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  • 1. Almer, Sven
    et al.
    Granerus, Göran
    Ström, Magnus
    Olaison, Gunnar
    Bonnet, Joëlle
    Lémann, Marc
    Smedh, Kennet
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Centrum för klinisk forskning, Västerås.
    Franzén, Lennart
    Bertheau, Philippe
    Cattan, Pierre
    Rain, Jean-Didier
    Modigliani, Robert
    Leukocyte scintigraphy compared to intraoperative small bowel enteroscopy and laparotomy findings in Crohn's disease2007Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 13, nr 2, s. 164-174Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Leukocyte scintigraphy is a noninvasive investigation to assess inflammation. We evaluated the utility of labeled leukocytes to detect small bowel inflammation and disease complications in Crohn's disease and compared it to whole small bowel enteroscopy and laparotomy findings.Methods: Scintigraphy with technetium-99m exametazime-labeled leukocytes was prospectively performed in 48 patients with Crohn's disease a few days before laparotomy; 41 also had an intraoperative small bowel enteroscopy. The same procedures were performed in 8 control patients. Independent grading of scans was compared with the results of enteroscopy and with surgical, histopathologic, and clinical data.Results: In the 8 control patients leukocyte scan, endoscopy, and histopathology were all negative for the small bowel. In patients with Crohn's disease and small bowel inflammation seen at enteroscopy and/or laparotomy (n = 39) the scan was positive in 33. In 8 patients without macroscopic small bowel inflammation, the scan was positive for the small bowel in 3 patients; at histology, 2 of 3 had inflammation. When combining results for patients and controls, the sensitivity of leukocyte scan for macroscopically evident small bowel inflammation was 0.85, specificity 0.81, accuracy 0.84, positive predictive value 0.92, and negative predictive value 0.68. Scintigraphy detected inflammatory lesions not known before laparotomy in 16 of 47 (34%) Crohn's disease patients and showed uptake in 25 of 35 (71%) bowel strictures. It was diagnostic regarding 4 of 8 abscesses and 9 of 15 fistulas. In 6 patients (13%) lesions first demonstrated by leukocyte scintigraphy were treated during the surgery performed.Conclusions: Leukocyte scintigraphy reliably detects small bowel inflammation in Crohn's disease. It gives additional information on the presence of inflammatory lesions in a fraction of patients planned for surgery.

  • 2.
    Almer, Sven
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Gastroenterologi och hepatologi. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Granerus, Göran
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Klinisk fysiologi. Östergötlands Läns Landsting, Hjärtcentrum, Fysiologiska kliniken.
    Ström, Magnus
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Gastroenterologi och hepatologi. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Olaison, Gunnar
    Bonnet, Joëlle
    Lémann, Marc
    Smedh, Kennet
    Franzén, Lennart
    Bertheau, Philippe
    Cattan, Pierre
    Rain, Jean-Didier
    Modigliani, Robert
    Leukocyte scintigraphy compared to intraoperative small bowel enteroscopy and laparotomy findings in Crohn's disease2007Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 13, nr 2, s. 164-174Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Leukocyte scintigraphy is a noninvasive investigation to assess inflammation. We evaluated the utility of labeled leukocytes to detect small bowel inflammation and disease complications in Crohn's disease and compared it to whole small bowel enteroscopy and laparotomy findings. Methods: Scintigraphy with technetium-99m exametazime-labeled leukocytes was prospectively performed in 48 patients with Crohn's disease a few days before laparotomy, 41 also had an intraoperative small bowel enteroscopy. The same procedures were performed in 8 control patients. Independent grading of scans was compared with the results of enteroscopy and with surgical, histopathologic, and clinical data. Results: In the 8 control patients leukocyte scan, endoscopy, and histopathology were all negative for the small bowel. In patients with Crohn's disease and small bowel inflammation seen at enteroscopy and/or laparotomy (n = 39) the scan was positive in 33. In 8 patients without macroscopic small bowel inflammation, the scan was positive for the small bowel in 3 patients, at histology, 2 of 3 had inflammation. When combining results for patients and controls, the sensitivity of leukocyte scan for macroscopically evident small bowel inflammation was 0.85, specificity 0.81, accuracy 0.84, positive predictive value 0.92, and negative predictive value 0.68. Scintigraphy detected inflammatory lesions not known before laparotomy in 16 of 47 (34%) Crohn's disease patients and showed uptake in 25 of 35 (71 %) bowel strictures. It was diagnostic regarding 4 of 8 abscesses and 9 of 15 fistulas. In 6 patients (13%) lesions first demonstrated by leukocyte scintigraphy were treated during the surgery performed. Conclusions: Leukocyte scintigraphy reliably detects small bowel inflammation in Crohn's disease. It gives additional information on the presence of inflammatory lesions in a fraction of patients planned for surgery. Copyright © 2006 Crohn's & Colitis Foundation of America, Inc.

  • 3.
    Ardesjö, Brita
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Portela-Gomes, Guida M.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för genetik och patologi.
    Rorsman, Fredrik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Gerdin, Eva
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kvinnors och barns hälsa.
    Lööf, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Centrum för klinisk forskning, Västerås.
    Grimelius, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för genetik och patologi.
    Kämpe, Olle
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Ekwall, Olov
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Immunoreactivity against goblet cells in patients with inflammatory bowel disease2008Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 14, nr 5, s. 652-661Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: A number of autoantibodies have been reported in inflammatory bowel disease (IBD). The aim of this study was to investigate to what extent sera from patients with IBD contain autoantibodies directed against normal human gastrointestinal mucosa. METHODS: Samples of sera from 50 patients with IBD and 50 healthy subjects were used for immunostaining of normal and affected human gastrointestinal tissues. RESULTS: Eighty-four percent of the sera from IBD patients showed immunoreactivity against goblet cells in the appendix compared with 8% of the sera from healthy subjects. Goblet cell reactivity of IBD patient sera varied between regions in the gastrointestinal tract. Sera from healthy subjects only reacted with goblet cells in the appendix. In the colon and the appendix, goblet cell reactivity of IBD sera was generally weak at the base of the crypts and gradually increased toward the lumen. Three IBD sera samples reacted with gastrin cells in the antrum. In colon biopsies from patients with ulcerative colitis, immunoreactivity against the remaining goblet cells showed an inverse correlation with inflammatory activity. CONCLUSIONS: These findings suggest that immunoreactivity against goblet cells may be of central importance in the pathogenesis of IBD. Identification of goblet cell antigens could lead to a better understanding of IBD and provide a new diagnostic tool.

  • 4.
    Ardesjö, Brita
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Portela-Gomes, Guida M.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för genetik och patologi.
    Rorsman, Fredrik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Grimelius, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för genetik och patologi.
    Ekwall, Olov
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Identification of a novel staining pattern of bile duct epithelial cells in primary sclerosing cholangitis2010Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 16, nr 2, s. 305-311Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Primary sclerosing cholangitis (PSC) is an inflammatory disease of the bile ducts with an unknown etiology. A number of autoantigens have been proposed, but an early diagnostic marker is still lacking. Our aim was to identify such an autoantigen. METHODS: Immunostaining was performed on normal human bile duct with sera from patients with PSC and controls. To identify an autoantigen a cDNA library from normal human choledochus was constructed and immunoscreened with patient sera. Using in vitro transcription and translation and immunoprecipitation we examined the immunoreactivity against PDZ domain containing 1 (PDZK1) in 35 patients with PSC, 198 control patients, and 94 healthy controls. RESULTS: We observed a previously unpublished staining pattern in which cytoplasmatic granules and apical cell membranes of biliary epithelial cells were stained by PSC sera. Strong immunoreactivity to these structures was obtained with 12 out of 35 PSC sera (34%) but not with sera from healthy controls. By screening the cDNA library we identified PDZK1 as a candidate antigen. Immunoreactivity against PDZK1 was detected in 9% of PSC patients, 2% of inflammatory bowel disease (IBD) patients, 8% of autoimmune pancreatitis patients, 18% of Grave's disease patients, and 1% of healthy controls. CONCLUSIONS: Previously unpublished, specific, and strong autoantibodies against epithelial cells of the bile duct in PSC sera were identified. Furthermore, PDZK1 is suggested as a potential new autoantigen.

  • 5.
    Berglund, Martin
    et al.
    Dept Microbiol & Immunol, Inst Biomed, Sahlgrenska Acad, Univ Gothenburg, Gothenburg, Sweden.
    Melgar, Silvia
    Alimentary Pharmabiot Ctr, Univ Coll Cork, Cork, Ireland; Immunoinflammat CEDD GlaxoSmithKline, Stevenage Herts, England.
    Kobayashi, Koichi S.
    Harvard Univ, Boston MA, USA.
    Flavell, Richard A.
    Yale Univ, New Haven CT, USA.
    Hultgren Hörnquist, Elisabeth
    Örebro universitet, Hälsoakademin.
    Hultgren, Olof H.
    Department of Medicine, School of Health and Medical Sciences, Örebro University, Örebro, Sweden; Örebro University Hospital, Örebro, Sweden.
    IL-1 receptor-associated kinase M downregulates DSS-induced colitis2010Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 16, nr 10, s. 1778-1786Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Ulcerative colitis is associated with increased colon permeability resulting in bacterial translocation into the lamina propria. We investigate the importance of the Toll-like receptor (TLR) regulating protein IL-1 receptor-associated kinase M (IRAK-M) using the erosive dextran sulfate sodium (DSS)-induced model of colitis. Methods: IRAK-M-competent and -incompetent mice were treated with 3% DSS for 5 days followed by 2 days of regular drinking water. Clinical signs of disease were followed for 7 days. At day 7 the mice were sacrificed and plasma and tissue were collected for histopathological examination and analyses of the production of cytokines and chemokines as well as expression of T-cell transcription factors. Results: At day 7 IRAK-M-deficient mice display a reduced total body weight (77.1 +/- 2.1 versus 88.5 +/- 2.0, *P=0.002) and an increased macroscopical (2.7 +/- 0.2 versus 1.6 +/- 0.1, *P 0.002) and histopathological (6.0 +/- 0 versus 3.3 +/- 60.5, *P < 0.001) colon score compared to wildtype mice. Furthermore, IRAK-M-deficient mice have increased colon mRNA expression of proinflammatory cytokines and increased tumor necrosis factor concentrations (41.1 +/- 13.5 versus 12.8 +/- 2.0 pg/mL, *P = 0.010) in plasma. Conclusions: This is the first report examining the role of IRAK-M in colitis. We find that IRAK-M is of critical importance in downregulating induction and progression of DSS colitis, and thereby suggesting that IRAK-M might be a target for future interventional therapies. (Inflamm Bowel Dis 2010; 16: 1778-1786)

  • 6.
    Burisch, Johan
    et al.
    Med Sect, Ctr Digest Dis, Herlev Univ Hosp, Copenhagen, Denmark.
    Pedersen, Natalia
    Med Sect, Ctr Digest Dis, Herlev Univ Hosp, Copenhagen, Denmark.
    Cukovic-Cavka, Silvja
    Univ Hosp Ctr Zagreb, Div Gastroenterol & Hepatol, Univ Zagreb School of Medicine, Zagreb, Croatia.
    Turk, Niksa
    Univ Hosp Ctr Zagreb, Div Gastroenterol & Hepatol, Univ Zagreb School of Medicine, Zagreb, Croatia.
    Kaimakliotis, Ioannis
    Nicosia Private Practice, Nicosia, Cyprus.
    Duricova, Dana
    IBD Ctr ISCARE, Charles Univ Prague, Prague, Czech Republic.
    Shonova, Olga
    Dept Gastroenterol, Hosp Ceske Budejovice, Ceske Budejovice, Czech Republic.
    Vind, Ida
    Dept Med, Amager Hosp, Amager, Denmark.
    Avnstrom, Soren
    Dept Med, Amager Hosp, Amager, Denmark.
    Thorsgaard, Niels
    Dept Med, Herning Cent Hosp, Herning, Denmark.
    Krabbe, Susanne
    Dept Med, Viborg Reg Hosp, Viborg, Denmark.
    Andersen, Vibeke
    Medical Department, Viborg Regional Hospital, Viborg, Denmark; Medical Department, Hospital of Southern Jutland, Aabenraa, Denmark; Institute of Regional Health Research, University of Southern Denmark, Odense, Denmark.
    Jens, Frederik Dahlerup
    Dept Med Hepatol & Gastroenterol 5, Aarhus Univ Hosp, Aarhus, Denmark.
    Kjeldsen, Jens
    Dept Med Gastroenterol, Odense Univ Hosp, Odense, Denmark.
    Salupere, Riina
    Div Gastroenterol & Endocrinol, Tartu Univ Hosp, Tartu, Estonia.
    Olsen, Jongero
    Dept Med, Natl Hosp Faroe Islands, Torshavn, Denmark.
    Nielsen, Kari Rubek
    Dept Med, Natl Hosp Faroe Islands, Torshavn, Denmark.
    Manninen, Pia
    Dept Gastroenterol & Alimentary Tract Surg, Tampere Univ Hosp, Tampere, Finland.
    Collin, Pekka
    Dept Gastroenterol & Alimentary Tract Surg, Tampere Univ Hosp, Tampere, Finland.
    Katsanos, Konstantinnos H.
    Div Internal Med 1, Univ Hosp, Ioannina, Greece ; Hepatogastroenterol Unit, Univ Hosp, Ioannina, Greece.
    Tsianos, Epameinondas V.
    Div Internal Med 1, Univ Hosp, Ioannina, Greece ; Hepatogastroenterol Unit, Univ Hosp, Ioannina, Greece.
    Ladefoged, Karin
    Dept Med, Dronning Ingrids Hosp, Nuuk, Greenland.
    Lakatos, Laszlo
    Dept Med, Csolnoky F Prov Hosp, Veszprem, Hungary.
    Bailey, Yvonne
    Adelaide & Meath Hosp, Dept Gastroenterol, Trinity Coll Dublin, Dublin, Ireland.
    O'Morain, Colm
    Dept Gastroenterol, Adelaide & Meath Hosp, Dublin, Ireland.
    Schwartz, Doron
    Dept Gastroenterol & Hepatol, Soroka Med Ctr, Beer Sheva, Israel; Ben Gurion Univ of the Negev, Beer Sheva, Israel .
    Odes, Selwyn
    Dept Gastroenterol & Hepatol, Soroka Med Ctr, Beer Sheva, Israel; Ben Gurion Univ of the Negev, Beer Sheva, Israel .
    Martinato, Matteo
    U.O. Gastroenterologia, Azienda Ospedaliera, Università di Padova, Padova, Italy.
    Lombardini, Silvia
    UO Medicina 38 e Gastroenterologia, Azienda Ospedaliera Arcispedale S Maria Nuova, Reggio Emilia, Italy.
    Jonaitis, Laimas
    Institute for Digestive Research, Lithuanian University of Health Sciences, Kaunas, Lithuania.
    Kupcinskas, Limas
    Department of Gastroenterology, State University of Medicine and Pharmacy of the Republic of Moldova, Chisinau, Moldova.
    Turcan, Svetlana
    Dept Gastroenterol, State Univ Med & Pharm Republ Moldova, Kishinev, Moldova.
    Barros, Louisa
    Dept Med, Hosp Vale de Sousa, Oporto, Portugal.
    Magro, Fernando
    Dept Gastroenterol, Hosp Sao Joao, Oporto, Portugal ; Inst Pharmacol & Therapeut, Oporto Med Sch, Oporto, Portugal ; Inst Mol & Cell Biol, Univ Porto, Oporto, Portugal .
    Lazar, Daniela
    Gastroenterol Clin, Univ Med 'Victor Babes', Timisoara, Romania.
    Goldis, Adrian
    Gastroenterol Clin, Univ Med 'Victor Babes', Timisoara, Romania.
    Nikulina, Inna
    Department of Gastroenterology, Moscow Regional Research Clinical Institute, Moscow, Russian Federation.
    Belousova, Elena
    Dept Gastroenterol, Moscow Reg Res Clin Inst, Moscow, Russia.
    Fernandez, Alberto
    Dept Gastroenterol, POVISA Hosp, Vigo, Spain.
    Hernandez, Vicent
    Dept Gastroenterol, Complexo Hospitalario Univ Vigo, Vigo, Spain.
    Almer, Sven
    Div Gastroenterol & Hepatol, Karolinska Instutue, Stockholm, Sweden ; Dept Gastroenterol UHL, Cty Council Östergötland,Linköping, Sweden .
    Zhulina, Yaroslava
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Region Örebro län. Div Gastroenterol, Dept Med, Örebro University Hospital, Örebro, Sweden.
    Halfvarson, Jonas
    Örebro universitet, Institutionen för läkarutbildning. Region Örebro län. Div Gastroenterol, Dept Med, Örebro University Hospital, Örebro, Sweden.
    Tsai, Her-Hsin
    Hull and East Yorkshire NHS Trust, Kingston-Upon-Hull, UK; Hull and York Medical School, Kingston-Upon-Hull, UK; Hull Royal Infirmary, Kingston-Upon-Hull, UK.
    Sebastian, Shaji
    Hull and East Yorkshire NHS Trust, Kingston-Upon-Hull, UK; Hull and York Medical School, Kingston-Upon-Hull, UK; Hull Royal Infirmary, Kingston-Upon-Hull, UK.
    Lakatos, Peter Laszlo
    Dept Med 1, Semmelweis Univ, Budapest, Hungary.
    Langholz, Ebbe
    Dept Med Gastroenterol, Gentofte Univ Hosp, Copenhagen, Denmark.
    Munkholm, Pia
    Med Sect, Ctr Digest Dis, Herlev Univ Hosp, Copenhagen, Denmark.
    EpiCom Northern Italy Centre Based in Crema and Cremona, Padova and Reggio Emilia, Italy (Lombardini & Martinato, on behalf of ), Group author
    Initial Disease Course and Treatment in an Inflammatory Bowel Disease Inception Cohort in Europe: The ECCO-EpiCom Cohort2014Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 20, nr 1, s. 36-46Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background:The EpiCom cohort is a prospective, population-based, inception cohort of inflammatory bowel disease (IBD) patients from 31 European centers covering a background population of 10.1 million. The aim of this study was to assess the 1-year outcome in the EpiCom cohort.

    Methods:Patients were followed-up every third month during the first 12 (3) months, and clinical data, demographics, disease activity, medical therapy, surgery, cancers, and deaths were collected and entered in a Web-based database (www.epicom-ecco.eu).

    Results:In total, 1367 patients were included in the 1-year follow-up. In western Europe, 65 Crohn's disease (CD) (16%), 20 ulcerative colitis (UC) (4%), and 4 IBD unclassified (4%) patients underwent surgery, and in eastern Europe, 12 CD (12%) and 2 UC (1%) patients underwent surgery. Eighty-one CD (20%), 80 UC (14%), and 13 (9%) IBD unclassified patients were hospitalized in western Europe compared with 17 CD (16%) and 12 UC (8%) patients in eastern Europe. The cumulative probability of receiving immunomodulators was 57% for CD in western (median time to treatment 2 months) and 44% (1 month) in eastern Europe, and 21% (5 months) and 5% (6 months) for biological therapy, respectively. For UC patients, the cumulative probability was 22% (4 months) and 15% (3 months) for immunomodulators and 6% (3 months) and 1% (12 months) for biological therapy, respectively in the western and eastern Europe.

    Discussion:In this cohort, immunological therapy was initiated within the first months of disease. Surgery and hospitalization rates did not differ between patients from eastern and western Europe, although more western European patients received biological agents and were comparable to previous population-based inception cohorts.

  • 7.
    Burisch, Johan
    et al.
    Digestive Disease Centre, Medical Section, Herlev University Hospital, Copenhagen, Denmark.
    Vardi, Hillel
    Department of Public Health, Faculty of Health Sciences, Ben Gurion University of the Negev, Beer Sheva, Israel.
    Pedersen, Natalia
    Digestive Disease Centre, Medical Section, Herlev University Hospital, Copenhagen, Denmark.
    Brinar, Marko
    Division of Gastroenterology and Hepatology, University Hospital Center Zagreb, University of Zagreb School of Medicine, Zagreb, Croatia.
    Cukovic-Cavka, Silvja
    Division of Gastroenterology and Hepatology, University Hospital Center Zagreb, University of Zagreb School of Medicine, Zagreb, Croatia.
    Kaimakliotis, Ioannis
    Private Practice, Nicosia, Cyprus.
    Duricova, Dana
    IBD Center ISCARE, Charles University, Prague, Czech Republic.
    Bortlik, Martin
    IBD Center ISCARE, Charles University, Prague, Czech Republic.
    Shonová, Olga
    Department of Gastroenterology, Hospital Ceske Budejovice, Ceske Budejovice, Czech Republic.
    Vind, Ida
    Department of Medicine, Amager Hospital, Amager, Denmark.
    Avnstrøm, Søren
    Department of Medicine, Amager Hospital, Amager, Denmark.
    Thorsgaard, Niels
    Department of Medicine, Herning Central Hospital, Herning, Denmark.
    Krabbe, Susanne
    Medical Department, Viborg Regional Hospital, Viborg, Denmark.
    Andersen, Vibeke
    Medical Department, Viborg Regional Hospital, Viborg, Denmark; Organ Center, Hospital of Southern Jutland, Aabenraa, Denmark; Institute of Regional Health Research, University of Southern Denmark, Odense, Denmark.
    Dahlerup, Jens F
    Department of Medicine V (Hepatology and Gastroenterology), Aarhus University Hospital, Arhus, Denmark.
    Kjeldsen, Jens
    Department of Medical Gastroenterology, Odense University Hospital, Odense, Denmark.
    Salupere, Riina
    Division of Endocrinology and Gastroenterology, Tartu University Hospital, Tartu, Estonia.
    Olsen, Jónger
    Medical Department, The National Hospital of the Faroe Islands, Torshavn, Faroe Islands.
    Nielsen, Kári R
    Medical Department, The National Hospital of the Faroe Islands, Torshavn, Faroe Islands.
    Manninen, Pia
    Department of Gastroenterology and Alimentary Tract Surgery, Tampere University Hospital, Tampere, Finland.
    Collin, Pekka
    Department of Gastroenterology and Alimentary Tract Surgery, Tampere University Hospital, Tampere, Finland.
    Katsanos, Konstantinnos H
    First Division of Internal Medicine and Hepato-Gastroenterology Unit, University Hospital, Ioannina, Greece.
    Tsianos, Epameinondas V
    First Division of Internal Medicine and Hepato-Gastroenterology Unit, University Hospital, Ioannina, Greece.
    Ladefoged, Karin
    Medical Department, Dronning Ingrids Hospital, Nuuk, Greenland.
    Lakatos, Laszlo
    First Department of Medicine, Semmelweis University, Budapest, Hungary.
    Bailey, Yvonne
    Department of Gastroenterology, Adelaide and Meath Hospital, TCD, Dublin, Ireland.
    OʼMorain, Colm
    Department of Gastroenterology, Adelaide and Meath Hospital, TCD, Dublin, Ireland.
    Schwartz, Doron
    Department of Gastroenterology and Hepatology, Soroka Medical Center, Ben Gurion University of the Negev, Beer Sheva, Israel.
    Lupinacci, Guido
    U.O. di Gastroenterologia e Endoscopia Digestiva, Az.Ospedaliera Ospedale Maggiore di Crema, Crema, Italy; EpiCom Northern Italy centre based in Crema and Cremona, Firenze, Forli, Padova and Reggio Emilia, Italy.
    De Padova, Angelo
    EpiCom Northern Italy centre based in Crema and Cremona, Firenze, Forli, Padova and Reggio Emilia, Italy; U.O. Gastroenterologia ed Endoscopia Digestiva, Ospedale Morgagni, Pierantoni, Forli, Italy.
    Jonaitis, Laimas
    Institute for Digestive Research, Lithuanian University of Health Sciences, Kaunas, Lithuania.
    Kupcinskas, Limas
    Institute for Digestive Research, Lithuanian University of Health Sciences, Kaunas, Lithuania.
    Turcan, Svetlana
    Department of Gastroenterology, State University of Medicine and Pharmacy of the Republic of Moldova, Chisinau, Republic of Moldova.
    Barros, Louisa
    Department of Medicine, Hospital de Vale de Sousa, Porto, Portugal.
    Magro, Fernando
    Department of Gastroenterology, Hospital de Sao Joao, Porto, Portugal; Institute of Pharmacology and Therapeutics, Oporto Medical School, Porto, Portugal; Institute for molecular and cell biology, University of Porto, Porto, Portugal.
    Lazar, Daniela
    Clinic of Gastroenterology, University of Medicine "Victor Babes," Timisoara, Romania.
    Goldis, Adrian
    Clinic of Gastroenterology, University of Medicine "Victor Babes," Timisoara, Romania.
    Nikulina, Inna
    Department of Gastroenterology, Moscow Regional Research Clinical Institute, Moscow, Russia.
    Belousova, Elena
    Department of Gastroenterology, Moscow Regional Research Clinical Institute, Moscow, Russia.
    Fernandez, Alberto
    Gastroenterology Department, POVISA Hospital, Vigo, Spain.
    Pineda, Juan R
    Gastroenterology Department, Complexo Hospitalario Universitario de Vigo, Vigo, Spain.
    Almer, Sven
    GastroCentrum, Karolinska University Hospital, Stockholm, Sweden; Department of Medicine, Solna, Karolinska University Hospital, Stockholm, Sweden.
    Halfvarson, Jonas
    Örebro universitet, Institutionen för läkarutbildning. Department of Medicine, Division of Gastroenterology, Örebro University Hospital, Örebro, Sweden; School of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Tsai, Her-Hsin
    Hull and East Yorkshire NHS Trust and Hull and York Medical School, Hull Royal Infirmary, Hull, United Kingdom.
    Sebastian, Shaji
    Hull and East Yorkshire NHS Trust and Hull and York Medical School, Hull Royal Infirmary, Hull, United Kingdom.
    Friger, Michael
    Department of Public Health, Faculty of Health Sciences, Ben Gurion University of the Negev, Beer Sheva, Israel.
    Greenberg, Dan
    Department of Health Systems Management, Faculty of Health Sciences, Ben Gurion University of the Negev, Beer Sheva, Israel; Guilford Glazer Faculty of Business and Management, Ben Gurion University of the Negev, Beer Sheva, Israel.
    Lakatos, Peter L
    First Department of Medicine, Semmelweis University, Budapest, Hungary.
    Langholz, Ebbe
    Department of Medical Gastroenterology, Gentofte Hospital, Copenhagen, Denmark.
    Odes, Selwyn
    Department of Gastroenterology and Hepatology, Soroka Medical Center, Ben Gurion University of the Negev, Beer Sheva, Israel.
    Munkholm, Pia
    Digestive Disease Centre, Medical Section, Herlev University Hospital, Copenhagen, Denmark.
    Costs and resource utilization for diagnosis and treatment during the initial year in a European inflammatory bowel disease inception cohort: an ECCO-EpiCom Study2015Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 21, nr 1, s. 121-131Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: No direct comparison of health care cost in patients with inflammatory bowel disease across the European continent exists. The aim of this study was to assess the costs of investigations and treatment for diagnostics and during the first year after diagnosis in Europe.

    METHODS: The EpiCom cohort is a prospective population-based inception cohort of unselected inflammatory bowel disease patients from 31 Western and Eastern European centers. Patients were followed every third month from diagnosis, and clinical data regarding treatment and investigations were collected. Costs were calculated in euros (&OV0556;) using the Danish Health Costs Register.

    RESULTS: One thousand three hundred sixty-seven patients were followed, 710 with ulcerative colitis, 509 with Crohn's disease, and 148 with inflammatory bowel disease unclassified. Total expenditure for the cohort was &OV0556;5,408,174 (investigations: &OV0556;2,042,990 [38%], surgery: &OV0556;1,427,648 [26%], biologicals: &OV0556;781,089 [14%], and standard treatment: &OV0556;1,156,520 [22%)]). Mean crude expenditure per patient in Western Europe (Eastern Europe) with Crohn's disease: investigations &OV0556;1803 (&OV0556;2160) (P = 0.44), surgery &OV0556;11,489 (&OV0556;13,973) (P = 0.14), standard treatment &OV0556;1027 (&OV0556;824) (P = 0.51), and biologicals &OV0556;7376 (&OV0556;8307) (P = 0.31). Mean crude expenditure per patient in Western Europe (Eastern Europe) with ulcerative colitis: investigations &OV0556;1189 (&OV0556;1518) (P < 0.01), surgery &OV0556;18,414 (&OV0556;12,395) (P = 0.18), standard treatment &OV0556;896 (&OV0556;798) (P < 0.05), and biologicals &OV0556;5681 (&OV0556;72) (P = 0.51).

    CONCLUSIONS: In this population-based unselected cohort, costs during the first year of disease were mainly incurred by investigative procedures and surgeries. However, biologicals accounted for >15% of costs. Long-term follow-up of the cohort is needed to assess the cost-effectiveness of biological agents.

  • 8.
    Canova, Cristina
    et al.
    Department of Molecular Medicine, University of Padua, Padua, Italy.
    Pitter, Gisella
    Department of Molecular Medicine, University of Padua, Padua, Italy; School of Specialization in Hygiene and Preventive Medicine, University of Padua, Padua, Italy.
    Zanier, Loris
    Epidemiological Service, Udine, Italy.
    Zanotti, Renzo
    Department of Molecular Medicine, University of Padua, Padua, Italy.
    Simonato, Lorenzo
    Department of Cardiological, Thoracic and Vascular Sciences, University of Padua, Padua, Italy.
    Ludvigsson, Jonas F.
    Örebro universitet, Institutionen för medicinska vetenskaper. 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, United Kingdom; Department of Medicine, College of Physicians and Surgeons, Columbia University, New York NY, USA.
    Inflammatory Bowel Diseases in Children and Young Adults with Celiac Disease: A Multigroup Matched Comparison2017Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 23, nr 11, s. 1996-2000Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Celiac disease (CD) has been linked to inflammatory bowel disease (IBD) but previous reports have been inconsistent and may have been affected by surveillance bias.

    METHODS: Matched birth cohort study in Friuli-Venezia Giulia Region, Italy. We identified 1294 individuals with CD aged 0 to 23 years at diagnosis using pathology reports, hospital discharge records, or copayment exemptions. Each CD individual was matched with up to 5 general population reference individuals from the regional Medical Birth Register in Friuli-Venezia Giulia (n = 5681). As secondary comparison groups, we used individuals undergoing small intestinal biopsy but not having villous atrophy (either Marsh 0-1-2 or exclusively Marsh 0). Individuals with IBD were identified through hospital discharge records or copayment exemptions. Conditional logistic regression was used to estimate odds ratios (ORs) for having IBD among CD individuals (before or after CD diagnosis) compared with their matched references.

    RESULTS: Overall 35 individuals with IBD were identified (29 with CD and 6 general population controls). This corresponded to an increased risk of IBD in CD (OR = 24.17; 95% CI, 10.03-58.21). However, compared with individuals with Marsh 0-1-2 the OR decreased to 1.41 (95% CI, 0.91-2.18) and restricting our comparison group to individuals with Marsh 0, the OR was 1.28 (95% CI, 0.61-2.70).

    CONCLUSIONS: In conclusion, this article found a highly increased risk of IBD in individuals with CD when comparing with the general population. Bias is the likely explanation for the very high risk increase for IBD in CD because the excess risk was substantially lower when we used individuals with a small intestinal biopsy without villous atrophy as our reference.

  • 9. Chan, Simon S. M.
    et al.
    Luben, Robert
    van Schaik, Fiona
    Oldenburg, Bas
    Bueno-De-Mesquita, H. Bas
    Hallmans, Göran
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Näringsforskning.
    Karling, Pontus
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Lindgren, Stefan
    Grip, Olof
    Key, Timothy
    Crowe, Francesca L.
    Bergmann, Manuela M.
    Overvad, Kim
    Palli, Domenico
    Masala, Giovanna
    Khaw, Kay-Tee
    Racine, Antoine
    Carbonnel, Franck
    Boutron-Rualt, Marie-Christine
    Olsen, Anja
    Tjonneland, Anne
    Kaaks, Rudolf
    Tumino, Rosario
    Trichopoulou, Antonia
    Hart, Andrew R.
    Carbohydrate Intake in the Etiology of Crohn's Disease and Ulcerative Colitis2014Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 20, nr 11, s. 2013-2021Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Diet may have a role in the etiology of inflammatory bowel disease. In previous studies, the associations between increased intakes of carbohydrates, sugar, starch, and inflammatory bowel disease are inconsistent. However, few prospective studies have investigated the associations between these macronutrients and incident Crohn's disease (CD) or ulcerative colitis (UC). Methods: A total of 401,326 men and women were recruited between 1991 and 1998. At recruitment, dietary intakes of carbohydrate, sugar, and starch were measured using validated food frequency questionnaires. The cohort was monitored identifying participants who developed incident CD or UC. Cases were matched with 4 controls, and odds ratios were calculated for quintiles of total carbohydrate, sugar, and starch intakes adjusted for total energy intake, body mass index, and smoking. Results: One hundred ten participants developed CD, and 244 participants developed UC during follow-up. The adjusted odds ratio for the highest versus the lowest quintiles of total carbohydrate intake for CD was 0.87, 95% CI = 0.24 to 3.12 and for UC 1.46, 95% CI = 0.62 to 3.46, with no significant trends across quintiles for either (CD, P-trend = 0.70; UC, P-trend = 0.41). Similarly, no associations were observed with intakes of total sugar (CD, P-trend = 0.50; UC, P-trend = 0.71) or starch (CD, P-trend = 0.69; UC, P-trend = 0.17). Conclusions: The lack of associations with these nutrients is in agreement with many case-control studies that have not identified associations with CD or UC. As there is biological plausibility for how specific carbohydrates could have an etiological role in inflammatory bowel disease, future epidemiological work should assess individual carbohydrates, although there does not seem to be a macronutrient effect.

  • 10.
    Da Silva, Stéphanie
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för Kirurgi, Ortopedi och Onkologi. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Centrum för kirurgi, ortopedi och cancervård, Kirurgiska kliniken US.
    Keita, Åsa V.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för Kirurgi, Ortopedi och Onkologi. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Centrum för kirurgi, ortopedi och cancervård, Kirurgiska kliniken US.
    Mohlin, Sofie
    Translational Cancer Research, Cancer Center at Medicon Village, Lund University, Lund, Sweden.
    Påhlman, Sven
    Translational Cancer Research, Cancer Center at Medicon Village, Lund University, Lund, Sweden.
    Théodorou, Vassilia
    Toxalim UMR 1331 INRA/INP/UPS Neuro-Gastroenterology and Nutrition Unit, Toulouse, France.
    Påhlman, Ingrid
    Albireo AB, Arvid Wallgrens Backe, Gothenburg, Sweden.
    Mattson, Jan P.
    Albireo AB, Arvid Wallgrens Backe, Gothenburg, Sweden.
    Söderholm, Johan D.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för Kirurgi, Ortopedi och Onkologi. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Centrum för kirurgi, ortopedi och cancervård, Kirurgiska kliniken US.
    A novel topical PPARγ agonist induces PPARγ-activity in ulcerative colitis mucosa and prevents and reverses inflammation in induced-colitis models2018Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 24, nr 4, s. 792-805Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Peroxisome proliferator-activated receptor-gamma (PPARγ) exerts anti-inflammatory effects and is therefore a potential target in ulcerative colitis (UC). A novel PPARγ agonist (AS002) developed for local action was evaluated ex vivo in biopsies from UC patients and in vivo in mice with low-grade dextran sodium sulfate (DSS)- and trinitrobenzene sulfonic acid (TNBS)-induced colitis.Methods: Colonic biopsies from UC patients (n = 18) and healthy controls (n = 6) were incubated with AS002 or rosiglitazone (positive control) to measure mRNA expression of the PPARγ-responsive gene ADIPOPHILIN and protein levels of UC-related cytokines (enzyme-linked immunosorbent assay). AS002 absorption was determined in the colonic mucosa of UC patients. DSS-colitis mice received PPARγ agonists or vehicle daily by intrarectal administration starting 2 days before induction of colitis (preventive) or from days 3 to 8 (curative). Myeloperoxidase (MPO) and cytokine levels in colonic mucosa were determined. In addition, AS002 effects were studied in TNBS colitis.Results: AS002 displayed an absorption pattern of a lipophilic drug totally metabolized in the mucosa. AS002 and rosiglitazone increased ADIPOPHILIN mRNA expression (3-fold) and decreased TNF-α, IL-1β, and IL-13 levels in human UC biopsies. In DSS, in both preventive and curative treatment and in TNBS colitis, AS002 protected against macroscopic and histological damage and lowered MPO and TNF-α, IL-1β, and IL-13 levels.Conclusions: AS002 triggers anti-inflammatory PPARγ activity in the human colonic mucosa of UC patients and prevents and reverses colitis in mice. Our data suggest that AS002 has potential for topical maintenance treatment of UC, which warrants further studies in vivo in patients.

  • 11. de Ridder, Lissy
    et al.
    Turner, Dan
    Wilson, David C.
    Koletzko, Sibylle
    Martin-de-Carpi, Javier
    Fagerberg, Ulrika L.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Centrum för klinisk forskning, Västerås.
    Spray, Christine
    Sladek, Malgorzata
    Shaoul, Ron
    Roma-Giannikou, Eleftheria
    Bronsky, Jiri
    Serban, Daniela E.
    Cucchiara, Salvatore
    Veres, Gabor
    Ruemmele, Frank M.
    Hojsak, Iva
    Kolho, Kaija L.
    Davies, Ieuan H.
    Aloi, Marina
    Lionetti, Paolo
    Veereman-Wauters, Gigi
    Braegger, Christian P.
    Trindade, Eunice
    Wewer, Anne V.
    Hauer, Almuthe
    Levine, Arie
    Malignancy and Mortality in Pediatric Patients with Inflammatory Bowel Disease: A Multinational Study from the Porto Pediatric IBD Group2014Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 20, nr 2, s. 291-300Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: The combination of the severity of pediatric-onset inflammatory bowel disease (IBD) phenotypes and the need for intense medical treatment may increase the risk of malignancy and mortality, but evidence regarding the extent of the problem is scarce. Therefore, the Porto Pediatric IBD working group of ESPGHAN conducted a multinational-based survey of cancer and mortality in pediatric IBD. Methods: A survey among pediatric gastroenterologists of 20 European countries and Israel on cancer and/or mortality in the pediatric patient population with IBD was undertaken. One representative from each country repeatedly contacted all pediatric gastroenterologists from each country for reporting retrospectively cancer and/or mortality of pediatric patients with IBD after IBD onset, during 2006-2011. Results: We identified 18 cases of cancers and/or 31 deaths in 44 children (26 males) who were diagnosed with IBD (ulcerative colitis, n = 21) at a median age of 10.0 years (inter quartile range, 3.0-14.0). Causes of mortality were infectious (n = 14), cancer (n = 5), uncontrolled disease activity of IBD (n = 4), procedure-related (n = 3), other non-IBD related diseases (n = 3), and unknown (n = 2). The most common malignancies were hematopoietic tumors (n = 11), of which 3 were hepatosplenic T-cell lymphoma and 3 Ebstein-Barr virus-associated lymphomas. Conclusions: Cancer and mortality in pediatric IBD are rare, but cumulative rates are not insignificant. Mortality is primarily related to infections, particularly in patients with 2 or more immunosuppressive agents, followed by cancer and uncontrolled disease. At least 6 lymphomas were likely treatment-associated by virtue of their phenotype.

  • 12.
    Drobin, Kimi
    et al.
    Royal Inst Technol, KTH, Sch Biotechnol, Affin Prote, SciLifeLab, Stockholm, Sweden.
    Assadi, Ghazaleh
    Karolinska Inst, Dept Biosci & Nutr, Stockholm, Sweden.
    Hong, Mun-Gwan
    Royal Inst Technol, KTH, Sch Biotechnol, Affin Prote, SciLifeLab, Stockholm, Sweden.
    Andersson, Eni
    Royal Inst Technol, KTH, Sch Biotechnol, Affin Prote, SciLifeLab, Stockholm, Sweden.
    Fredolini, Claudia
    Royal Inst Technol, KTH, Sch Biotechnol, Affin Prote, SciLifeLab, Stockholm, Sweden.
    Forsström, Björn
    Royal Inst Technol, KTH, Sch Biotechnol, Affin Prote, SciLifeLab, Stockholm, Sweden.
    Reznichenko, Anna
    Karolinska Inst, Dept Biosci & Nutr, Stockholm, Sweden.
    Akhter, Tahmina
    Karolinska Inst, Dept Biosci & Nutr, Stockholm, Sweden.
    Ek, Weronica E
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Medicinsk genetik och genomik. Uppsala universitet, Science for Life Laboratory, SciLifeLab. Karolinska Inst, Dept Biosci & Nutr, Stockholm, Sweden.
    Bonfiglio, Ferdinando
    Karolinska Inst, Dept Biosci & Nutr, Stockholm, Sweden; Biodonostia Hlth Res Inst, Dept Gastrointestinal & Liver Dis, San Sebastian, Spain.
    Berner Hansen, Mark
    AstraZeneca R&D, Innovat & Global Med, Mölndal, Sweden; Univ Copenhagen, Bispebjerg Hosp, Ctr Digest Dis, Copenhagen, Denmark.
    Sandberg, Kristian
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Farmaceutiska fakulteten, Institutionen för läkemedelskemi. Uppsala universitet, Science for Life Laboratory, SciLifeLab. Karolinska Inst, Dept Physiol & Pharmacol, Stockholm, Sweden.
    Greco, Dario
    Univ Helsinki, Inst Biotechnol, Helsinki, Finland.
    Repsilber, Dirk
    Örebro Univ, Sch Med Sci, Örebro, Sweden.
    Schwenk, Jochen M.
    Royal Inst Technol, KTH, Sch Biotechnol, Affin Prote, SciLifeLab, Stockholm, Sweden.
    D’Amato, Mauro
    Karolinska Inst, Dept Biosci & Nutr, Stockholm, Sweden; BioDonostia Hlth Res Inst, San Sebastian, Spain; Ikerbasque, Basque Fdn Sci, Bilbao, Spain.
    Halfvarson, Jonas
    Örebro Univ, Fac Med & Hlth, Dept Gastroenterol, Örebro, Sweden.
    Targeted Analysis of Serum Proteins Encoded at Known Inflammatory Bowel Disease Risk Loci2019Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 25, nr 2, s. 306-316Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Few studies have investigated the blood proteome of inflammatory bowel disease (IBD). We characterized the serum abundance of proteins encoded at 163 known IBD risk loci and tested these proteins for their biomarker discovery potential.

    Methods: Based on the Human Protein Atlas (HPA) antibody availability, 218 proteins from genes mapping at 163 IBD risk loci were selected. Targeted serum protein profiles from 49 Crohn’s disease (CD) patients, 51 ulcerative colitis (UC) patients, and 50 sex- and age-matched healthy individuals were obtained using multiplexed antibody suspension bead array assays. Differences in relative serum abundance levels between disease groups and controls were examined. Replication was attempted for CD-UC comparisons (including disease subtypes) by including 64 additional patients (33 CD and 31 UC). Antibodies targeting a potentially novel risk protein were validated by paired antibodies, Western blot, immuno-capture mass spectrometry, and epitope mapping.

    Results: By univariate analysis, 13 proteins mostly related to neutrophil, T-cell, and B-cell activation and function were differentially expressed in IBD patients vs healthy controls, 3 in CD patients vs healthy controls and 2 in UC patients vs healthy controls (q < 0.01). Multivariate analyses further differentiated disease groups from healthy controls and CD subtypes from UC (P < 0.05). Extended characterization of an antibody targeting a novel, discriminative serum marker, the laccase (multicopper oxidoreductase) domain containing 1 (LACC1) protein, provided evidence for antibody on-target specificity.

    Conclusions: Using affinity proteomics, we identified a set of IBD-associated serum proteins encoded at IBD risk loci. These candidate proteins hold the potential to be exploited as diagnostic biomarkers of IBD.

  • 13.
    Drobin, Kimi
    et al.
    Affinity Proteomics, SciLifeLab, School of Biotechnology, KTH, Royal Institute of Technology, Stockholm, Sweden.
    Assadi, Ghazaleh
    Department of Biosciences and Nutrition, Karolinska Institutet, Stockholm, Sweden.
    Hong, Mun-Gwan
    Affinity Proteomics, SciLifeLab, School of Biotechnology, KTH, Royal Institute of Technology, Stockholm, Sweden.
    Andersson, Eni
    Affinity Proteomics, SciLifeLab, School of Biotechnology, KTH, Royal Institute of Technology, Stockholm, Sweden.
    Fredolini, Claudia
    Affinity Proteomics, SciLifeLab, School of Biotechnology, KTH, Royal Institute of Technology, Stockholm, Sweden.
    Forsström, Björn
    Affinity Proteomics, SciLifeLab, School of Biotechnology, KTH, Royal Institute of Technology, Stockholm, Sweden.
    Reznichenko, Anna
    Department of Biosciences and Nutrition, Karolinska Institutet, Stockholm, Sweden.
    Akhter, Tahmina
    Department of Biosciences and Nutrition, Karolinska Institutet, Stockholm, Sweden.
    Ek, Weronica E.
    Department of Biosciences and Nutrition, Karolinska Institutet, Stockholm, Sweden; Department of Immunology, Genetics and Pathology, Science for Life Laboratory, Uppsala University, Uppsala, Sweden.
    Bonfiglio, Ferdinando
    Department of Biosciences and Nutrition, Karolinska Institutet, Stockholm, Sweden; Department of Gastrointestinal and Liver Diseases, Biodonostia Health Research Institute, San Sebastián, Spain.
    Hansen, Mark Berner
    AstraZeneca R&D Mölndal, Innovative and Global Medicines, Mölndal, Sweden; Digestive Disease Center, Bispebjerg Hospital, University of Copenhagen, Copenhagen, Denmark.
    Sandberg, Kristian
    Science for Life Laboratory, Drug Discovery & Development Platform & Organic Pharmaceutical Chemistry, Department of Medicinal Chemistry, Uppsala Biomedical Center, Uppsala University, Uppsala, Sweden; Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Greco, Dario
    Institute of Biotechnology, University of Helsinki, Helsinki, Finland.
    Repsilber, Dirk
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Schwenk, Jochen M.
    Affinity Proteomics, SciLifeLab, School of Biotechnology, KTH, Royal Institute of Technology, Stockholm, Sweden.
    D'Amato, Mauro
    Department of Biosciences and Nutrition, Karolinska Institutet, Stockholm, Sweden; BioDonostia Health Research Institute, San Sebastian, Spain; IKERBASQUE, Basque Foundation for Science, Bilbao, Spain.
    Halfvarson, Jonas
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Gastroenterology.
    Targeted Analysis of Serum Proteins Encoded at Known Inflammatory Bowel Disease Risk Loci2019Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 25, nr 2, s. 306-316Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Few studies have investigated the blood proteome of inflammatory bowel disease (IBD). We characterized the serum abundance of proteins encoded at 163 known IBD risk loci and tested these proteins for their biomarker discovery potential.

    Methods: Based on the Human Protein Atlas (HPA) antibody availability, 218 proteins from genes mapping at 163 IBD risk loci were selected. Targeted serum protein profiles from 49 Crohn's disease (CD) patients, 51 ulcerative colitis (UC) patients, and 50 sex- and age-matched healthy individuals were obtained using multiplexed antibody suspension bead array assays. Differences in relative serum abundance levels between disease groups and controls were examined. Replication was attempted for CD-UC comparisons (including disease subtypes) by including 64 additional patients (33 CD and 31 UC). Antibodies targeting a potentially novel risk protein were validated by paired antibodies, Western blot, immuno-capture mass spectrometry, and epitope mapping.

    Results: By univariate analysis, 13 proteins mostly related to neutrophil, T-cell, and B-cell activation and function were differentially expressed in IBD patients vs healthy controls, 3 in CD patients vs healthy controls and 2 in UC patients vs healthy controls (q < 0.01). Multivariate analyses further differentiated disease groups from healthy controls and CD subtypes from UC (P < 0.05). Extended characterization of an antibody targeting a novel, discriminative serum marker, the laccase (multicopper oxidoreductase) domain containing 1 (LACC1) protein, provided evidence for antibody on-target specificity.

    Conclusions: Using affinity proteomics, we identified a set of IBD-associated serum proteins encoded at IBD risk loci. These candidate proteins hold the potential to be exploited as diagnostic biomarkers of IBD.

  • 14.
    Drobin, Kimi
    et al.
    KTH, Skolan för kemi, bioteknologi och hälsa (CBH), Proteinvetenskap, Affinity Proteomics. KTH, Centra, Science for Life Laboratory, SciLifeLab.
    Assadi, Ghazaleh
    Karolinska Inst, Dept Biosci & Nutr, Stockholm, Sweden..
    Hong, Mun-Gwan
    KTH, Skolan för kemi, bioteknologi och hälsa (CBH), Proteinvetenskap, Affinity Proteomics. KTH, Centra, Science for Life Laboratory, SciLifeLab.
    Anggraeni Andersson, Margaretha
    KTH, Skolan för kemi, bioteknologi och hälsa (CBH), Proteinvetenskap, Affinity Proteomics. KTH, Centra, Science for Life Laboratory, SciLifeLab.
    Fredolini, Claudia
    KTH, Skolan för kemi, bioteknologi och hälsa (CBH), Proteinvetenskap, Affinity Proteomics. KTH, Centra, Science for Life Laboratory, SciLifeLab. Royal Inst Technol, KTH, Sch Biotechnol, Affin Prote,SciLifeLab, Stockholm, Sweden..
    Forsström, Björn
    KTH, Skolan för kemi, bioteknologi och hälsa (CBH), Proteinvetenskap, Affinity Proteomics. KTH, Centra, Science for Life Laboratory, SciLifeLab.
    Reznichenko, Anna
    Karolinska Inst, Dept Biosci & Nutr, Stockholm, Sweden..
    Akhter, Tahmina
    Karolinska Inst, Dept Biosci & Nutr, Stockholm, Sweden..
    Ek, Weronica E.
    Karolinska Inst, Dept Biosci & Nutr, Stockholm, Sweden.;Uppsala Univ, Sci Life Lab, Dept Immunol Genet & Pathol, Uppsala, Sweden..
    Bonfiglio, Ferdinando
    Karolinska Inst, Dept Biosci & Nutr, Stockholm, Sweden.;Biodonostia Hlth Res Inst, Dept Gastrointestinal & Liver Dis, San Sebastian, Spain..
    Hansen, Mark Berner
    AstraZeneca R&D, Innovat & Global Med, Molndal, Sweden.;Univ Copenhagen, Bispebjerg Hosp, Ctr Digest Dis, Copenhagen, Denmark..
    Sandberg, Kristian
    Uppsala Univ, Sci Life Lab, Drug Discovery & Dev Platform, Uppsala, Sweden.;Uppsala Univ, Uppsala Biomed Ctr, Dept Med Chem, Organ Pharmaceut Chem, Uppsala, Sweden.;Karolinska Inst, Dept Physiol & Pharmacol, Stockholm, Sweden..
    Greco, Dario
    Univ Helsinki, Inst Biotechnol, Helsinki, Finland..
    Repsilber, Dirk
    Orebro Univ, Sch Med Sci, Orebro, Sweden..
    Schwenk, Jochen M.
    KTH, Skolan för kemi, bioteknologi och hälsa (CBH), Proteinvetenskap, Affinity Proteomics. KTH, Centra, Science for Life Laboratory, SciLifeLab.
    D'Amato, Mauro
    Karolinska Inst, Dept Biosci & Nutr, Stockholm, Sweden.;BioDonostia Hlth Res Inst, San Sebastian, Spain.;Ikerbasque, Basque Fdn Sci, Bilbao, Spain..
    Halfvarson, Jonas
    Orebro Univ, Fac Med & Hlth, Dept Gastroenterol, SE-70182 Orebro, Sweden..
    Targeted Analysis of Serum Proteins Encoded at Known Inflammatory Bowel Disease Risk Loci2019Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 25, nr 2, s. 306-316Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Few studies have investigated the blood proteome of inflammatory bowel disease (IBD). We characterized the serum abundance of proteins encoded at 163 known IBD risk loci and tested these proteins for their biomarker discovery potential. Based on the Human Protein Atlas (HPA) antibody availability, 218 proteins from genes mapping at 163 IBD risk loci were selected. Targeted serum protein profiles from 49 Crohns disease (CD) patients, 51 ulcerative colitis (UC) patients, and 50 sex- and age-matched healthy individuals were obtained using multiplexed antibody suspension bead array assays. Differences in relative serum abundance levels between disease groups and controls were examined. Replication was attempted for CD-UC comparisons (including disease subtypes) by including 64 additional patients (33 CD and 31 UC). Antibodies targeting a potentially novel risk protein were validated by paired antibodies, Western blot, immuno-capture mass spectrometry, and epitope mapping. By univariate analysis, 13 proteins mostly related to neutrophil, T-cell, and B-cell activation and function were differentially expressed in IBD patients vs healthy controls, 3 in CD patients vs healthy controls and 2 in UC patients vs healthy controls (q < 0.01). Multivariate analyses further differentiated disease groups from healthy controls and CD subtypes from UC (P < 0.05). Extended characterization of an antibody targeting a novel, discriminative serum marker, the laccase (multicopper oxidoreductase) domain containing 1 (LACC1) protein, provided evidence for antibody on-target specificity. Using affinity proteomics, we identified a set of IBD-associated serum proteins encoded at IBD risk loci. These candidate proteins hold the potential to be exploited as diagnostic biomarkers of IBD.

  • 15.
    Englund, Gunilla
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Farmaceutiska fakulteten, Institutionen för farmaci.
    Jacobson, Annica
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Rorsman, Fredrik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Artursson, Per
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Farmaceutiska fakulteten, Institutionen för farmaci.
    Kindmark, Andreas
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Rönnblom, Anders
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Efflux transporters in ulcerative colitis: decreased expression of BCRP (ABCG2) and Pgp (ABCB1)2007Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 13, nr 3, s. 291-297Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Efflux transport proteins are important components of the intestinal barrier against bacterial toxins, carcinogens, and drugs. This investigation was conducted to determine the expression of Breast Cancer Resistance Protein (BCRP/ABCG2), P-glycoprotein (Pgp/MDR1/ABCB1), and Multidrug Resistance Protein 2 (MRP2/ABCC2) in the gut mucosa of patients with ulcerative colitis (UC). Methods: Patients were thoroughly diagnosed according to well-established clinical, endoscopic, and histologic criteria to be included in the group of patients with active UC (n = 16) or UC in remission (n = 17). Colonic and rectal mucosa from patients with UC were compared with tissues from control subjects (n = 15). The mRNA expression (TaqMan) of the efflux transporters and the proinflammatory cytokines interleukin (IL)-1β and IL-6 was determined. Western blot was used in the analysis of protein expression and the tissue localization of BCRP was determined with confocal microscopy. Results: BCRP and Pgp expression was strongly reduced in individuals with active inflammation compared with controls and was negatively correlated with the levels of IL-6 mRNA. The BCRP staining of colonic epithelium seen in healthy mucosa was diminished in inflamed tissues, with concurrent disruption of epithelial F-actin structure. Conclusions: Two of the efflux transporters of importance for the barrier function of the gut mucosa, Pgp and BCRP, are expressed at strongly reduced levels during active inflammation in patients with UC. Investigations are warranted to determine whether the low levels of efflux transporters during active UC contribute to altered transport and tissue exposure of carcinogens, bacterial toxins, and drugs.

  • 16.
    Escudero-Hernández, Celia
    et al.
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för molekylär medicin och virologi. Linköpings universitet, Medicinska fakulteten. Univ Valladolid, Spain.
    Montalvillo, Enrique
    Univ Valladolid, Spain.
    Antolin, Beatriz
    Hosp Clin Univ Valladolid, Spain.
    Bernardo, David
    Univ Valladolid, Spain.
    Antonio Garrote, Jose
    Univ Valladolid, Spain; Hosp Univ Rio Hortega, Spain.
    Arranz, Eduardo
    Univ Valladolid, Spain.
    Fernandez-Salazar, Luis
    Hosp Clin Univ Valladolid, Spain.
    Different Intraepithelial CD3(+) Cell Numbers in Crohns Disease and Ulcerative Colitis2020Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 26, nr 3, s. E14-E15Artikel i tidskrift (Övrigt vetenskapligt)
    Abstract [en]

    Intraepithelial immune response can be studied by flow cytometry. The proportion of CD3(+) cells differs between Crohns disease and ulcerative colitis.

  • 17.
    Everhov, Asa H.
    et al.
    Karolinska Inst, Sweden.
    Khalili, Hamed
    Karolinska Inst, Sweden; Harvard Med Sch, MA 02115 USA.
    Askling, Johan
    Karolinska Inst, Sweden.
    Myrelid, Pär
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för Kirurgi, Ortopedi och Onkologi. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Centrum för kirurgi, ortopedi och cancervård, Kirurgiska kliniken US.
    Ludvigsson, Jonas F.
    Karolinska Inst, Sweden; Orebro Univ Hosp, Sweden.
    Halfvarson, Jonas
    Orebro Univ, Sweden.
    Nordenvall, Caroline
    Karolinska Inst, Sweden; Karolinska Univ Hosp, Sweden.
    Neovius, Martin
    Karolinska Inst, Sweden.
    Soderling, Jonas
    Karolinska Inst, Sweden.
    Olen, Ola
    Karolinska Inst, Sweden; Sachs Children and Youth Hosp, Sweden.
    Work Loss Before and After Diagnosis of Crohns Disease2019Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 25, nr 7, s. 1237-1247Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background The aim of this study was to examine work loss in patients with Crohns disease. Methods Using nationwide registers, we identified incident patients with Crohns disease (2007-2010) and population comparator subjects without inflammatory bowel disease, matched by age, sex, calendar year, health care region, and education level. We assessed the number of lost workdays due to sick leave and disability pension from 5 years before to 5 years after first diagnosis of Crohns disease or end of follow-up (September 30, 2015). Results Among the 2015 incident Crohns disease patients (median age, 35 years; 50% women), both the proportion with work loss and the mean annual number of lost workdays were larger 5 years before diagnosis (25%; mean, 45 days) than in the 10,067 comparators (17%; mean, 29 days). Increased work loss was seen during the year of diagnosis, after which it declined to levels similar to before diagnosis. Of all patients, 75% had no work loss 24-12 months before diagnosis. Of them, 84% had full work ability also 12-24 months after diagnosis. In patients with total work loss (8.3% of all) before diagnosis, 83% did not work after. Among those with full work ability before diagnosis, the absolute risk of having total work loss after diagnosis was 1.4% (0.43% in the comparators). Our results were consistent across several sensitivity analyses using alternative definitions for date of diagnosis. Conclusions Patients with Crohns disease had increased work loss several years before diagnosis, possibly explained by comorbidity or by diagnostic delay.

  • 18.
    Everhov, Åsa H.
    et al.
    Department of Clinical Science and Education, Södersjukhuset, Karolinska Institutet, Stockholm, Sweden; Clinical Epidemiology Division, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Khalili, Hamed
    Clinical Epidemiology Division, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden; Gastroenterology Unit, Massachusetts General Hospital, Harvard Medical School, Boston, Masschusetts, USA.
    Askling, Johan
    Clinical Epidemiology Division, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    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, Linköping, Sweden.
    Ludvigsson, Jonas F.
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro University, Örebro, Sweden.
    Halfvarson, Jonas
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Gastroenterology.
    Nordenvall, Caroline
    Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden; Center for Digestive Disease, Division of Coloproctology, Karolinska University Hospital, Stockholm, Sweden.
    Neovius, Martin
    Clinical Epidemiology Division, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Söderling, Jonas
    Clinical Epidemiology Division, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Olén, Ola
    Department of Clinical Science and Education, Södersjukhuset, Karolinska Institutet, Stockholm, Sweden; Clinical Epidemiology Division, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden; Department of Pediatric Gastroenterology and Nutrition, Sachs' Children and Youth Hospital, Stockholm, Sweden.
    Work Loss Before and After Diagnosis of Crohn's Disease2019Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 25, nr 7, s. 1237-1247Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: The aim of this study was to examine work loss in patients with Crohn's disease.

    Methods: Using nationwide registers, we identified incident patients with Crohn's disease (2007-2010) and population comparator subjects without inflammatory bowel disease, matched by age, sex, calendar year, health care region, and education level. We assessed the number of lost workdays due to sick leave and disability pension from 5 years before to 5 years after first diagnosis of Crohn's disease or end of follow-up (September 30, 2015).

    Results: Among the 2015 incident Crohn's disease patients (median age, 35 years; 50% women), both the proportion with work loss and the mean annual number of lost workdays were larger 5 years before diagnosis (25%; mean, 45 days) than in the 10,067 comparators (17%; mean, 29 days). Increased work loss was seen during the year of diagnosis, after which it declined to levels similar to before diagnosis. Of all patients, 75% had no work loss 24-12 months before diagnosis. Of them, 84% had full work ability also 12-24 months after diagnosis. In patients with total work loss (8.3% of all) before diagnosis, 83% did not work after. Among those with full work ability before diagnosis, the absolute risk of having total work loss after diagnosis was 1.4% (0.43% in the comparators). Our results were consistent across several sensitivity analyses using alternative definitions for date of diagnosis.

    Conclusions: Patients with Crohn's disease had increased work loss several years before diagnosis, possibly explained by comorbidity or by diagnostic delay.

  • 19.
    Fritsch Fredin, Maria
    et al.
    Astra-Zeneca, Mölndal.
    Hultin, Leif
    Astra-Zeneca, Mölndal.
    Hyberg, Gina
    Astra-Zeneca, Mölndal.
    Rehnström, Erika
    Astra-Zeneca, Mölndal.
    Hultgren Hörnquist, Elisabeth
    Örebro universitet, Hälsoakademin.
    Melgar, Silvia
    Astra-Zeneca, Mölndal.
    Jansson, Liselotte
    Astra-Zeneca, Mölndal.
    Predicting and monitoring colitis development in mice by micro-computed tomography2008Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 14, nr 4, s. 491-499Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Computed tomography (CT) has been developed as a tool for monitoring human inflammatory bowel disease (IBD). The aim of this study was to evaluate colon wall thickness as a noninvasive marker in the dextran sodium sulfate (DSS) mouse model of colitis using micro-CT. METHODS: Mice were examined by micro-CT 1, 2, or 4 times between day 0 (d0) and d26 after induction of colitis to document the kinetics of changes in colon wall thickness and its relation to colitis development. RESULTS: DSS-treated mice displayed a significantly thicker colon wall at all timepoints (days 5, 8, 12, 19, and 26) investigated compared to healthy controls. Colon wall thickness showed a good correlation to the macroscopic grading of colitis (r = 0.81). The increase in colon wall thickness occurred mainly during the acute phase of colitis (between days 5 and 12) and did not progress much further in the chronic phase of colitis (d26). Colon wall thickness at d26 was thereby predicted by measurements at d12. All mice did not respond equally to DSS and this difference was manifest during the first 2 weeks of colitis, providing an important tool in stratifying responders from nonresponders. CONCLUSIONS: While the potential impact of handling and anesthesia should be considered on repeated micro-CT, irradiation exposure during repeated micro-CT did not affect the development of colitis. Thus, the results suggest that micro-CT can be used for monitoring and prediction of the inflammatory response in mouse colitis in future therapeutic studies.

  • 20.
    Ganda Mall, John-Peter
    et al.
    School of Medical Sciences, Nutrition-Gut-Brain Interactions Research Centre, Örebro University, Örebro, Sweden.
    Casado-Bedmar, Maite
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för Kirurgi, Ortopedi och Onkologi. Linköpings universitet, Medicinska fakulteten.
    Winberg, Martin E.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för Kirurgi, Ortopedi och Onkologi. Linköpings universitet, Medicinska fakulteten.
    Brummer, Robert J.
    School of Medical Sciences, Nutrition-Gut-Brain Interactions Research Centre, Örebro University, Örebro, Sweden.
    Schoultz, Ida
    School of Medical Sciences, Nutrition-Gut-Brain Interactions Research Centre, Örebro University, Örebro, Sweden.
    Keita, Åsa
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för Kirurgi, Ortopedi och Onkologi. Linköpings universitet, Medicinska fakulteten. School of Medical Sciences, Nutrition-Gut-Brain Interactions Research Centre, Örebro University, Örebro, Sweden.
    A ß-Glucan-Based Dietary Fiber Reduces Mast Cell-Induced Hyperpermeability in Ileum From Patients With Crohns Disease and Control Subjects2018Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 24, nr 1, s. 166-178Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Administration of ß-glucan has shown immune-enhancing effects. Our aim was to investigate whether ß-glucan could attenuate mast cell (MC)-induced hyperpermeability in follicle-associated epithelium (FAE) and villus epithelium (VE) of patients with Crohns disease (CD) and in noninflammatory bowel disease (IBD)-controls. Further, we studied mechanisms of ß-glucan uptake and effects on MCs in vitro.

  • 21.
    Ganda Mall, John-Peter
    et al.
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Casado-Bedmar, Maite
    Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
    Winberg, Martin E.
    Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
    Brummer, Robert Jan
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Schoultz, Ida
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Keita, Åsa V.
    A β-Glucan-Based Dietary Fiber Reduces Mast Cell-Induced Hyperpermeability in Ileum From Patients With Crohn's Disease and Control Subjects2017Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 24, nr 1, s. 166-178Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Administration of β-glucan has shown immune-enhancing effects. Our aim was to investigate whether β-glucan could attenuate mast cell (MC)-induced hyperpermeability in follicle-associated epithelium (FAE) and villus epithelium (VE) of patients with Crohn's disease (CD) and in noninflammatory bowel disease (IBD)-controls. Further, we studied mechanisms of β-glucan uptake and effects on MCs in vitro.

    Methods: Segments of FAE and VE from 8 CD patients and 9 controls were mounted in Ussing chambers. Effects of the MC-degranulator compound 48/80 (C48/80) and yeast-derived β-1,3/1,6 glucan on hyperpermeability were investigated. Translocation of β-glucan and colocalization with immune cells were studied by immunofluorescence. Caco-2-cl1- and FAE-cultures were used to investigate β-glucan-uptake using endocytosis inhibitors and HMC-1.1 to study effects on MCs.

    Results: β-glucan significantly attenuated MC-induced paracellular hyperpermeability in CD and controls. Transcellular hyperpermeability was only significantly attenuated in VE. Baseline paracellular permeability was higher in FAE than VE in both groups, P<0.05, and exhibited a more pronounced effect by C48/80 and β-glucan P<0.05. No difference was observed between CD and controls. In vitro studies showed increased passage, P<0.05, of β-glucan through FAE-culture compared to Caco-2-cl1. Passage was mildly attenuated by the inhibitor methyl-β-cyclodextrin. HMC-1.1 experiments showed a trend to decreasing MC-degranulation and levels of TNF-α but not IL-6 by β-glucan. Immunofluorescence revealed more β-glucan-uptake and higher percentage of macrophages and dendritic cells close to β-glucan in VE of CD compared to controls.

    Conclusions: We demonstrated beneficial effects of β-glucan on intestinal barrier function and increased β-glucan-passage through FAE model. Our results provide important and novel knowledge on possible applications of β-glucan in health disorders and diseases characterized by intestinal barrier dysfunction.

  • 22. Gasche, C
    et al.
    Berstad, A
    Befrits, R
    Beglinger, C
    Dignass, A
    Erichsen, K
    Gomollon, F
    Hjortswang, Henrik
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Gastroenterologi och hepatologi. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Koutroubakis, I
    Kulnigg, S
    Oldenburg, B
    Rampton, D
    Schroeder, O
    Stein, J
    Travis, S
    Van Assche, G
    Guidelines on the diagnosis and management of iron deficiency and anemia in inflammatory bowel diseases2007Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 13, nr 12, s. 1545-1553Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Anemia is a common complication of inflammatory bowel diseases. An international working party has formed and developed guidelines for evaluation and treatment of anemia and iron deficiency that should serve practicing gastroenterologists. Within a total of 16 statements, recommendations are made regarding diagnostic measures to screen for iron- and other anemia-related deficiencies regarding the triggers for medical intervention, treatment goals, and appropriate therapies. Anemia is a common cause of hospitalization, prevents physicians from discharging hospitalized patients, and is one of me most frequent comorbid conditions in patients with inflammatory bowel disease. It therefore needs appropriate attention and specific care. Copyright © 2007 Crohn's & Colitis Foundation of America, Inc.

  • 23.
    Gunaltay, Sezin
    et al.
    Örebro universitet, Institutionen för medicinska vetenskaper. Nutrition-Gut-Brain Interactions Research Centre, Örebro University, Örebro, Sweden.
    Repsilber, Dirk
    Örebro universitet, Institutionen för medicinska vetenskaper. Nutrition-Gut-Brain Interactions Research Centre, Örebro University, Örebro, Sweden.
    Helenius, Gisela
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län. Department of Pathology, Örebro University Hospital, Örebro, Sweden.
    Nyhlin, Nils
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län. Department of Medicine, Div. of Gastroenterol., Örebro University Hospital, Örebro, Sweden.
    Bohr, Johan
    Department of Medicine, Div of Gastroenterol, Örebro Univ Hosp, Örebro, Sweden; Fac of Med and Hlth, Örebro Univ, Örebro, Sweden.
    Hultgren, Olof
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Microbiology and Immunology, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Hultgren Hörnquist, Elisabeth
    Örebro universitet, Institutionen för medicinska vetenskaper. Nutrition-Gut-Brain Interactions Research Centre, Örebro University, Örebro, Sweden.
    Oligoclonal T-cell Receptor Repertoire in Colonic Biopsies of Patients with Microscopic Colitis and Ulcerative Colitis2017Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 23, nr 6, s. 932-945Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Microscopic colitis (MC), comprising collagenous colitis (CC) and lymphocytic colitis (LC), is a type of variation of inflammatory bowel diseases. Local T-cell infiltration in the mucosa plays a major role in MC immunopathology.

    Methods: To understand diversity and clonality of infiltrating T cells, we analyzed the T-cell receptor beta (TCR beta) chains in colonic biopsies of MC, ulcerative colitis (UC), and their remission counterparts (CC/LC-HR [histological remission] or UC-R [remission]) compared with patients with non-inflamed colons using next-generation sequencing.

    Results: Compared with controls and patients with CC, patients with LC had significantly lower diversity with significantly lower evenness and richness in TCRVb-Jb gene segments. Similarly, patients with LC-HR had lower diversity because of significantly lower TCRVb-Jb clone richness. Patients with UC and UC-R showed significantly higher diversity and richness. Univariate and multivariate analyses were performed to identify TCRVb-Jb gene segments differentiating disease types from controls or their remission counterparts. Patients with LC were discriminated from controls by 12 clones and from patients with CC by 8 clones. Neither univariate nor multivariate analyses showed significance for patients with CC or CC-HR compared with controls. Patients with UC and UC-R had 16 and 14 discriminating clones, respectively, compared with controls.

    Conclusions: Altogether, patients with MC and UC showed an oligoclonal TCRb distribution. TCRVb-Jb clone types and their diversity were distinctive between patients with CC and LC, as well as for patients with UC, suggesting different pathophysiological mechanisms according to disease type and stage. This study suggests that CC and LC are different entities because of differences in immunoregulatory responses, as mirrored by their T-cell repertoire.

  • 24.
    Halfvarson, Jonas
    Örebro universitet, Hälsoakademin. Department of Internal Medicine, Division of Gastroenterology.
    Genetics in twins with Crohn's disease: less pronounced than previously believed?2011Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 17, nr 1, s. 6-12Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: The influence of genetics in inflammatory bowel disease is emphasized by twin concordance. Previous studies have methodological limitations. The aims were to establish reliable concordance rates and compare phenotypic characteristics in concordant and discordant monozygotic pairs, anticipating the former reflects a genetically determined subgroup.

    METHODS: By re-running the Swedish twin registry with the Swedish hospital discharge register, observation time was extended. Diagnoses and phenotype were based on medical notes. Pairs with unknown zygosity and where both twins were not alive or not responding to the questionnaire were excluded. In all, 149 new twin pairs of the same sex, born 1909-1980 were identified.

    RESULTS: Of new pairs, 4/29 monozygotic, 0/38 dizygotic, and 0/1 twin pairs with unknown zygosity were concordant for Crohn's disease (CD). In ulcerative colitis (UC), 4/31 monozygotic, 4/48 dizygotic, and 0/1 twin pairs with unknown zygosity were concordant. New pairs were added to the original cohort. Restricting analyses to pairs born 1886-1958, the time period used in the original cohort, 9/33 monozygotic and 1/50 dizygotic pairs were concordant for CD (P = 0.008), 6/41 and 3/49, correspondingly, for UC (P = 0.29). There was a trend for concordant twins to have less colonic CD than discordant twins, 15% versus 35% (P = 0.09) in twins born 1886-1980.

    CONCLUSIONS: Previous twin studies have overestimated the influence of genetics in CD. A trend for phenotypic difference between concordant and discordant pairs was observed, suggesting that the clinical entity represents diseases with different pathophysiological backgrounds.

  • 25.
    Halfvarson, Jonas
    et al.
    Örebro University Hospital.
    Jess, T
    University of Copenhagen.
    Bodin, L
    Örebro University Hospital.
    Järnerot, Gunnar
    Örebro University Hospital.
    Munkholm, P
    University of Copenhagen.
    Binder, V
    University of Copenhagen.
    Tysk, Curt
    Örebro University Hospital.
    Longitudinal concordance for clinical characteristics in a Swedish-Danish twin population with inflammatory bowel disease.2007Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 13, nr 12, s. 1536-1544Artikel i tidskrift (Refereegranskat)
    Abstract [en]

      Background: The genetic influence on disease course in inflammatory bowel disease (IBD) remains unknown. We therefore aimed to study longitudinal concordance for clinical characteristics and longitudinal stability using the Montreal Classification in an IBD twin population.Methods: A total of 158 twins with ulcerative colitis (UC) (18 belonging to 9 concordant monozygotic pairs) and 141 twins with Crohn's disease (CD) (34 belonging to 17 concordant monozygotic pairs) were enrolled. Medical notes were scrutinized for clinical characteristics at diagnosis and after 10 years. Using the binominal distribution, we tested the hypothesis that clinical characteristics were independent within individuals in disease concordant monozygotic pairs.Results: In CD, location was identical in 11/17 monozygotic concordant pairs at diagnosis (P = 0.008) and in 11/16 pairs after 10 years (P = 0.02). Behavior at diagnosis was identical in 13/17 pairs (P = 0.03) and in 11/16 pairs after 10 years (P = 0.01). Monozygotic UC twins were concordant (within 5 years) for age at diagnosis (6/9 pairs; P < 0.001) and symptomatic onset (4/9 pairs; P = 0.02) but not for extent of disease at diagnosis or after 10 years. The Montreal Classification did not demonstrate longitudinal stability, either regarding location or behavior of CD or extent of UC.Conclusions: The high phenotypic concordance, both at diagnosis and longitudinally, in monozygotic twins with CD supports a genetic influence not only on disease occurrence but also on disease course. This contrasts with UC, where the genetic impact appears less. Montreal Classification characteristics changed over time and should be used cautiously.

  • 26.
    Halfvarson, Jonas
    et al.
    Örebro universitet, Institutionen för läkarutbildning.
    Jess, Tine
    Bodin, Lennart
    Örebro universitet, Handelshögskolan vid Örebro Universitet.
    Järnerot, Gunnar
    Munkholm, Pia
    Binder, Vibeke
    Tysk, Curt
    Örebro universitet, Hälsoakademin.
    Longitudinal concordance for clinical characteristics in a Swedish-Danish twin population with inflammatory bowel disease2007Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 13, nr 12, s. 1536-1544Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: The genetic influence on disease course in inflammatory bowel disease (IBD) remains unknown. We therefore aimed to study longitudinal concordance for clinical characteristics and longitudinal stability using the Montreal Classification in an IBD twin population. METHODS: A total of 158 twins with ulcerative colitis (UC) (18 belonging to 9 concordant monozygotic pairs) and 141 twins with Crohn's disease (CD) (34 belonging to 17 concordant monozygotic pairs) were enrolled. Medical notes were scrutinized for clinical characteristics at diagnosis and after 10 years. Using the binominal distribution, we tested the hypothesis that clinical characteristics were independent within individuals in disease concordant monozygotic pairs. RESULTS: In CD, location was identical in 11/17 monozygotic concordant pairs at diagnosis (P = 0.008) and in 11/16 pairs after 10 years (P = 0.02). Behavior at diagnosis was identical in 13/17 pairs (P = 0.03) and in 11/16 pairs after 10 years (P = 0.01). Monozygotic UC twins were concordant (within 5 years) for age at diagnosis (6/9 pairs; P < 0.001) and symptomatic onset (4/9 pairs; P = 0.02) but not for extent of disease at diagnosis or after 10 years. The Montreal Classification did not demonstrate longitudinal stability, either regarding location or behavior of CD or extent of UC. CONCLUSIONS: The high phenotypic concordance, both at diagnosis and longitudinally, in monozygotic twins with CD supports a genetic influence not only on disease occurrence but also on disease course. This contrasts with UC, where the genetic impact appears less. Montreal Classification characteristics changed over time and should be used cautiously.

  • 27. Halfvarson, Jonas
    et al.
    Jess, Tine
    Magnuson, Anders
    Montgomery, Scott M.
    Örebro universitet, Institutionen för klinisk medicin.
    Orholm, Marianne
    Tysk, Curt
    Örebro universitet, Institutionen för klinisk medicin.
    Binder, Vibeke
    Järnerot, Gunnar
    Environmental factors in inflammatory bowel disease: a co-twin control study of a Swedish-Danish twin population2006Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 12, nr 10, s. 925-933Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND:

    Genetics and environmental factors are implicated in the etiology of inflammatory bowel disease (IBD). We studied environmental factors in a population-based Swedish-Danish twin cohort using the co-twin control method.

    SUBJECTS AND METHODS:

    A questionnaire was sent to 317 twin pairs regarding markers of exposures in the following areas: infections/colonization and diet as well as smoking, appendectomy, and oral contraceptives. Odds ratios (OR) were calculated by conditional logistic regression. When confounding appeared plausible, multivariate conditional logistic regression was added. The questions were also divided into topic groups, and adjustment was made for multiple testing within each of the groups.

    RESULTS:

    The response rate to the questionnaire was 83%. In consideration of the study design, only discordant pairs were included (Crohn's disease [CD], n = 102; ulcerative colitis [UC], n = 125). Recurrent gastrointestinal infections were associated with both UC (OR, 8.0; 95% confidence interval [CI], 1.0-64) and CD (OR, 5.5; 95% CI, 1.2-25). Hospitalization for gastrointestinal infections was associated with CD (OR, 12; 95% CI, 1.6-92). Smoking was inversely associated with UC (OR, 0.4; 95% CI, 0.2-0.9) and associated with CD (OR, 2.9; 95% CI, 1.2-7.1).

    CONCLUSIONS:

    The observed associations indicate that markers of possible infectious events may influence the risk of IBD. Some of these effects might be mediated by long-term changes in gut flora or alterations in reactivity to the flora. The influence of smoking in IBD was confirmed.

  • 28.
    Halfvarson, Jonas
    et al.
    Division of Gastroenterology, Department of Internal Medicine, Örebro University Hospital, Örebro, Sweden.
    Jess, Tine
    Department of Medical Gastroenterology C, Herlev Hospital, University of Copenhagen, Copenhagen, Denmark.
    Magnusson, Andreas
    Statistical and Epidemiological Unit, Clinical Research Centre, Örebro University Hospital, Örebro, Sweden.
    Montgomery, Scott M.
    Statistical and Epidemiological Unit, Clinical Research Centre, Örebro University Hospital, Örebro, Sweden.
    Orholm, Marianne
    Department of Internal Medicine, Elsinore Hospital, Elsinore, Denmark.
    Tysk, Curt
    Division of Gastroenterology, Department of Internal Medicine, Örebro University Hospital, Örebro, Sweden and Department of Clinical Medicine, Örebro University, Örebro, Sweden.
    Binder, Vibeke
    Department of Medical Gastroenterology C, Herlev Hospital, University of Copenhagen, Copenhagen, Denmark.
    Järnerot, Gunnar
    Division of Gastroenterology, Department of Internal Medicine, Örebro University Hospital, Örebro, Sweden.
    Environmental factors in inflammatory bowel disease: a co-twin control study of a Swedish-Danish twin population2006Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 12, nr 10, s. 925-933Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Genetics and environmental factors are implicated in the etiology of inflammatory bowel disease (IBD). We studied environmental factors in a population-based Swedish-Danish twin cohort using the co-twin control method.

    Subjects and Methods: A questionnaire was sent to 317 twin pairs regarding markers of exposures in the following areas: infections/colonization and diet as well as smoking, appendectomy, and oral contraceptives. Odds ratios (OR) were calculated by conditional logistic regression. When confounding appeared plausible, multivariate conditional logistic regression was added. The questions were also divided into topic groups, and adjustment was made for multiple testing within each of the groups.

    Results: The response rate to the questionnaire was 83%. In consideration of the study design, only discordant pairs were included (Crohn's disease [CD], n = 102; ulcerative colitis [UC], n > = 125). Recurrent gastrointestinal infections were associated with both UC (OR, 8.0; 95% confidence interval [CI], 1.0–64) and CD (OR, 5.5; 95% CI, 1.2–25). Hospitalization for gastrointestinal infections was associated with CD (OR, 12; 95% CI, 1.6–92). Smoking was inversely associated with UC (OR, 0.4; 95% CI, 0.2–0.9) and associated with CD (OR, 2.9; 95% CI, 1.2–7.1).

    Conclusions: The observed associations indicate that markers of possible infectious events may influence the risk of IBD. Some of these effects might be mediated by long-term changes in gut flora or alterations in reactivity to the flora. The influence of smoking in IBD was confirmed.

  • 29.
    Halfvarson, Jonas
    et al.
    Division of Gastroenterology, Department of Internal Medicine, Örebro University Hospital, Sweden.
    Järnerot, Gunnar
    Division of Gastroenterology, Department of Internal Medicine, Örebro University Hospital, Sweden.
    Treatment of choice for acute severe steroid-refractory ulcerative colitis is remicade2009Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 15, nr 1, s. 143-145Artikel i tidskrift (Refereegranskat)
  • 30.
    Hallert, Claes
    et al.
    Linköpings universitet, Institutionen för vård och välfärd. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Närsjukvården i östra Östergötland, Medicinkliniken ViN.
    Björck, Inger
    Department of Applied Nutrition and Food Chemistry, Chemical Center, Lund University, Lund, Sweden.
    Nyman, Margareta
    Department of Applied Nutrition and Food Chemistry, Chemical Center, Lund University, Lund, Sweden.
    Pousette, Anneli
    Östergötlands Läns Landsting, Närsjukvården i östra Östergötland, Medicinkliniken ViN.
    Grännö, Christer
    Departments of Internal Medicine, Ryhov Hospital, Jönköping.
    Svensson, Hans
    Östergötlands Läns Landsting, Närsjukvården i östra Östergötland, Medicinkliniken ViN.
    Increasing Fecal Butyrate in Ulcerative Colitis Patients by Diet: Controlled Pilot Study2003Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 9, nr 2, s. 116-121Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Topical butyrate has been shown to be effective in the treatment of ulcerative colitis (UC). Butyrate is derived from colonic fermentation of dietary fiber, and our aim was to study whether UC patients could safely increase the fecal butyrate level by dietary means. We enrolled 22 patients with quiescent UC (mean age, 44 years; 45% women; median time from last relapse, 1 year) in a controlled pilot trial lasting 3 months. The patients were instructed to add 60 g oat bran (corresponding to 20 g dietary fiber) to the daily diet, mainly as bread slices. Fecal short-chain fatty acids (SCFAs) including butyrate, disease activity, and gastrointestinal symptoms were recorded every 4 weeks. During the oat bran intervention the fecal butyrate concentration increased by 36% at 4 weeks (from 11 +/- 2 (mean +/- SEM) to 15 +/- 2 mumol/g feces) (p < 0.01). The mean butyrate concentration over the entire test period was 14 +/-1 &mu;mol/g feces (p < 0.05). Remaining fecal SCFA levels were unchanged. No patient showed signs of colitis relapse. Unlike controls, the patients showed no increase in gastrointestinal complaints during the trial. Yet patients reporting abdominal pain and reflux complaints at entry showed significant improvement at 12 weeks that returned to baseline 3 months later. This pilot study shows that patients with quiescent UC can safely take a diet rich in oat bran specifically to increase the fecal butyrate level. This may have clinical implications and warrants studies of the long-term benefits of using oat bran in the maintenance therapy in UC.

  • 31. Hjortswang, Henrik
    et al.
    Tysk, Curt
    Örebro universitet, Hälsoakademin.
    Bohr, Johan
    Benoni, Cecilia
    Kilander, Anders
    Larsson, Lasse
    Vigren, Lina
    Ström, Magnus
    Defining clinical criteria for clinical remission and disease activity in collagenous colitis2009Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 15, nr 12, s. 1875-1881Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Collagenous colitis is a chronic inflammatory bowel disease accompanied mainly by nonbloody diarrhea. The objectives of treatment are to alleviate the symptoms and minimize the deleterious effects on health-related quality of life (HRQOL). There is still no generally accepted clinical definition of remission or relapse. The purpose of this study was to analyze the impact of bowel symptoms on HRQOL and accordingly suggest criteria for remission and disease activity based on impact of patient symptoms on HRQOL.

    METHODS: The design was a cross-sectional postal survey of 116 patients with collagenous colitis. The main outcome measures were 4 HRQOL questionnaires: the Short Health Scale, the Inflammatory Bowel Disease Questionnaire, the Rating Form of IBD Patient Concerns, and the Psychological General Well-Being Index, and a 1-week symptom diary recording number of stools/day and number of watery stools/day.

    RESULTS: Severity of bowel symptoms had a deleterious impact on patients' HRQOL. Patients with a mean of >/=3 stools/day or a mean of >/=1 watery stool/day had a significantly impaired HRQOL compared to those with <3 stools/day and <1 watery stool/day.

    CONCLUSIONS: We propose that clinical remission in collagenous colitis is defined as a mean of <3 stools/day and a mean of <1 watery stool per day and disease activity to be a daily mean of >/=3 stools or a mean of >/=1 watery stool.

  • 32.
    Hjortswang, Henrik
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Gastroenterologi och hepatologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Tysk, Curt
    Orebro Univ Hosp, Dept Med, Div Gastroenterol, Orebro, Sweden.
    Bohr, Johan
    Orebro Univ Hosp, Dept Med, Div Gastroenterol, Orebro, Sweden.
    Benoni, Cecilia
    MAS Univ Hosp, Dept Med, Div Gastroenterol, Malmo, Sweden.
    Kilander, Anders
    Sahlgrenska Univ Hospital, Div Gastroenterol, Dept Med, Gothenburg, Sweden.
    Larsson, Lasse
    Sahlgrenska Univ Hospital, Div Gastroenterol, Dept Med, Gothenburg, Sweden.
    Vigren, Lira
    MAS Univ Hosp, Dept Med, Div Gastroenterol, Malmo, Sweden.
    Ström, Magnus
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Gastroenterologi och hepatologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärt- och Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Defining Clinical Criteria for Clinical Remission and Disease Activity in Collagenous Colitis2009Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 15, nr 12, s. 1875-1881Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Collagenous colitis is a chronic inflammatory bowel disease accompanied mainly by nonbloody diarrhea. The objectives of treatment are to alleviate the symptoms and minimize the deleterious effects on health-related quality of life (HRQOL). There is still no generally accepted clinical definition of remission or relapse. The purpose of this study was to analyze the impact of bowel symptoms on HRQOL and accordingly suggest criteria for remission and disease activity based on impact of patient symptoms on HRQOL. Methods: The design was a cross-sectional postal survey of 116 patients with collagenous colitis. The main outcome measures were 4 HRQOL questionnaires: the Short Health Scale, the Inflammatory Bowel Disease Questionnaire, the Rating Form of IBD Patient Concerns, and the Psychological General Well-Being Index, and a 1-week symptom diary recording number of stools/day and number of watery stools/day. Results: Severity of bowel symptoms had a deleterious impact on patients HRQOL. Patients with a mean of greater than= 3 stools/day or a mean of greater than= 1 watery stool/day had a significantly impaired HRQOL compared to those with less than3 stools/day and less than 1 watery stool/day. Conclusions: We propose that clinical remission in collagenous colitis is defined as a mean of less than3 stools/day and a mean of less than 1 watery stool per clay and disease activity to be a daily mean of greater than= 3 stools or a mean of greater than= 1 watery stool.

  • 33.
    Jansson, A.
    et al.
    School of Life Sciences, Systems Biology Research Centre, University of Skövde, Skövde, Sweden.
    Pernestig, A.-K.
    School of Life Sciences, Systems Biology Research Centre, University of Skövde, Skövde, Sweden.
    Nilsson, P.
    School of Life Sciences, Systems Biology Research Centre, University of Skövde, Skövde, Sweden.
    Jirstrand, M.
    Fraunhofer-Chalmers Research Centre for Industrial Mathematics, Gothenburg, Sweden.
    Hultgren Hörnquist, Elisabeth
    Örebro universitet, Institutionen för läkarutbildning. Department of Biomedicine.
    Toward quantifying the thymic dysfunction state in mouse models of inflammatory bowel disease2013Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 19, nr 4, s. 881-888Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    Inflammatory bowel disease is characterized by a number of immunological alterations, not the least in the T-cell compartment. Numerous animal models of colitis have revealed aberrant thymocyte dynamics associated with skewed thymocyte development. The recent advancements in quantitative methods have proposed critical kinetic alterations in the thymocyte development during the progression of colitis. This review focuses on the aberrant thymocyte dynamics in Gαi2-deficient mice as this mouse model provides most quantitative data of the thymocyte development associated with colitis. Herein, we discuss several dynamic changes during the progression of colitis and propose a hypothesis for the underlying causes for the skewed proportions of the thymocyte populations seen in the Gαi2-deficient mice and in other mouse models of colitis.

  • 34.
    Jansson, Andreas
    et al.
    Högskolan i Skövde, Institutionen för vård och natur. Högskolan i Skövde, Forskningscentrum för Systembiologi.
    Pernestig, Anna-Karin
    Högskolan i Skövde, Institutionen för vård och natur. Högskolan i Skövde, Forskningscentrum för Systembiologi.
    Nilsson, Patric
    Högskolan i Skövde, Institutionen för vård och natur. Högskolan i Skövde, Forskningscentrum för Systembiologi.
    Jirstrand, Mats
    Fraunhofer-Chalmers Research Centre for Industrial Mathematics, Gothenburg, Sweden.
    Hornquist, Elisabeth Hultgren
    Univ Örebro, Sch Hlth & Med Sci, Dept Biomed, Örebro, Sweden.
    Toward Quantifying the Thymic Dysfunctional State in Mouse Models of Inflammatory Bowel Disease2013Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 19, nr 4, s. 881-888Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    Inflammatory bowel disease is characterized by a number of immunological alterations, not the least in the T-cell compartment. Numerous animal models of colitis have revealed aberrant thymocyte dynamics associated with skewed thymocyte development. The recent advancements in quantitative methods have proposed critical kinetic alterations in the thymocyte development during the progression of colitis. This review focuses on the aberrant thymocyte dynamics in G alpha i2-deficient mice as this mouse model provides most quantitative data of the thymocyte development associated with colitis. Herein, we discuss several dynamic changes during the progression of colitis and propose a hypothesis for the underlying causes for the skewed proportions of the thymocyte populations seen in the G alpha i2-deficient mice and in other mouse models of colitis. (Inflamm Bowel Dis 2013; 19: 881-888)

  • 35.
    Johansson, Malin
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Anatomi.
    Jönsson, Maria
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Anatomi.
    Norrgård, Orjan
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Forsgren, Sture
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Anatomi.
    New aspects concerning ulcerative colitis and colonic carcinoma: analysis of levels of neuropeptides, neurotrophins, and TNFalpha/TNF receptor in plasma and mucosa in parallel with histological evaluation of the intestine2008Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 14, nr 10, s. 1331-1340Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: The levels of neuropeptides, neurotrophins, and TNFalpha (TNFalpha)/TNF receptor in plasma and mucosa for patients with ulcerative colitis (UC) and colonic carcinoma, and concerning plasma also for healthy controls, were examined. Moreover, the relationships between the different substances and the influence of mucosal derangement on the levels were analyzed.

    METHODS: The levels of VIP, SP, CGRP, BDNF, NGF, and TNFalpha/TNF receptor 1 were measured using ELISA/EIA.

    RESULTS: Patients with UC demonstrated the highest levels of all analyzed substances in plasma, with the exception of BDNF. However, there were differences within the UC group, patients treated with corticosteroids, and/or nonsteroid antiinflammatory/immunosuppressive treatment having higher plasma levels than those not given these treatments. Patients with colonic carcinoma showed higher SP and TNF receptor 1 levels in plasma compared to healthy controls. Concerning mucosa, the levels of almost all analyzed substances were elevated for patients with UC compared to noncancerous mucosa of colonic carcinoma patients. There were correlations between many of the substances in both plasma and mucosa, especially concerning the 3 neuropeptides examined. There were also marked associations with mucosa derangement.

    CONCLUSIONS: Via analysis of correlations for the respective patients and via comparisons between the different patient groups, new and original information was obtained. Interestingly, the degree of mucosal affection was markedly correlated with tissue levels of the substances and the treatments were found to be of importance concerning plasma but not tissue levels of these. Combined plasma analysis of neuropeptides, neurotrophins, and TNF receptor 1 may help to distinguish UC and colonic carcinoma patients.

  • 36.
    Johansson, Malin
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Anatomi.
    Norrgård, Örjan
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap.
    Forsgren, Sture
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Anatomi.
    Study of expression patterns and levels of neurotrophins and neurotrophin receptors in ulcerative colitis2007Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 13, nr 4, s. 398-409Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Neurotrophins may be involved in ulcerative colitis (UC). Yet, it is unclear whether if their effects should be blocked.

    Methods: In this study, the neurotrophins nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) and their receptors were examined by immunohistochemistry, ELISA, and RT-PCR.

    Results: BDNF immunoreaction was detected in nerve structures in particular, and NGF immunoreaction was detected in lamina propria cells. Cellular NGF immunoreaction was generally observed to be higher in the mucosa of UC patients than in the controls. In addition, UC patients demonstrated significantly higher p75 immunoreaction (P = 0.010) in lamina propria cells. The controls expressed significantly higher BDNF immunoreaction in the nerve structures than did UC patients (P = 0.000). However, the UC group showed marked interindividual variation in expression of neurotrophins and neurotrophin receptors. This included variation at the mRNA level for NGF. Differences with the controls were most pronounced in UC specimens demonstrating great infiltration of inflammatory cells and marked tissue derangement. Corticosteroid treatment seemed to affect neurotrophin production in lamina propria cells but not in nerve structures. These observations demonstrate that up-regulation and down-regulation of neurotrophins occur in different structural components in response to the disease process. Massive inflammation seemed to be correlated with decreased neurotrophin immunoreaction in nerve structures, but there was a tendency toward increased neurotrophin production in lamina propria cells.

    Conclusions: Our study shows that UC patients are not a uniform group in their expression of neurotrophins, a fact that should be considered when discussing therapeutic interventions.

  • 37.
    Jonefjäll, Börje
    et al.
    Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden / Department of Internal Medicine, Kungälv Hospital, Kungälv, Sweden.
    Öhman, Lena
    Högskolan i Skövde, Institutionen för hälsa och lärande. Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden / Department of Microbiology and Immunology, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Simrén, Magnus
    Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden / Center for Functional GI and Motility Disorders, University of North Carolina, USA.
    Strid, Hans
    Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden / Department of Internal Medicine, Södra Älvsborg Hospital, Borås, Sweden.
    IBS-like Symptoms in Patients with Ulcerative Colitis in Deep Remission Are Associated with Increased Levels of Serum Cytokines and Poor Psychological Well-being2016Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 22, nr 11, s. 2630-2640Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Gastrointestinal symptoms (GI) compatible with irritable bowel syndrome (IBS) are common in patients with ulcerative colitis (UC) in remission. The causes of these symptoms remain to be clarified. Our aim was to investigate prevalence and factors associated with IBS-like symptoms in patients with UC in deep remission.

    METHODS: We included 298 patients with UC and used Mayo score, sigmoidoscopy, and fecal calprotectin to define deep remission versus active disease. Presence of IBS-like symptoms according to the Rome III criteria, severity of GI, extraintestinal and psychological symptoms, stress levels, and quality of life were measured with validated questionnaires. Serum cytokines and high-sensitive C-reactive peptide were determined.

    RESULTS: The criteria for deep remission was fulfilled by 132 patients (44%) and 24 of these fulfilled the Rome III criteria for IBS (18%). Patients with UC in deep remission with IBS-like symptoms had comparable levels of GI symptoms, non-GI somatic symptoms, and quality of life as patients with active UC. The patients with UC in deep remission with IBS-like symptoms had similar levels of fecal calprotectin as patients in deep remission without IBS-like symptoms (18 versus 31 μg/g, P = 0.11), but higher levels of serum cytokines (interleukin [IL]-1β, IL-6, IL-13, IL-10 and IL-8, P < 0.05) and higher levels of anxiety (P < 0.001), depression (P = 0.02) and perceived stress (P = 0.03).

    CONCLUSIONS: IBS-like symptoms in patients with UC in deep remission are common, but not as prevalent as previously reported. Poor psychological well-being and increased serum cytokine levels, but not colonic low-grade inflammation, were associated with IBS-like symptoms.

  • 38.
    Jönsson, Maria
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB).
    Norrgård, Orjan
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Forsgren, Sture
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB).
    Presence of a marked nonneuronal cholinergic system in human colon: study of normal colon and colon in ulcerative colitis2007Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 13, nr 11, s. 1347-1356Artikel i tidskrift (Övrigt vetenskapligt)
    Abstract [en]

    BACKGROUND: The body has not only a neuronal but also a nonneuronal cholinergic system. Both systems are likely to be very important, particularly in inflammatory conditions. The patterns and importance of the nonneuronal cholinergic system in patients with ulcerative colitis (UC) are largely unknown.

    METHODS: The colons of UC and non-UC patients were examined for expression patterns of choline acetyltransferase (ChAT), vesicular acetylcholine transporter (VAChT), and the muscarinic receptor of the M(2) subtype.

    RESULTS: ChAT and VAChT immunoreactions and mRNA reactions for ChAT were detected in epithelial and endocrine cells, in cells in the lamina propria, and in blood vessel walls. Furthermore, a marked M(2) immunoreaction was noted for epithelium, blood vessel walls, and smooth musculature. ChAT and VAChT immunoreactions were significantly higher in endocrine and epithelial cells, respectively, in non-UC mucosa than in UC mucosa. On the other hand, there was a tendency toward higher M(2) levels in epithelium of UC patients.

    CONCLUSIONS: There is a pronounced nonneuronal cholinergic system in the colon, which has previously been ignored when discussing cholinergic influences in UC. Furthermore, it is evident that certain changes in the nonneuronal cholinergic system occur in response to inflammation/derangement in UC. Cholinergic effects in the colon can be considered to be related not only to nerve-related effects but also to effects of acetylcholine from nonneuronal local cells. Thus, the recently discussed phenomenon of a "cholinergic antiinflammatory pathway" in the intestine may have a pronounced nonneuronal component.

  • 39.
    Lewis, Kimberley
    et al.
    University of Calgary.
    Lutgendorff, Femke
    Linköpings universitet, Institutionen för klinisk och experimentell medicin. Linköpings universitet, Hälsouniversitetet.
    Phan, Van
    University of Calgary.
    Söderholm, Johan D
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Kirurgi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Kirurgi- och onkologicentrum, Kirurgiska kliniken i Östergötland med verksamhet i Linköping, Norrköping och Motala.
    Sherman, Philip M.
    University of Toronto.
    McKay, Derek M.
    University of Calgary.
    Enhanced Translocation of Bacteria Across Metabolically Stressed Epithelia is Reduced by Butyrate2010Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 16, nr 7, s. 1138-1148Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: The gut microflora in some patients with Crohns disease can be reduced in numbers of butyrate-producing bacteria and this could result in metabolic stress in the colonocytes. Thus, we hypothesized that the short-chain fatty acid, butyrate, is important in the maintenance and regulation of the barrier function of the colonic epithelium. Methods: Confluent monolayers of the human colon-derived T84 or HT-29 epithelial cell lines were exposed to dinitrophenol (DNP (0.1 mM), uncouples oxidative phosphorylation) + Escherichia coil (strain HB101, 10(6) cfu) +/- butyrate (3-50 mM). Transepithelial resistance (TER), and bacterial internalization and translocation were assessed over a 24-hour period. Epithelial ultrastructure was assessed by transmission electron microscopy. Results: Epithelia under metabolic stress display decreased TER and increased numbers of pseudopodia that is consistent with increased internalization and translocation of the E. coli. Butyrate (but not acetate) significantly reduced the bacterial translocation across DNP-treated epithelia but did not ameliorate the drop in TER in the DNP+E. coli exposed monolayers. Inhibition of bacterial transcytosis across metabolically stressed epithelia was associated with reduced I-kappa B phosphorylation and hence NF-kappa B activation. Conclusions: Reduced butyrate-producing bacteria could result in increased epithelial permeability particularly in the context of concomitant exposure to another stimulus that reduces mitochondria function. We speculate that prebiotics, the substrate for butyrate synthesis, is a valuable prophylaxis in the regulation of epithelial permeability and could be of benefit in preventing relapses in IBD.

  • 40. Lu, Yunxia
    et al.
    Zamora-Ros, Raul
    Chan, Simon
    Cross, Amanda J.
    Ward, Heather
    Jakszyn, Paula
    Luben, Robert
    Opstelten, Jorrit L.
    Oldenburg, Bas
    Hallmans, Göran
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Näringsforskning.
    Karling, Pontus
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Grip, Olof
    Key, Timothy
    Bergmann, Manuela M.
    Boeing, Heiner
    Overvad, Kim
    Palli, Domenico
    Masala, Giovanna
    Khaw, Kay-Tee
    Racine, Antoine
    Carbonnel, Franck
    Boutron-Ruault, Marie-Christine
    Andersen, Vibeke
    Olsen, Anja
    Tjonneland, Anne
    Kaaks, Rudolf
    Tumino, Rosario
    Trichopoulou, Antonia
    Scalbert, Augustin
    Riboli, Elio
    Hart, Andrew R.
    Dietary Polyphenols in the Aetiology of Crohn's Disease and Ulcerative Colitis-A Multicenter European Prospective Cohort Study (EPIC)2017Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 23, nr 12, s. 2072-2082Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Oxidative stress may be involved in the aetiology of inflammatory bowel disease and whether dietary polyphenols, which possess antioxidants properties, prevent its development is unknown.

    Methods: A total of 401,326 men and women aged 20 to 80 years from 8 countries were recruited between 1991 and 1998 and at baseline completed validated food frequency questionnaires. Dietary polyphenol intake was measured using Phenol-Explorer, a database with information on the content of 502 polyphenols. Incident cases of Crohn's diseases (CD) and ulcerative colitis (UC) were identified during the follow-up period of up to December 2010. A nested case–control study using conditional logistic regression estimated the odds ratios (ORs), and 95% confidence intervals, for polyphenol intake (categories based on quartiles) and developing CD or UC.

    Results: In total, 110 CD (73% women) and 244 UC (57% women) cases were identified and matched to 440 and 976 controls, respectively. Total polyphenol intake was not associated with CD ( P trend = 0.17) or UC ( P trend = 0.16). For flavones and CD, there were reduced odds for all quartiles, which were statistically significant for the third (OR 3rd versus 1st quartile = 0.33; 95% confidence interval, 0.15–0.69) and there was an inverse trend across quartiles ( P = 0.03). Similarly, for resveratrol, there was an inverse association with CD (OR 4th versus 1st quartile = 0.40; 95% confidence interval, 0.20–0.82) with an inverse trend across quartiles ( P = 0.02). No significant associations between subtypes of polyphenols and UC were found. Effect modification by smoking in CD was documented with borderline statistical significance.

    Conclusions: The data supports a potential role of flavones and resveratrol in the risk of developing CD; future aetiological studies should investigate these dietary components and further examine the potential for residual confounding.

  • 41.
    Magnusson, Maria K.
    et al.
    Department of Microbiology and Immunology, Institute for Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden / Department of Internal Medicine and Clinical Nutrition, Institute for Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Strid, Hans
    Department of Internal Medicine, Södra Älvsborg Hospital, Borås, Sweden.
    Isaksson, Stefan
    Department of Microbiology and Immunology, Institute for Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden / Department of Internal Medicine and Clinical Nutrition, Institute for Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Simrén, Magnus
    Department of Internal Medicine and Clinical Nutrition, Institute for Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Öhman, Lena
    Högskolan i Skövde, Institutionen för hälsa och lärande. Högskolan i Skövde, Forskningsspecialiseringen Hälsa och Lärande. Department of Microbiology and Immunology, Institute for Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden / Department of Internal Medicine and Clinical Nutrition, Institute for Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Swede.
    The Mucosal Antibacterial Response Profile and Fecal Microbiota Composition Are Linked to the Disease Course in Patients with Newly Diagnosed Ulcerative Colitis2017Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 23, nr 6, s. 956-966Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: The clinical disease course of ulcerative colitis (UC) varies substantially between individuals and can currently not be reliably predicted. The gut microbiota and the host's immune defense are key players for gut homeostasis and may be linked to disease outcome. The aim of this study was to determine fecal microbiota composition and mucosal antibacterial response profile in untreated patients with newly diagnosed UC and the impact of these factors on disease course. Methods: Stool samples and intestinal biopsies were obtained from therapy-naive newly diagnosed patients with UC. Patients were defined to have mild or moderate/severe disease course assessed by disease activity during the 3 years follow-up. Fecal microbiota was analyzed by the GA-map Dysbiosis test (n = 18), and gene expression in intestinal biopsies was analyzed by RT2 Profiler polymerase chain reaction array (n = 13) and real-time polymerase chain reaction (n = 44). Results: At the time of diagnosis of UC, the fecal microbiota composition discriminated between patients with mild versus moderate/severe disease course. Also, the mucosal antibacterial gene expression response profile differed between patients with mild versus moderate/severe disease course with bactericidal/permeability-increasing protein (BPI) being most important for the discrimination. Mucosal bactericidal/permeability-increasing protein gene expression at diagnosis was higher in patients with mild versus moderate/severe disease course when confirmed in a larger patient cohort (P = 0.0004, n = 44) and was a good predictor for the number of flares during the 3 years follow-up (R-2 = 0.395, P < 0.0001). Conclusions: In patients with newly diagnosed UC, fecal microbiota composition and mucosal antibacterial response profile, especially bactericidal/permeability-increasing protein, are linked to disease course.

  • 42.
    Malmborg, Petter
    et al.
    Department of Women and Child Health, Karolinska Institutet, Stockholm, Sweden.
    Bahmanyar, Shahram
    Clinical Epidemiology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden; Faculty of Medicine, Golestan University of Medical Sciences, Gorgan, Iran.
    Grahnquist, Lena
    Department of Women and Child Health, Karolinska Institutet, Stockholm, Sweden.
    Hildebrand, Hans
    Department of Women and Child Health, Karolinska Institutet, Stockholm, Sweden.
    Montgomery, Scott
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Clinical Epidemiology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden; Department of Primary Care and Public Health, Charing Cross Hospital, Imperial College, London, UK.
    Cesarean section and the risk of pediatric Crohn's disease2012Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 18, nr 4, s. 703-708Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Crohn's disease (CD) could involve an inappropriate immune response against normal bowel flora. Disrupted or atypical patterns of microbial bowel colonization may impair development of homeostasis between gut flora and the immune system. Perinatal microbial exposures may be particularly important in stimulating intestinal immune recognition. As birth by cesarean section is thought to represent an atypical pattern of early bowel colonization, we examined its association with pediatric CD. Methods: Some 1536 patients diagnosed with pediatric CD and 15,439 controls matched by delivery unit, week of birth, sex, and born between 1973 and 2006 were identified through Swedish registers. The association of birth by cesarean section with pediatric CD was examined using conditional logistic regression, with stratification by sex and adjustment for parental socioeconomic index and maternal infections during pregnancy. Results: Birth by cesarean section is associated with a modestly increased risk for pediatric CD among boys (odds ratio [OR] 1.25, 95% confidence interval [CI] 1.01-1.54) but not girls, (OR = 0.99, 95% CI 0.76-1.29) and elective cesarean section is associated with a modest increased risk for the entire population (OR = 1.36, 95% CI 1.02-1.80). Conclusions: This study does not suggest that the delivery procedure should be altered, but the findings may be of etiological significance in CD, indicating a potential role for perinatal exposures associated with delivery mode. Although the sex difference may have arisen by chance, the modestly increased CD risk for boys delivered by cesarean section is consistent with sex-specific differences in susceptibility to some exposures.

  • 43.
    Malmborg, Petter
    et al.
    Department of Women's and Children's Health, Astrid Lindgren Children's Hospital, Karolinska Institutet, Stockholm, Sweden.
    Grahnquist, Lena
    Department of Women's and Children's Health, Astrid Lindgren Children's Hospital, Karolinska Institutet, Stockholm, Sweden.
    Ideström, Maja
    Department of Women's and Children's Health, Astrid Lindgren Children's Hospital, Karolinska Institutet, Stockholm, Sweden.
    Lindholm, Johan
    Departments of Oncology-Pathology, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Befrits, Ragnar
    Departments of Medicine, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden .
    Björk, Jan
    Departments of Medicine, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden .
    Montgomery, Scott
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Region Örebro län. Clinical Epidemiology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology and Public Health, University College London, London, United Kingdom .
    Hildebrand, Hans
    Department of Women's and Children's Health, Astrid Lindgren Children's Hospital, Karolinska Institutet, Stockholm, Sweden.
    Presentation and progression of childhood-onset inflammatory bowel disease in northern Stockholm County2015Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 21, nr 5, s. 1098-1108Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Some studies have suggested that childhood-onset inflammatory bowel disease (IBD) is characterized by extensive intestinal involvement and rapid progression to complications. Here, we report the presentation and progression of patients diagnosed with IBD during childhood in a population-based cohort from northern Stockholm County.

    Methods: Medical records for all 280 patients diagnosed in the period 1990-2007 with childhood-onset IBD in northern Stockholm County were followed until 2011 (median follow-up time, 8.8 yr). Disease phenotypes were classified according to the Paris pediatric IBD classification.

    Results: Among the 74 patients with ulcerative colitis, 72% presented with pancolitis. Among the 200 patients with Crohn's disease (CD), 75% presented with colitis. Complicated disease behavior was observed in 18% of patients with CD by end of follow-up. Extension of the disease territory was observed in 22% of patients with ulcerative colitis and 15% of patients with CD. The cumulative risk of intra-abdominal surgery after 10 years was 8% (95% confidence interval, 4%-20%) for ulcerative colitis and 22% (95% confidence interval, 15%-28%) for patients with CD. Nonmucosal healing at 1 year was associated with a complicated disease course in patients with CD (hazard ratio = 14.56; 95% confidence interval, 1.79-118.68; P = 0.01).

    Conclusions: Patients with childhood-onset IBD were characterized by extensive colitis that was relatively stable over time and associated with a relatively low risk of complications and abdominal surgery. Our findings confirm the more extensive disease location in pediatric IBD but did not identify the proposed dynamic and aggressive nature of the childhood-onset phenotype. The association of nonmucosal healing with a complicated disease course suggests that endoscopy should guide treatment intensity in childhood-onset CD.

  • 44.
    Malmborg, Petter
    et al.
    Sach’ Children and Youth Hospital, South General Hospital, Stockholm, Sweden; Clinical Epidemiology Unit, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.
    Mouratidou, Natalia
    Astrid Lindgren Children’s Hospital, Karolinska University Hospital, Stockholm, Sweden.
    Sachs, Michael C.
    Unit of Biostatistics, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Hammar, Ulf
    Unit of Biostatistics, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Khalili, Hamed
    Clinical Epidemiology Unit, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden; Division of Gastroenterology, Massachusetts General Hospital, Harvard Medical School, Boston Massachusetts, USA.
    Neovius, Martin
    Clinical Epidemiology Unit, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.
    Hjern, Anders
    Clinical Epidemiology Unit, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden; Centre for Health Equity Studies, Stockholm University/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.
    Askling, Johan
    Clinical Epidemiology Unit, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro, Sweden.
    Olén, Ola
    Sach’ Children and Youth Hospital, South General Hospital, Stockholm, Sweden; Clinical Epidemiology Unit, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.
    Effects of Childhood-onset Inflammatory Bowel Disease on School Performance: A Nationwide Population-based Cohort Study Using Swedish Health and Educational Registers2019Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 25, nr 10, s. 1663-1673Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Childhood-onset inflammatory bowel disease (IBD) might negatively impact academic school performance. We conducted a nationwide study to examine the association between childhood-onset IBD and school results.

    Methods: Our study population was selected from Swedish health registers. In the National Patient Register (1990 to 2013), we identified 2827 children with IBD: Crohn's disease (CD), n = 1207, and ulcerative colitis (UC), n = 1370. Patients were matched with 10 reference individuals by age, sex, birth year, and place of residence (n = 28,235). Final compulsory school grades (0 to 320 grade points) and qualification for high school (yes or no) were obtained through the National School Register. Regression models controlling for socioeconomic factors were used to analyze the association of IBD with school performance.

    Results: Children with IBD had a lower final grade point average (adjusted mean grade difference [AMGD] -4.9, 95% confidence interval [CI] -7.1 to -2.6) but not a significantly higher risk to not qualify for high school (odds ratio [OR] 1.14, CI 0.99-1.31). The results were similar in children with UC (AMGD -5.5, CI -8.7 to -2.3) and CD (AMGD -4.7, CI -8.2 to -1.2). Underperformance was more common in subsets of IBD children characterized by markers associated with long-standing active disease (eg, >30 inpatient days [AMGD-18.1, CI -25.8 to -10.4]).

    Conclusion: Most children with IBD achieve comparable results in the final year of compulsory school as their healthy peers. Care should be improved for the subgroup of children for which IBD has a stronger negative impact on school performance.

  • 45. Malmborg, Petter
    et al.
    Mouratidou, Natalia
    Sachs, Michael C.
    Hammar, Ulf
    Khalili, Hamed
    Neovius, Martin
    Hjern, Anders
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Institutionen för folkhälsovetenskap, Centrum för forskning om ojämlikhet i hälsa (CHESS). Karolinska Institutet, Sweden.
    Smedby, Karin E.
    Ekbom, Anders
    Askling, Johan
    Ludvigsson, Jonas F.
    Olén, Ola
    Effects of Childhood-onset Inflammatory Bowel Disease on School Performance: A Nationwide Population-based Cohort Study Using Swedish Health and Educational Registers2019Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 25, nr 10, s. 1663-1673Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Childhood-onset inflammatory bowel disease (IBD) might negatively impact academic school performance. We conducted a nationwide study to examine the association between childhood-onset IBD and school results. METHODS: Our study population was selected from Swedish health registers. In the National Patient Register (1990 to 2013), we identified 2827 children with IBD: Crohn's disease (CD), n = 1207, and ulcerative colitis (UC), n = 1370. Patients were matched with 10 reference individuals by age, sex, birth year, and place of residence (n = 28,235). Final compulsory school grades (0 to 320 grade points) and qualification for high school (yes or no) were obtained through the National School Register. Regression models controlling for socioeconomic factors were used to analyze the association of IBD with school performance. RESULTS: Children with IBD had a lower final grade point average (adjusted mean grade difference [AMGD] -4.9, 95% confidence interval [CI] -7.1 to -2.6) but not a significantly higher risk to not qualify for high school (odds ratio [OR] 1.14, CI 0.99-1.31). The results were similar in children with UC (AMGD -5.5, CI -8.7 to -2.3) and CD (AMGD -4.7, CI -8.2 to -1.2). Underperformance was more common in subsets of IBD children characterized by markers associated with long-standing active disease (eg, >30 inpatient days [AMGD-18.1, CI -25.8 to -10.4]). CONCLUSION: Most children with IBD achieve comparable results in the final year of compulsory school as their healthy peers. Care should be improved for the subgroup of children for which IBD has a stronger negative impact on school performance.

  • 46.
    Mesterton, Johan
    et al.
    i3 Innovus, Stockholm, Sweden.
    Jonsson, Linus
    i3 Innovus, Stockholm, Sweden.
    Almer, Sven
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Gastroenterologi och hepatologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Befrits, Ragnar
    Karolinska Univ Hosp, Div Gastroenterol, Stockholm, Sweden.
    Friis-Liby, Ingalill
    Sahlgrens Univ Hosp, Div Gastroenterol Hepatol, Gothenburg, Sweden.
    Lindgren, Stefan
    Univ Hosp MAS, Dept Clin Sci, Div Gastroenterol Hepatol, S-20502 Malmo, Sweden.
    Resource Use and Societal Costs for Crohns Disease in Sweden2009Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 15, nr 12, s. 1882-1890Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: The usual onset of Crohns disease (CD) is between 15 and 30 years of age, thus affecting people during their most economically productive period in life. Methods: This study intended to estimate societal costs and health-related quality of life (HRQoL) in Swedish patients in different stages of CD. Cross-sectional data on disease activity (measured with the Harvey-Bradshaw Index [HBI]), direct medical resource use, work productivity, and HRQoL (assessed using the 15D instrument) were collected for 420 patients by questionnaires to patients, to the treating physician, and from medical records. Based on HBI, current treatment, and response to treatment, patients were classified into the following disease states: Remission, Response, Active, Refractory, and Surgery. Results: The average 4-week cost per patient in 2007 was estimated at (sic)721 (USD 988), of which 64% was due to lost productivity. The total 4-week cost of care was (sic)255 (USD 349) in Remission, (sic)831 (USD 1138) in Response, (sic)891 (USD 1220) in Active, (sic)1360 (USD 1864) in Refractory, and (sic)16984 (USD 23269) in Surgery. HBI was the most important predictor of costs of care-a 1-point increase in HBI increased total costs by 25% (P less than 0.001). HRQoL differed between the disease states: 0.92 in Remission, 0.90 in Response, 0.82 in Active, 0.81 in Refractory, and 0.77 in Surgery. Conclusions: Patients in remission have the lowest costs and the highest HRQoL. Patients responding to treatment have lower costs of care than patients with high disease activity who are not treated or do not respond to treatment:. Thus, total costs of care might be reduced by efficient treatment.

  • 47.
    Nordenvall, Caroline
    et al.
    Karolinska Inst, Sweden; Karolinska Univ Hosp, Sweden.
    Olen, Ola
    Karolinska Inst, Sweden; Sachs Childrens Hosp, Sweden.
    Nilsson, Per Johan
    Karolinska Inst, Sweden; Karolinska Univ Hosp, Sweden.
    Ekbom, Anders
    Karolinska Inst, Sweden.
    Bottai, Matteo
    Karolinska Inst, Sweden.
    Myrelid, Pär
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för Kirurgi, Ortopedi och Onkologi. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Centrum för kirurgi, ortopedi och cancervård, Kirurgiska kliniken US.
    Bergquist, Annika
    Karolinska Inst, Sweden; Karolinska Univ Hosp, Sweden.
    Restorative Surgery in Patients With Primary Sclerosing Cholangitis and Ulcerative Colitis Following a Colectomy2018Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 24, nr 3, s. 624-632Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Studies on surgical procedures in patients with concomitant primary sclerosing cholangitis (PSC) and ulcerative colitis (UC) have mainly been restricted to single centers. The aim was to compare surgical treatment of UC with or without PSC in a nationwide study. Methods: A cohort study including all patients diagnosed with UC between 1987 and 2014 in Sweden was undertaken. The impact of PSC on the risk of colectomy, the chance of restorative surgery, and risk of failure (presence of a stoma) following restorative surgery were estimated. Survival analyses were performed using the Kaplan-Meier method and multivariable Cox regression models. Results: Of 49 882 UC patients, 2079 had a PSC diagnosis at the end of follow-up. The risk of colectomy was unaffected by PSC diagnosis, whereas the chance of restorative surgery was elevated in PSC-UC patients (hazard ratio [HR], 1.22; 95% confidence interval [CI], 1.02-1.44). Ileorectal anastomosis (IRA) was performed in 63% of the PSC-UC patients and 43% of the non-PSC-UC-patients, and the corresponding numbers for ileal pouch anal anastomosis (IPAA) were 35% and 53%. There was no significantly increased risk of failure following restorative surgery in PSC patients (HR, 1.44; 95% CI, 0.93-2.22). In PSC-UC patients, the cumulative failure rates following an IRA at 3 and 5 years were 15% and 18%, and following an IPAA they were 11% and 18%, respectively. Conclusions: Presence of PSC is not associated with the risk of colectomy, whereas the chance of restorative surgery in PSC-UC patients is higher than in UC alone.

  • 48. Opstelten, Jorrit L
    et al.
    Leenders, Max
    Dik, Vincent K
    Chan, Simon S M
    van Schaik, Fiona D M
    Khaw, Kay-Tee
    Luben, Robert
    Hallmans, Göran
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Näringsforskning.
    Karling, Pontus
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Lindgren, Stefan
    Grip, Olof
    Key, Timothy J
    Crowe, Francesca L
    Boeing, Heiner
    Bergmann, Manuela M
    Overvad, Kim
    Palli, Domenico
    Masala, Giovanna
    Racine, Antoine
    Carbonnel, Franck
    Boutron-Ruault, Marie-Christine
    Tjønneland, Anne
    Olsen, Anja
    Andersen, Vibeke
    Kaaks, Rudolf
    Katzke, Verena A
    Tumino, Rosario
    Trichopoulou, Antonia
    Siersema, Peter D
    Bueno-de-Mesquita, H Bas
    Hart, Andrew R
    Oldenburg, Bas
    Dairy Products, Dietary Calcium, and Risk of Inflammatory Bowel Disease: Results From a European Prospective Cohort Investigation.2016Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 22, nr 6Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Dairy products may be involved in the etiology of inflammatory bowel disease by modulating gut microbiota and immune responses, but data from epidemiological studies examining this relationship are limited. We investigated the association between prediagnostic intake of these foods and dietary calcium, and the subsequent development of Crohn's disease (CD) and ulcerative colitis (UC).

    METHODS: In total, 401,326 participants were enrolled in the European Prospective Investigation into Cancer and Nutrition cohort. At recruitment, consumption of total and specific dairy products (milk, yogurt, and cheese) and dietary calcium was measured using validated food frequency questionnaires. Cases developing incident CD (n = 110) or UC (n = 244) during follow-up were matched with 4 controls. Conditional logistic regression analyses were used to calculate odds ratios (ORs) with 95% confidence intervals (CIs), adjusted for total energy intake and smoking.

    RESULTS: Compared with the lowest quartile, the ORs for the highest quartile of total dairy products and dietary calcium intake were 0.61 (95% CI, 0.32-1.19, p trend = 0.19) and 0.63 (95% CI, 0.28-1.42, p trend = 0.23) for CD, and 0.80 (95% CI, 0.50-1.30, p trend = 0.40) and 0.81 (95% CI, 0.49-1.34, p trend = 0.60) for UC, respectively. Compared with nonconsumers, individuals consuming milk had significantly reduced odds of CD (OR 0.30, 95% CI, 0.13-0.65) and nonsignificantly reduced odds of UC (OR 0.85, 95% CI, 0.49-1.47).

    CONCLUSIONS: Milk consumption may be associated with a decreased risk of developing CD, although a clear dose-response relationship was not established. Further studies are warranted to confirm this possible protective effect.

  • 49.
    Oxelmark, Lena
    et al.
    Karolinska Institutet / Sophiahemmet högskola.
    Magnusson, Anna
    S:t Lukasföreningen.
    Löfberg, Robert
    Karolinska Institutet / Sophiahemmet högskola.
    Hillerås, Pernilla
    Sophiahemmet högskola / Karolinska Institutet.
    Group‐based intervention program in inflammatory bowel disease patients: Effects on quality of life2007Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 13, nr 2, s. 182-190Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Inflammatory bowel diseases (IBD) such as ulcerative colitis (UC) and Crohn's disease (CD) have great impact on patients' health‐related quality of life (HRQOL). The aim of this study was to develop an integrated medical and psychological/psychosocial group‐based intervention program for IBD patients and to evaluate if such a program could influence the patients' HRQOL and coping abilities.

    Methods: IBD patients in remission or with low disease activity were randomized to intervention or control groups. The intervention comprised nine weekly sessions, alternating lectures, and group therapy sessions. The Inflammatory Bowel Disease Questionnaire (IBDQ) and the Sense of Coherence scale (SOC) were used to measure HRQOL and coping ability at 0, 6, and 12 months. The intervention was evaluated by a visual analog scale (VAS) and written comments by a content analysis.

    Results: In all, 24 patients were included in the intervention group and 20 in the control group. The mean IBDQ score showed no statistically significant differences before (173.9) or after the intervention at month 6 (175.7) or at month 12 (171.8), or when comparing intervention and controls at month 12. Similarly, there were no statistically significant differences in mean SOC before or after intervention or when comparing groups. The VAS and the content analysis showed that the intervention was well appreciated by the patients.

    Conclusions: The group‐based intervention program was feasible and highly appreciated. There were no statistically significant differences in average IBDQ or SOC over time or in comparison with controls, although a significant increase was seen in patients with short disease duration.

  • 50.
    Oxelmark, Lena
    et al.
    Sophiahemmet Högskola.
    Magnusson, Anne
    Löfberg, Robert
    Hillerås, Pernilla
    Sophiahemmet Högskola.
    Group-based intervention program in inflammatory bowel disease patients: effects on quality of life2007Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 13, nr 2, s. 182-90Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Inflammatory bowel diseases (IBD) such as ulcerative colitis (UC) and Crohn's disease (CD) have great impact on patients' health-related quality of life (HRQOL). The aim of this study was to develop an integrated medical and psychological/ psychosocial group-based intervention program for IBD patients and to evaluate if such a program could influence the patients' HRQOL and coping abilities.

    METHODS: IBD patients in remission or with low disease activity were randomized to intervention or control groups. The intervention comprised nine weekly sessions, alternating lectures, and group therapy sessions. The Inflammatory Bowel Disease Questionnaire (IBDQ) and the Sense of Coherence scale (SOC) were used to measure HRQOL and coping ability at 0, 6, and 12 months. The intervention was evaluated by a visual analog scale (VAS) and written comments by a content analysis.

    RESULTS: In all, 24 patients were included in the intervention group and 20 in the control group. The mean IBDQ score showed no statistically significant differences before (173.9) or after the intervention at month 6 (175.7) or at month 12 (171.8), or when comparing intervention and controls at month 12. Similarly, there were no statistically significant differences in mean SOC before or after intervention or when comparing groups. The VAS and the content analysis showed that the intervention was well appreciated by the patients.

    CONCLUSIONS: The group-based intervention program was feasible and highly appreciated. There were no statistically significant differences in average IBDQ or SOC over time or in comparison with controls, although a significant increase was seen in patients with short disease duration.

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