology Unit, Massachusetts General Hospital, Harvard Medical School, Boston MA, USA.
    Aumais, Guy
    Université de Montréal, Montréal QC, Canada; Hopital Maisonneuve Rosemont, Montréal QC, Canada.
    Baidoo, Leonard
    Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, School of Medicine, University of Pittsburgh, Pittsburgh PA, USA.
    Dubinsky, Marla
    F. Widjaja Foundation Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, USA; Department of Pediatrics, Icahn School of Medicine at Mount Sinai, New York NY, USA.
    Fiocchi, Claudio
    Pathobiology Department, Cleveland Clinic, Cleveland OH, USA.
    Glas, Jürgen
    Department of Preventive Dentistry and Periodontology, Ludwig-Maximilians-University, Munich, Germany.
    Milgrom, Raquel
    Zane Cohen Centre for Digestive Diseases, Mount Sinai Hospital, University of Toronto, Toronto, ON, Canada.
    Proctor, Deborah D.
    Division of Gastroenterology, Department of Medicine, Yale University, New Haven CT, USA.
    Regueiro, Miguel
    Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, School of Medicine, University of Pittsburgh, Pittsburgh PA, USA.
    Simms, Lisa A.
    Inflammatory Bowel Diseases, Genetics and Computational Biology, QIMR Berghofer Medical Research Institute, Brisbane, Australia.
    Stempak, Joanne M.
    Zane Cohen Centre for Digestive Diseases, Mount Sinai Hospital, University of Toronto, Toronto ON, Canada.
    Targan, Stephan R.
    F. Widjaja Foundation Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, USA.
    Törkvist, Leif
    Department of Clinical Science Intervention and Technology, Karolinska Institutet, Stockholm, Sweden; Center for Digestive Disease, IBD-unit, Karolinska University Hospital, Stockholm, Sweden.
    Sharma, Yashoda
    Department of Genetic & Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York NY, USA.
    Devlin, Bernie
    Department of Psychiatry, School of Medicine, University of Pittsburgh, Pittsburgh PA, USA; Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh PA, USA.
    Borneman, James
    Department of Plant Pathology and Microbiology, University of California, Riverside, Riverside CA, USA.
    Hakonarson, Hakon
    Center for Applied Genomics, The Children’s Hospital of Philadelphia, Philadelphia PA, USA.
    Xavier, Ramnik J.
    Gastroenterology Unit, Massachusetts General Hospital, Harvard Medical School, Boston , USA; Broad Institute of MIT and Harvard, Cambridge MA, USA.
    Daly, Mark
    Broad Institute of MIT and Harvard, Cambridge MA, USA; Analytic and Translational Genetics Unit, Massachusetts General Hospital, Harvard Medical School, Boston MA, USA.
    Brant, Steven R.
    Division of Gastroenterology and Hepatology, School of Medicine, Johns Hopkins University, Baltimore MD, USA; Bloomberg School of Public Health, Johns Hopkins University, Baltimore MD, USA.
    Rioux, John D.
    Université de Montréal, Montréal QC, Canada; Montreal Heart Institute, Montréal OC, Canada.
    Silverberg, Mark S.
    Zane Cohen Centre for Digestive Diseases, Mount Sinai Hospital, University of Toronto, Toronto ON, Canada.
    Cho, Judy H.
    Department of Genetic & Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York NY, USA; Division of Gastroenterology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York NY, USA.
    Braun, Jonathan
    Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California, Los Angeles CA, USA; .
    McGovern, Dermot P. B.
    F. Widjaja Foundation Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, USA.
    Duerr, Richard H.
    Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, School of Medicine, University of Pittsburgh, Pittsburgh PA, USA; Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh PA, USA.
    A Pleiotropic Missense Variant in SLC39A8 Is Associated With Crohn's Disease and Human Gut Microbiome Composition2016In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 151, no 4, p. 724-732Article in journal (Refereed)
    Abstract [en]

    Background & Aims: Genome-wide association studies have identified 200 inflammatory bowel disease (IBD) loci, but the genetic architecture of Crohn's disease (CD) and ulcerative colitis remain incompletely defined. Here, we aimed to identify novel associations between IBD and functional genetic variants using the Illumina ExomeChip (San Diego, CA).

    Methods: Genotyping was performed in 10,523 IBD cases and 5726 non-IBD controls. There were 91,713 functional single-nucleotide polymorphism loci in coding regions analyzed. A novel identified association was replicated further in 2 independent cohorts. We further examined the association of the identified single-nucleotide polymorphism with microbiota from 338 mucosal lavage samples in the Mucosal Luminal Interface cohort measured using 16S sequencing.

    Results: We identified an association between CD and a missense variant encoding alanine or threonine at position 391 in the zinc transporter solute carrier family 39, member 8 protein (SLC39A8 alanine 391 threonine, rs13107325) and replicated the association with CD in 2 replication cohorts (combined meta-analysis P = 5.55 × 10(-13)). This variant has been associated previously with distinct phenotypes including obesity, lipid levels, blood pressure, and schizophrenia. We subsequently determined that the CD risk allele was associated with altered colonic mucosal microbiome composition in both healthy controls (P = .009) and CD cases (P = .0009). Moreover, microbes depleted in healthy carriers strongly overlap with those reduced in CD patients (P = 9.24 × 10(-16)) and overweight individuals (P = 6.73 × 10(-16)).

    Conclusions: Our results suggest that an SLC39A8-dependent shift in the gut microbiome could explain its pleiotropic effects on multiple complex diseases including CD.

  • 18.
    Ludvigsson, Jonas F.
    et al.
    Örebro University, School of Medical Sciences. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden; Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham, UK; Celiac Disease Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, USA.
    Höijer, Jonas
    Unit of Biostatistics, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Stephansson, Olof
    Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet,Stockholm, Sweden; School of Public Health, University of California, Berkeley CA, USA.
    Reply2017In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 153, no 1, p. 331-332Article in journal (Refereed)
  • 19.
    Ludvigsson, Jonas F.
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, Region Örebro County, Örebro, Sweden; Division of Epidemiology and Public Health, School of Medicine, City Hospital, University of Nottingham, Nottingham, UK.
    Lebwohl, Benjamin
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Celiac Disease Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, USA.
    Ekbom, Anders
    Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Sweden.
    Kiran, Ravi
    Division of Colorectal Surgery, New York Presbyterian, New York, USA; Columbia University Medical Center, New York, USA.
    Green, Peter H. R.
    Celiac Disease Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, USA.
    Höijer, Jonas
    Unit of Biostatistics, Institute of Environmental Medicine, Karolinska Institutet, Sweden.
    Stephansson, Olof
    Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Sweden; School of Public Health, University of California, Berkeley, USA.
    Outcomes of Pregnancies for Women Undergoing Endoscopy While They Were Pregnant-a Nationwide Cohort Study2017In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 152, no 3, p. 554-563Article in journal (Refereed)
    Abstract [en]

    Background &  & Aims: Endoscopy is an integral part of the investigation and management of gastrointestinal disease. We aimed to examine outcomes of pregnancies for women who underwent endoscopy during their pregnancy.

    Methods: We performed a nationwide population-based cohort study, linking data from the Swedish Medical Birth Registry (for births from 1992 through 2011) with those from the Swedish Patient Registry. We identified 3052 pregnancies exposed to endoscopy (2025 upper endoscopies, 1109 lower endoscopies, 58 endoscopic retrograde cholangiopancreatographies). Using Poisson regression, we calculated adjusted relative risks (ARRs) for adverse outcomes of pregnancy according to endoscopy status using 1,589,173 unexposed pregnancies as reference. To consider the effects of disease activity, we examined pregnancy outcomes (preterm birth, stillbirth, small for gestational age [SGA], or congenital malformations) in women who underwent endoscopy just before or after pregnancy. Secondary factors included induction of labor, low birth weight (<2500g), cesarean section, Apgar score below 7 at 5 minutes, and neonatal death within 28 days. To consider intra-familial factors, we compared pregnancies within the same mother.

    Results: Exposure to any endoscopy during pregnancy was associated with an increased risk of preterm birth (ARR, 1.54; 95% CI, 1.36-1.75) or SGA (ARR, 1.30; 95% CI, 1.07-1.57) but not of congenital malformation (ARR, 1.00; 95% CI, 0.83-1.20) or stillbirth (ARR, 1.45; 95% CI, 0.87-2.40). None of the 15 stillbirths to women with endoscopy occurred less than 2 weeks after endoscopy. ARRs were independent of trimester. Compared to women with endoscopy less than 1 year before or after pregnancy, endoscopy during pregnancy was associated with preterm birth (ARR, 1.16) but not with SGA (ARR, 1.19), stillbirth (ARR, 1.11), or congenital malformation (ARR, 0.90). Restricting the study population to women having an endoscopy during pregnancy or before/after, and only analyzing data from women without a diagnosis of inflammatory bowel disease, celiac disease, or liver disease, endoscopy during pregnancy was not linked to preterm birth (ARR, 1.03; 95% CI, 0.84-1.27). Comparing births within the same mother, for which only 1 birth had been exposed to endoscopy, we found no association between endoscopy and gestational age or birth weight.

    Conclusions: In a nationwide population-based cohort study, we found endoscopy during pregnancy to be associated with increased risk of preterm birth or SGA, but not of congenital malformation or stillbirth. However, these risks are small and likely due to intra-familial factors or disease activity.

  • 20.
    Mahadev, Srihari
    et al.
    Celiac Disease Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York New York, United States.
    Laszkowska, Monika
    Celiac Disease Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York New York, United States.
    Sundström, Johan
    Department of Medical Sciences, Uppsala University, Uppsala Clinical Research Center, Uppsala, Sweden.
    Björkholm, Magnus
    Department of Medicine, Division of Hematology, Karolinska University Hospital and Karolinska Institutet, Stockholm, Sweden.
    Lebwohl, Benjamin
    Celiac Disease Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York New York, United States.
    Green, Peter H. R.
    Celiac Disease Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York New York, United States.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Celiac Disease Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York New York, United States; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro, Sweden; Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham, United Kingdom.
    Prevalence of Celiac Disease in Patients With Iron Deficiency Anemia-A Systematic Review With Meta-analysis2018In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 155, no 2, p. 374-382Article, review/survey (Refereed)
    Abstract [en]

    BACKGROUND & AIMS: Anemia is common in patients with celiac disease (CD) and a frequent mode of presentation. Guidelines recommend screening patients with iron-deficiency anemia (IDA) for CD. However, the reported prevalence of CD in patients with IDA varies. We performed a systematic review to determine the prevalence of biopsy-verified CD in patients with IDA.

    METHODS: We performed a systematic review of articles published in PubMed Medline or EMBASE through July 2017 for the term "celiac disease" combined with "anemia" or "iron deficiency." We used fixed-effects inverse variance-weighted models to measure the pooled prevalence of CD. Meta-regression was used to assess subgroup heterogeneity.

    RESULTS: We identified 18 studies composed of 2998 patients with IDA for inclusion in our analysis. Studies originated from the United Kingdom, United States, Italy, Turkey, Iran, and Israel. The crude unweighted prevalence of CD was 4.8% (n = 143). Using a weighted pooled analysis, we found a prevalence of biopsy-confirmed CD of 3.2% (95% confidence interval = 2.6-3.9) in patients with IDA. However, heterogeneity was high (I-2 = 67.7%). The prevalence of CD was not significantly higher in studies with a mean participant age older or younger than 18 years or in studies with a mixed-sex vs female-predominant (>= 60%) population. On meta-regression, year of publication, female proportion, age at CD testing, and prevalence in the general population were not associated with the prevalence of CD in patients with IDA. In the 8 studies fulfilling all our quality criteria, the pooled prevalence of CD was 5.5% (95% confidence interval = 4.1-6.9).

    CONCLUSIONS: In a systematic review and meta-analysis, we found that approximately 1 in 31 patients with IDA have histologic evidence of CD. This prevalence value justifies the practice of testing patients with IDA for CD.

  • 21.
    Mårild, Karl
    et al.
    Department of Medicine, Örebro University Hospital, Örebro University, Örebro, Sweden.
    Stephansson, Olof
    Clinical Epidemiology Unit and Department of Women's and Children's Health, Karolinska University Hospital, Karolinska Institute, Stockholm, Sweden.
    Montgomery, Scott M.
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Clinical Epidemiology Unit and Department of Women's and Children's Health, Karolinska University Hospital, Karolinska Institute, Stockholm, Sweden.
    Murray, Joseph A.
    Division of Gastroenterology and Hepatology, Departments of Medicine and Immunology, Mayo Clinic College of Medicine, Rochester MN, USA.
    Ludvigsson, Jonas F.
    Clinical Epidemiology Unit and Department of Women's and Children's Health, Karolinska University Hospital and Institutet, Stockholm, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro University, Örebro, Sweden.
    Pregnancy outcome and risk of celiac disease in offspring: a nationwide case-control study2012In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 142, no 1, p. 39-45.e3Article in journal (Refereed)
    Abstract [en]

    Background & Aims: Studies on pregnancy characteristics and mode of delivery and risk of later celiac disease in offspring are inconsistent. In recent decades rates of cesarean delivery and preterm birth survival have increased while at the same time the prevalence of celiac disease has doubled.

    Methods: In this population-based case-control study we examined the risk of celiac disease in individuals exposed to cesarean delivery and adverse fetal events (ie, low Apgar score, small for gestational age, low birth weight, preterm birth, and neonatal infections). Prospectively recorded pregnancy data were obtained from the Swedish Medical Birth Register between 1973 and 2008. Study participants consisted of 11,749 offspring with biopsy-verified celiac disease identified through histopathology reports from Sweden's 28 pathology departments, and 53,887 age- and sex-matched controls from the general population.

    Results: We found a positive association between elective cesarean delivery and later celiac disease (adjusted odds ratio [OR], 1.15; 95% confidence interval [CI], 1.04-1.26), but no increased risk of celiac disease after emergency (adjusted OR, 1.02; 95% CI, 0.92-1.13) or any cesarean delivery (adjusted OR, 1.06; 95% CI, 0.99-1.13). Infants born small for gestational age were at a 21% increased risk of celiac disease (95% CI, 1.09-1.35), whereas other pregnancy exposures did not increase the risk of future celiac disease.

    Conclusions: The positive association with elective, but not emergency, cesarean delivery is consistent with the hypothesis that the bacterial flora of the newborn plays a role in the development of celiac disease.

  • 22.
    Olén, Ola
    et al.
    Sachs’ Children and Youth Hospital, Stockholm South General Hospital, Stockholm, Sweden; Department of Clinical Science and Education Södersjukhuset, Karolinska Institutet, Stockholm, Sweden; Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Askling, Johan
    Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Sachs, Michael C.
    Unit of Biostatistics, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Frumento, Paolo
    Unit of Biostatistics, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Neovius, Martin
    Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Smedby, Karin E.
    Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Ekbom, Anders
    Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Malmborg, Petter
    Sachs’ Children and Youth Hospital, Stockholm South General Hospital, Stockholm, Sweden; Department of Clinical Science and Education Södersjukhuset, Karolinska Institutet, Stockholm, Sweden; Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro, Sweden; Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham, UK; Department of Medicine, Columbia University College of Physicians and Surgeons, New York NY, USA.
    Increased Mortality of Patients With Childhood- Onset Inflammatory Bowel Diseases, Compared With the General Population2019In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 156, no 3, p. 614-622Article in journal (Refereed)
    Abstract [en]

    BACKGROUND & AIMS: Childhood-onset inflammatory bowel disease (IBD) is believed to be a more severe disease than adultonset IBD, but there is little information on all-cause and causespecific mortality in patients with childhood-onset IBD. We performed a population-based cohort study, with 50 years of follow-up, to estimate absolute and relative risks for overall and cause-specific mortality in patients with childhood-onset IBD, during childhood and adulthood.

    METHODS: We identified children with a diagnosis of IBD (younger than 18 years) in the Swedish nationwide health registers (1964-2014; n = 9442) and individuals from the general population matched for sex, age, calendar year, and place of residence (reference group; n = 93,180). Hazard ratios (HR) for death were estimated using Cox regression separately in patients with ulcerative colitis (n = 4671), Crohn's disease (n = 3780), and IBD unclassified (n = 991). HRs were compared among calendar periods.

    RESULTS: During 138,690 person-years of follow-up, 294 deaths (2.1/1000 person-years) occurred among the patients with IBD compared with 940 deaths in the reference group (0.7/1000 person-years; adjusted HR, 3.2; 95% confidence interval [CI] 2.8-3.7). Mean age at end of follow-up was 30 years. HRs were increased for patients with ulcerative colitis 4.0, 95% CI 3.4-4.7; Crohn's disease 2.3, 95% CI 1.8-3.0; and IBD unclassified 2.0, 95% CI 1.2-3.4. Among patients younger than 18 years, there were 27 deaths from IBD 4.9, 95% CI 3.0-7.7. Among young adults with IBD, we found no evidence that HRs for death decreased from 1964 through 2014 (P = .90).

    CONCLUSIONS: Children with IBD have a 3-fold increase in risk of death when followed through adulthood. The relative risk for death has not decreased with development of new drugs for treatment of IBD.

  • 23. Radford-Smith, Graham
    et al.
    Doecke, James D.
    Lees, Charlie W.
    McGovern, Dermot P.
    Vermeire, Severine
    Kupcinskas, Limas
    Gearry, Richard B.
    Hov, Johannes R.
    Andersen, Vibeke
    Colombel, Jean-Frederic
    Annese, Vito
    Weersma, Rinse K.
    Lawrance, Ian C.
    Brand, Stephan
    Brant, Steven R.
    Ahmad, Tariq
    Krishnaprasad, Krupa
    Schumm, L. Philip
    Silverberg, Mark S.
    Halfvarson, Jonas
    Örebro University, School of Medicine, Örebro University, Sweden.
    Clinical and molecular characterization of medically refractory acute, severe colitis: preliminary results from the international inflammatory bowel disease genetics consortium (IIBDGC) immunochip study2013In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 144, no 5, p. S470-S470Article in journal (Other academic)
  • 24.
    Schoultz, Ida
    et al.
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Verma, Deepti
    Törkvist, Leif
    Halfvarson, Jonas
    Örebro University, School of Medicine, Örebro University, Sweden.
    Lerm, Maria
    Söderkvist, Peter
    Söderholm, Johan D.
    M2080 Compound Polymorphisms in CARD8 and CIAS1 Predispose to Crohn's Disease in a Swedish Cohort2008In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 134, no 4, p. A464-A465Article in journal (Other academic)
  • 25.
    Sjöberg, Mats
    et al.
    Örebro University, School of Health and Medical Sciences.
    Almer, Sven
    Befrits, Ragnar
    Benoni, Cecilia
    Carlson, Marie
    Eriksson, Anders
    Friis-Liby, Ingalill
    Halfvarson, Jonas
    Örebro University, School of Health and Medical Sciences.
    Hertervig, Erik
    Karlen, Per
    Lapidus, Annika B.
    Magnuson, Anders
    Midhagen, Gunnar
    Tysk, Curt
    Örebro University, School of Health and Medical Sciences.
    Infliximab as Rescue Therapy in Steroid-Refractory Acute Ulcerative Colitis: A Retrospective Follow-up Study2011In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 140, no 5, p. S590-S590Article in journal (Other academic)
  • 26.
    Westerbacka, Jukka
    et al.
    Department of Medicine, Division of Diabetes, University of Helsinki, Helsinki, Finland.
    Kotronen, Anna
    Department of Medicine, Division of Diabetes, University of Helsinki, Helsinki, Finland: Minerva Medical Research Institute, Helsinki, Finland; Diabetes Prevention Unit, National Institute for Health and Welfare, Helsinki, Finland.
    Fielding, Barbara A.
    Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, United Kingdom.
    Wahren, John
    Department of Surgical Sciences, Division of Clinical Physiology, Karolinska Hospital, Stockholm, Sweden.
    Hodson, Leanne
    Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, United Kingdom.
    Perttilä, Julia
    Minerva Medical Research Institute, Helsinki, Finland.
    Seppänen-Laakso, Tuulikki
    VTT Technical Research Centre of Finland, Espoo, Finland.
    Suortti, Tapani
    VTT Technical Research Centre of Finland, Espoo, Finland.
    Arola, Johanna
    Department of Pathology, University of Helsinki and HUSLAB, Helsinki, Finland.
    Hultcrantz, Rolf
    Department of Gastroenterology and Hepatology, Karolinska University Hospital, Stockholm, Sweden.
    Castillo, Sandra
    VTT Technical Research Centre of Finland, Espoo, Finland.
    Olkkonen, Vesa M.
    Minerva Medical Research Institute, Helsinki, Finland.
    Frayn, Keith N.
    Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, United Kingdom.
    Oresic, Matej
    VTT Technical Research Centre of Finland, Espoo, Finland.
    Yki-Järvinen, Hannele
    Department of Medicine, Division of Diabetes, University of Helsinki, Helsinki, Finland.
    Splanchnic balance of free fatty acids, endocannabinoids, and lipids in subjects with nonalcoholic fatty liver disease2010In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 139, no 6, p. 1961-1971.e1Article in journal (Refereed)
    Abstract [en]

    BACKGROUND & AIMS: Animal studies suggest that endocannabinoids could contribute to the development of nonalcoholic fatty liver disease (NAFLD). In addition, NAFLD has been shown to be associated with multiple changes in lipid concentrations in liver biopsies. There are no data on splanchnic free fatty acid (FFA), glycerol, ketone body, endocannabinoid, and lipid fluxes in vivo in subjects with NAFLD.

    METHODS: We performed hepatic venous catheterization studies in combination with [(2)H(2)]palmitate infusion in the fasting state and during a low-dose insulin infusion in 9 subjects with various degrees of hepatic steatosis as determined using liver biopsy. Splanchnic balance of endocannabinoids and individual lipids was determined using ultra performance liquid chromatography coupled to mass spectrometry.

    RESULTS: Concentrations of the endocannabinoid 2-arachidonoylglycerol were higher in arterialized (91 ± 33 μg/L basally) than in hepatic venous (51 ± 19 μg/L; P < .05) plasma. Fasting arterial (r = 0.72; P = .031) and hepatic venous (r = 0.70; P = .037) concentrations of 2-arachidonoylglycerol were related positively to liver fat content. Analysis of fluxes of 85 different triglycerides showed that the fatty liver overproduces saturated triglycerides. In the plasma FFA fraction in the basal state, the relative amounts of palmitoleate and linoleate were lower and those of stearate and oleate were higher in the hepatic vein than in the artery. Absolute concentrations of all nontriglyceride lipids were comparable in arterialized venous plasma and the hepatic vein both in the basal and insulin-stimulated states.

    CONCLUSIONS: The human fatty liver takes up 2-arachidonoylglycerol and overproduces triacylglycerols containing saturated fatty acids, which might reflect increased de novo lipogenesis.

  • 27.
    Willing, Ben P.
    et al.
    Dept Microbiol, Swedish Univ Agr Sci, Uppsala, Sweden .
    Dicksved, Johan
    Dept Microbiol, Swedish Univ Agr Sci, Uppsala, Sweden .
    Halfvarson, Jonas
    Dept Med, Div Gastroenterol, Örebro Univ Hosp, Örebro, Sweden .
    Andersson, Anders F.
    Dept Bacteriol, Swedish Inst Infect Dis Control, Solna, Sweden.
    Lucio, Marianna
    Res Ctr Environ, Inst Ecol Chem, Helmholtz Zentrum Muenchen, Neuherberg, Germany .
    Zheng, Zongli
    Dept Med Epidemiol & Biostat, Karolinska Inst, Solna, Sweden.
    Järnerot, Gunnar
    Dept Med, Div Gastroenterol, Örebro Univ Hosp, Örebro, Sweden.
    Tysk, Curt
    Örebro University, School of Health and Medical Sciences.
    Jansson, Janet K.
    Lawrence Berkeley Lab, Div Earth Sci, Univ Calif Berkeley, Berkeley CA, USA.
    Engstrand, Lars
    Dept Bacteriol, Swedish Inst Infect Dis Control, Solna, Sweden.
    A pyrosequencing study in twins shows that gastrointestinal microbial profiles vary with inflammatory bowel disease phenotypes2010In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 139, no 6, p. 1844-1854.e1Article in journal (Refereed)
    Abstract [en]

    BACKGROUND & AIMS: The composition of the gastrointestinal microbiota is thought to have an important role in the etiology of inflammatory bowel diseases (IBDs) such as Crohn's disease (CD) and ulcerative colitis (UC). Interindividual variation and an inability to detect less abundant bacteria have made it difficult to correlate specific bacteria with disease.

    METHODS: We used 454 pyrotag sequencing to determine the compositions of microbial communities in feces samples collected from a cohort of 40 twin pairs who were concordant or discordant for CD or UC, and in mucosal samples from a subset of the cohort. The cohort primarily comprised patients who were in remission, but also some with active disease.

    RESULTS: The profiles of the microbial community differed with disease phenotypes; relative amounts of bacterial populations correlated with IBD phenotypes. The microbial compositions of individuals with CD differed from those of healthy individuals, but were similar between healthy individuals and individuals with UC. Profiles from individuals with CD that predominantly involved the ileum differed from those with CD that predominantly involved the colon; several bacterial populations increased or decreased with disease type. Changes specific to patients with ileal CD included the disappearance of core bacteria, such as Faecalibacterium and Roseburia, and increased amounts of Enterobacteriaceae and Ruminococcus gnavus.

    CONCLUSIONS: Bacterial populations differ in abundance among individuals with different phenotypes of CD. Specific species of bacteria are associated with ileal CD; further studies should investigate their role in pathogenesis.

  • 28. Wouters, Mira M.
    et al.
    Lambrechts, Diether
    Cleynen, Isabelle
    Whorwell, Peter J.
    Lambaerts, Kathleen
    Agreus, Lars
    Dlugosz, Aldona
    Schmidt, Peter T.
    Halfvarson, Jonas
    Örebro University, School of Medicine, Örebro University, Sweden.
    Simren, Magnus
    Ohlsson, Bodil
    Karling, Pontus
    Van Wanrooy, Sander
    Vermeire, Severine
    Lindberg, Greger
    Spiller, Robin C.
    D'Amato, Mauro
    Boeckxstaens, Guy E.
    Association of protective IL13 polymorphism with irritable bowel syndrome2012In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 142, no 5, p. S178-S178Article in journal (Other academic)
  • 29.
    Zhulina, Yaroslava
    et al.
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Carlson, Marie
    Peterson, Christer G.
    Tysk, Curt
    Örebro University, School of Health and Medical Sciences.
    Gustavsson, Anders
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Bohr, Johan
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Bodin, Lennart
    Örebro University, Örebro University School of Business.
    Halfvarson, Jonas
    Örebro University, School of Medicine, Örebro University, Sweden.
    Subclinical inflammation due to environmental exposure in health co-twins to twins with inflammatory bowel disease2009In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 136, no 5, p. A20-A20Article in journal (Other academic)
1 - 29 of 29
CiteExportLink to result list
Permanent link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf