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  • 1.
    Abdalla, Maie
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för Kirurgi, Ortopedi och Onkologi. Linköpings universitet, Medicinska fakulteten. Suez Canal University, Egypt.
    Landerholm, Kalle
    Ryhov County Hospital, Sweden.
    Andersson, Peter
    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.
    Andersson, Roland
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för Kirurgi, Ortopedi och Onkologi. Linköpings universitet, Medicinska fakulteten. Ryhov County Hospital, 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.
    Risk of Rectal Cancer After Colectomy for Patients With Ulcerative Colitis: A National Cohort Study2017Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 15, nr 7, s. 1055-1060, artikkel-id e2Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND amp; AIMS: Patients with ulcerative colitis (UC) have an increased risk of rectal cancer, therefore reconstruction with an ileal pouch-anal anastomosis (IPAA) generally is preferred to an ileorectal anastomosis (IRA) after subtotal colectomy. Similarly, completion proctectomy is recommended for patients with ileostomy and a diverted rectum, although this approach has been questioned because anti-inflammatory agents might reduce cancer risk. We performed a national cohort study in Sweden to assess the risk of rectal cancer in patients with UC who have an IRA, IPAA, or diverted rectum after subtotal colectomy.

    METHODS: We collected data from the Swedish National Patient Register for a cohort of 5886 patients with UC who underwent subtotal colectomy with an IRA, IPAA, or diverted rectum from 1964 through 2010. Patients who developed rectal cancer were identified from the Swedish National Cancer Register. The risk of rectal cancer was compared between this cohort and the general population by standardized incidence ratio analysis.

    RESULTS: Rectal cancer occurred in 20 of 1112 patients (1.8%) who received IRA, 1 of 1796 patients (0.06%) who received an IPAA, and 25 of 4358 patients (0.6%) with a diverted rectum. Standardized incidence ratios for rectal cancer were 8.7 in patients with an IRA, 0.4 in patients with an IPAA, and 3.8 in patients with a diverted rectum. Risk factors for rectal cancer were primary sclerosing cholangitis in patients with an IRA (hazard ratio, 6.12), and colonic severe dysplasia or cancer before subtotal colectomy in patients with a diverted rectum (hazard ratio, 3.67).

    CONCLUSIONS: In an analysis of the Swedish National Patient Register, we found that the risk for rectal cancer after colectomy in patients with UC is low, in relative and absolute terms, after reconstruction with an IPAA. An IRA and diverted rectum are associated with an increased risk of rectal cancer, compared with the general population, but the absolute risk is low. Patients and their health care providers should consider these findings in making decisions to leave the rectum intact, perform completion proctectomy, or reconstruct the colon with an IRA or IPAA.

  • 2. Aglago, Elom K.
    et al.
    Huybrechts, Inge
    Murphy, Neil
    Casagrande, Corinne
    Nicolas, Genevieve
    Pischon, Tobias
    Fedirko, Veronika
    Severi, Gianluca
    Boutron-Ruault, Marie-Christine
    Fournier, Agnès
    Katzke, Verena
    Kühn, Tilman
    Olsen, Anja
    Tjønneland, Anne
    Dahm, Christina C.
    Overvad, Kim
    Lasheras, Cristina
    Agudo, Antonio
    Sánchez, Maria-Jose
    Amiano, Pilar
    Huerta, José Maria
    Ardanaz, Eva
    Perez-Cornago, Aurora
    Trichopoulou, Antonia
    Karakatsani, Anna
    Martimianaki, Georgia
    Palli, Domenico
    Pala, Valeria
    Tumino, Rosario
    Naccarati, Alessio
    Panico, Salvatore
    Bueno-de-Mesquita, Bas
    May, Anne
    Derksen, Jeroen W. G.
    Hellstrand, Sophie
    Ohlsson, Bodil
    Wennberg, Maria
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Allmänmedicin.
    van Guelpen, Bethany
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Skeie, Guri
    Brustad, Magritt
    Weiderpass, Elisabete
    Cross, Amanda J.
    Ward, Heather
    Riboli, Elio
    Norat, Teresa
    Chajes, Veronique
    Gunter, Marc J.
    Consumption of Fish and Long-chain n-3 Polyunsaturated Fatty Acids Is Associated With Reduced Risk of Colorectal Cancer in a Large European Cohort2019Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND & AIMS: There is an unclear association between intake of fish and long-chain n-3 polyunsaturated fatty acids (n-3 LC-PUFAs) and colorectal cancer (CRC). We examined the association between fish consumption, dietary and circulating levels of n-3 LC-PUFAs, and ratio of n-6:n-3 LC-PUFA with CRC using data from the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort.

    METHODS: Dietary intake of fish (total, fatty/oily, lean/white) and n-3 LC-PUFA were estimated by food frequency questionnaires given to 521,324 participants in the EPIC study; among these, 6291 individuals developed CRC (median follow up, 14.9 years). Levels of phospholipid LC-PUFA were measured by gas chromatography in plasma samples from a sub-group of 461 CRC cases and 461 matched individuals without CRC (controls). Multivariable Cox proportional hazards and conditional logistic regression models were used to calculate hazard ratios (HRs) and odds ratios (ORs), respectively, with 95% CIs.

    RESULTS: Total intake of fish (HR for quintile 5 vs 1, 0.88; 95% CI, 0.80-0.96; Ptrend = .005), fatty fish (HR for quintile 5 vs 1, 0.90; 95% CI, 0.82-0.98; Ptrend = .009), and lean fish (HR for quintile 5 vs 1, 0.91; 95% CI, 0.83-1.00; Ptrend = .016) were inversely associated with CRC incidence. Intake of total n-3 LC-PUFA (HR for quintile 5 vs 1, 0.86; 95% CI, 0.78-0.95; Ptrend = .010) was also associated with reduced risk of CRC, whereas dietary ratio of n-6:n-3 LC-PUFA was associated with increased risk of CRC (HR for quintile 5 vs 1, 1.31; 95% CI, 1.18-1.45; Ptrend < .001). Plasma levels of phospholipid n-3 LC-PUFA was not associated with overall CRC risk, but an inverse trend was observed for proximal compared with distal colon cancer (Pheterogeneity = .026).

    CONCLUSIONS: In an analysis of dietary patterns of participants in the EPIC study, we found regular consumption of fish, at recommended levels, to be associated with a lower risk of CRC, possibly through exposure to n-3 LC-PUFA. Levels of n-3 LC-PUFA in plasma were not associated with CRC risk, but there may be differences in risk at different regions of the colon.

  • 3.
    Andreasson, Anna
    et al.
    Karolinska Inst, Dept Med, Stockholm, Sweden.;Stockholm Univ, Stress Res Inst, Stockholm, Sweden.;Macquarie Univ, Dept Psychol, N Ryde, NSW, Australia..
    Carlsson, Axel C
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi. Karolinska Inst, Dept Neurobiol Care Sci & Soc, Div Family Med, Huddinge, Sweden.
    Önnerhag, Kristina
    Skane Univ Hosp, Dept Gastroenterol & Hepatol, Malmo, Sweden..
    Hagström, Hannes
    Karolinska Inst, Dept Med, Stockholm, Sweden.;Karolinska Univ Hosp, Ctr Digest Dis, Div Hepatol, Stockholm, Sweden..
    Waist/Hip Ratio Better Predicts Development of Severe Liver Disease Within 20 Years Than Body Mass Index: A Population-based Cohort Study2017Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 15, nr 8, s. 1294-1301Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND & AIMS: Obesity, commonly assessed based on body mass index (BMI), is associated with an increased risk for severe liver disease. It is not known if other measures of body composition are better determinants of risk for severe liver disease, and/or if these differ between women and men. We investigated the body composition measures that best predict the development of severe liver disease.

    METHODS: We collected data from the Malmo Diet and Cancer study in Sweden, comprising 16,784 women and 10,833 (mean age, 58.1 years at baseline), and followed patients for a median 19.8 years. We analyzed data on measures of body composition including BMI, waist/hip ratio, and others. We determined whether subjects were diagnosed with severe liver disease, or died from severe liver disease, until the end of 2014 using Swedish national registers. Associations between body composition measures and severe liver disease were assessed using Cox regression models, stratified by sex and adjusted for age, alcohol consumption, smoking, education, and physical activity.

    RESULTS: All studied measures of body composition were significantly associated with severe liver disease. Waist/hip ratio was the best predictor of severe liver disease in women (hazard ratio [HR] per standard deviation increment, 1.30; 95% confidence interval [CI], 1.16-1.46) and men (HR, 1.46; 95% CI, 1.31-1.63). BMI had the lowest HR in women (HR, 1.12; 95% CI, 1.00-1.27) and men (HR, 1.26; 95% CI, 1.12-1.42). The association between waist/hip ratio and development of liver disease was independent of BMI.

    CONCLUSIONS: In a Swedish population-based cohort study, we associated all measures of body composition with risk of severe liver disease. However, measures of abdominal obesity were best at predicting development of severe liver disease.

  • 4.
    Andreasson, Anna
    et al.
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden; Macquarie University, Australia.
    Carlsson, Axel C.
    Önnerhag, Kristina
    Hagström, Hannes
    Waist/Hip Ratio Better Predicts Development of Severe Liver Disease Within 20 Years Than Body Mass Index: A Population-based Cohort Study2017Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 15, nr 8, s. 1294-+Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND & AIMS: Obesity, commonly assessed based on body mass index (BMI), is associated with an increased risk for severe liver disease. It is not known if other measures of body composition are better determinants of risk for severe liver disease, and/or if these differ between women and men. We investigated the body composition measures that best predict the development of severe liver disease. METHODS: We collected data from the Malmo Diet and Cancer study in Sweden, comprising 16,784 women and 10,833 (mean age, 58.1 years at baseline), and followed patients for a median 19.8 years. We analyzed data on measures of body composition including BMI, waist/hip ratio, and others. We determined whether subjects were diagnosed with severe liver disease, or died from severe liver disease, until the end of 2014 using Swedish national registers. Associations between body composition measures and severe liver disease were assessed using Cox regression models, stratified by sex and adjusted for age, alcohol consumption, smoking, education, and physical activity. RESULTS: All studied measures of body composition were significantly associated with severe liver disease. Waist/hip ratio was the best predictor of severe liver disease in women (hazard ratio [HR] per standard deviation increment, 1.30; 95% confidence interval [CI], 1.16-1.46) and men (HR, 1.46; 95% CI, 1.31-1.63). BMI had the lowest HR in women (HR, 1.12; 95% CI, 1.00-1.27) and men (HR, 1.26; 95% CI, 1.12-1.42). The association between waist/hip ratio and development of liver disease was independent of BMI. CONCLUSIONS: In a Swedish population-based cohort study, we associated all measures of body composition with risk of severe liver disease. However, measures of abdominal obesity were best at predicting development of severe liver disease.

  • 5.
    Axelrad, Jordan E.
    et al.
    Inflammatory Bowel Disease Center, Division of Gastroenterology, Department of Medicine, NYU Langone Health, New York NY, USA; Division of Digestive and Liver Disease, Department of Medicine, Columbia University Medical Center, New York NY, USA.
    Olén, Ola
    Sachs’ Children and Youth Hospital, Stockholm South General Hospital, Stockholm, Sweden; Department of Clinical Science and Education Södersjukhuset, Karolinska Institutet, Stockholm, Sweden; Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Askling, Johan
    Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Lebwohl, Benjamin
    Division of Digestive and Liver Disease, Department of Medicine, Columbia University Medical Center, New York NY, USA.
    Khalili, Hamed
    Inflammatory Bowel Disease Center, Division of Gastroenterology, Department of Medicine, Massachusetts General Hospital, Boston Massachusetts, USA.
    Sachs, Michael C.
    Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län. Division of Digestive and Liver Disease, Department of Medicine, Columbia University Medical Center, New York NY, USA; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro, Sweden; Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham, United Kingdom.
    Gastrointestinal Infection Increases Odds of Inflammatory Bowel Disease in a Nationwide Case-Control Study2019Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 17, nr 7, s. 1311-1322Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND & AIMS: Gastrointestinal infections have been associated with later development of inflammatory bowel diseases (IBD). However, studies have produced conflicting results. We performed a nationwide case-control study in Sweden to determine whether gastroenteritis is associated with the development of Crohn's disease (CD) or ulcerative colitis (UC).

    METHODS: Using the Swedish National Patient Register, we identified 44,214 patients with IBD (26,450 with UC; 13,387 with CD; and 4377 with IBD-unclassified) from 2002 to 2014 and matched them with 436,507 individuals in the general population (control subjects). We then identified patients and control subjects with reported episodes of gastroenteritis (from 1964 to 2014) and type of pathogen associated. We collected medical and demographic data and used logistic regression to estimate odds ratios (ORs) for IBD associated with enteric infection.

    RESULTS: Of the patients with IBD, 3105 (7.0%) (1672 with UC, 1050 with CD, and 383 with IBD-unclassified) had a record of previous gastroenteritis compared with 17,685 control subjects (4.1%). IBD cases had higher odds for an antecedent episode of gastrointestinal infection (aOR, 1.64; 1.57-1.71), bacterial gastrointestinal infection (aOR, 2.02; 1.82-2.24), parasitic gastrointestinal infection (aOR, 1.55; 1.03-2.33), and viral gastrointestinal infection (aOR, 1.55; 1.34-1.79). Patients with UC had higher odds of previous infection with Salmonella, Escherichia coli, Campylobacter, or Clostridium difficile compared to control subjects. Patients with CD had higher odds of previous infection with Salmonella, Campylobacter, Yersinia enterocolitica, C difficile, amoeba, or norovirus compared to control subjects. Increasing numbers of gastroenteritis episodes were associated with increased odds of IBD, and a previous episode of gastroenteritis remained associated with odds for IBD more than 10 years later (aOR, 1.26; 1.19-1.33).

    CONCLUSIONS: In an analysis of the Swedish National Patient Register, we found previous episodes of gastroenteritis to increase odds of later development of IBD. Although we cannot formally exclude misclassification bias, enteric infections might induce microbial dysbiosis that contributes to the development of IBD in susceptible individuals.

  • 6.
    Bergquist, A.
    et al.
    Department of Gastroenterology and Hepatology, Karolinska University Hospital, Karolinska Institute, Huddinge and Solna, Stockholm.
    Montgomery, S.M.
    Clinical Epidemiology Unit, Department of Medicine, Karolinska Hospital, Stockholm, Clinical Research Centre, Örebro University Hospital, Örebro.
    Bahmanyar, S.
    Clinical Epidemiology Unit, Department of Medicine, Karolinska Hospital, Stockholm.
    Olsson, R.
    Department of Medicine, Sahlgrenska University Hospital, Gothenburg, Sweden.
    Danielsson, A.
    Danielsson, Å., Department of Medicine, Section for Gastroenterology and Hepatology, University Hospital, Umeå.
    Lindgren, S.
    Department of Gastroenterology and Hepatology, University Hospital, Malmö.
    Prytz, H.
    Division of Gastroenterology and Hepatology, University Hospital, Lund.
    Hultcrantz, R.
    Department of Gastroenterology and Hepatology, Karolinska University Hospital, Karolinska Institute, Huddinge and Solna, Stockholm.
    Loof, L.A.R.S.
    Lööf, L.A.R.S., Centre for Clinical Research, Central Hospital, Västerås.
    Sandberg-Gertzen, H.
    Sandberg-Gertzén, H., Division of Gastroenterology and Hepatology, Department of Medicine, Medical Center Hospital, Örebro.
    Almer, Sven
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Gastroenterologi och hepatologi. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Askling, J.
    Clinical Epidemiology Unit, Department of Medicine, Karolinska Hospital, Stockholm.
    Ehlin, A.
    Clinical Epidemiology Unit, Department of Medicine, Karolinska Hospital, Stockholm.
    Ekbom, A.
    Clinical Epidemiology Unit, Department of Medicine, Karolinska Hospital, Stockholm.
    Increased Risk of Primary Sclerosing Cholangitis and Ulcerative Colitis in First-Degree Relatives of Patients With Primary Sclerosing Cholangitis2008Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 6, nr 8, s. 939-943Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background & Aims: The importance of genetic factors for the development of primary sclerosing cholangitis (PSC) is incompletely understood. This study assessed the risk of PSC and inflammatory bowel disease (IBD) among first-degree relatives of patients with PSC, compared with the first-degree relatives of a cohort without PSC. Methods: Subjects from the national Swedish cohort of PSC patients (n = 678) were matched for date of birth, sex, and region to up to 10 subjects without a diagnosis of PSC (n = 6347). Linkage through general population registers identified first-degree relatives of subjects in both the PSC and comparison cohorts (n = 34,092). Diagnoses among first-degree relatives were identified by using the Inpatient Register. Results: The risk of cholangitis was statistically significantly increased in offspring, siblings, and parents of the PSC patient cohort, compared with relatives of the comparison cohort, with the hazard ratios and 95% confidence intervals, 11.5 (1.6-84.4), 11.1 (3.3-37.8), and 2.3 (0.9-6.1), respectively. The hazard ratios for ulcerative colitis (UC) among first-degree relatives of all PSC patients was 3.3 (2.3-4.9) and for Crohn's disease 1.4 (0.8-2.5). The risk of UC for relatives of PSC patients without IBD was also increased, 7.4 (2.9-18.9). Conclusions: First-degree relatives of patients with PSC run an increased risk of PSC, indicating the importance of genetic factors in the etiology of PSC. First-degree relatives of PSC patients without IBD are also at an increased risk of UC, which might indicate shared genetic susceptibility factors for PSC and UC. © 2008 AGA Institute.

  • 7. Bergquist, Annika
    et al.
    Montgomery, Scott M.
    Bahmanyar, Shahram
    Olsson, Rolf
    Danielsson, Åke
    Lindgren, Stefan
    Prytz, Hanne
    Hultcrantz, Rolf
    Lööf, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Centrum för klinisk forskning, Västerås.
    Sandberg-Gertzén, Hanna
    Almer, Sven
    Askling, Johan
    Ehlin, Anna
    Ekbom, Anders
    Increased risk of primary sclerosing cholangitis and ulcerative colitis in first-degree relatives of patients with primary sclerosing cholangitis2008Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 6, nr 8, s. 939-943Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background & Aims: The importance of genetic factors for the development of primary sclerosing cholangitis (PSC) is incompletely understood. This study assessed the risk of PSC and inflammatory bowel disease (IBD) among first-degree relatives of patients with PSC, compared with the first-degree relatives of a cohort without PSC. Methods: Subjects from the national Swedish cohort of PSC patients (n = 678) were matched for date of birth, sex, and region to up to 10 subjects without a diagnosis of PSC (n = 6347). Linkage through general population registers identified first-degree relatives of subjects in both the PSC and comparison cohorts (n = 34,092). Diagnoses among first-degree relatives were identified by using the Inpatient Register. Results: The risk of cholangitis was statistically significantly increased in offspring, siblings, and parents of the PSC patient cohort, compared with relatives of the comparison cohort, with the hazard ratios and 95% confidence intervals, 11.5 (1.6-84.4), 11.1 (3.3-37.8), and 2.3 (0.9-6.1), respectively. The hazard ratios for ulcerative colitis (UC) among first-degree relatives of all PSC patients was 3.3 (2.3-4.9) and for Crohn's disease 1.4 (0.8-2.5). The risk of UC for relatives of PSC patients without IBD was also increased, 7.4 (2.9-18.9). Conclusions: First-degree relatives of patients with PSC run an increased risk of PSC, indicating the importance of genetic factors in the etiology of PSC. First-degree relatives of PSC patients without IBD are also at an increased risk of UC, which might indicate shared genetic susceptibility factors for PSC and UC.

  • 8. Bergquist, Annika
    et al.
    Montgomery, Scott M.
    Örebro universitet, Hälsoakademin.
    Bahmanyar, Shahram
    Olsson, Rolf
    Danielsson, Åke
    Lindgren, Stefan
    Prytz, Hanne
    Hultcrantz, Rolf
    Lööf, Lars
    Sandberg-Gertzén, Hanna
    Almer, Sven
    Askling, Johan
    Ehlin, Anna
    Ekbom, Anders
    Increased risk of primary sclerosing cholangitis and ulcerative colitis in first-degree relatives of patients with primary sclerosing cholangitis2008Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 6, nr 8, s. 939-943Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background & Aims: The importance of genetic factors for the development of primary sclerosing cholangitis (PSC) is incompletely understood. This study assessed the risk of PSC and inflammatory bowel disease (IBD) among first-degree relatives of patients with PSC, compared with the first-degree relatives of a cohort without PSC. Methods: Subjects from the national Swedish cohort of PSC patients (n = 678) were matched for date of birth, sex, and region to up to 10 subjects without a diagnosis of PSC (n = 6347). Linkage through general population registers identified first-degree relatives of subjects in both the PSC and comparison cohorts (n = 34,092). Diagnoses among first-degree relatives were identified by using the Inpatient Register. Results: The risk of cholangitis was statistically significantly increased in offspring, siblings, and parents of the PSC patient cohort, compared with relatives of the comparison cohort, with the hazard ratios and 95% confidence intervals, 11.5 (1.6–84.4), 11.1 (3.3–37.8), and 2.3 (0.9–6.1), respectively. The hazard ratios for ulcerative colitis (UC) among first-degree relatives of all PSC patients was 3.3 (2.3–4.9) and for Crohn's disease 1.4 (0.8–2.5). The risk of UC for relatives of PSC patients without IBD was also increased, 7.4 (2.9–18.9). Conclusions: First-degree relatives of patients with PSC run an increased risk of PSC, indicating the importance of genetic factors in the etiology of PSC. First-degree relatives of PSC patients without IBD are also at an increased risk of UC, which might indicate shared genetic susceptibility factors for PSC and UC. 

  • 9. Bergquist, Annika
    et al.
    Montgomery, Scott M
    Bahmanyar, Shahram
    Olsson, Rolf
    Danielsson, Åke
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Lindgren, Stefan
    Prytz, Hanne
    Hultcrantz, Rolf
    Lööf, Lars
    Sandberg-Gertzén, Hanna
    Almer, Sven
    Askling, Johan
    Ehlin, Anna
    Ekbom, Anders
    Increased risk of primary sclerosing cholangitis and ulcerative colitis in first-degree relatives of patients with primary sclerosing cholangitis2008Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 6, nr 8, s. 939-943Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND & AIMS: The importance of genetic factors for the development of primary sclerosing cholangitis (PSC) is incompletely understood. This study assessed the risk of PSC and inflammatory bowel disease (IBD) among first-degree relatives of patients with PSC, compared with the first-degree relatives of a cohort without PSC.

    METHODS: Subjects from the national Swedish cohort of PSC patients (n = 678) were matched for date of birth, sex, and region to up to 10 subjects without a diagnosis of PSC (n = 6347). Linkage through general population registers identified first-degree relatives of subjects in both the PSC and comparison cohorts (n = 34,092). Diagnoses among first-degree relatives were identified by using the Inpatient Register.

    RESULTS: The risk of cholangitis was statistically significantly increased in offspring, siblings, and parents of the PSC patient cohort, compared with relatives of the comparison cohort, with the hazard ratios and 95% confidence intervals, 11.5 (1.6-84.4), 11.1 (3.3-37.8), and 2.3 (0.9-6.1), respectively. The hazard ratios for ulcerative colitis (UC) among first-degree relatives of all PSC patients was 3.3 (2.3-4.9) and for Crohn's disease 1.4 (0.8-2.5). The risk of UC for relatives of PSC patients without IBD was also increased, 7.4 (2.9-18.9).

    CONCLUSIONS: First-degree relatives of patients with PSC run an increased risk of PSC, indicating the importance of genetic factors in the etiology of PSC. First-degree relatives of PSC patients without IBD are also at an increased risk of UC, which might indicate shared genetic susceptibility factors for PSC and UC.

  • 10. Bhoo-Pathy, Nirmala
    et al.
    Uiterwaal, Cuno S. P. M.
    Dik, Vincent K.
    Jeurnink, Suzanne M.
    Bech, Bodil H.
    Overvad, Kim
    Halkjær, Jytte
    Tjønneland, Anne
    Boutron-Ruault, Marie-Christine
    Fagherazzi, Guy
    Racine, Antoine
    Katzke, Verena A.
    Li, Kuanrong
    Boeing, Heiner
    Floegel, Anna
    Androulidaki, Anna
    Bamia, Christina
    Trichopoulou, Antonia
    Masala, Giovanna
    Panico, Salvatore
    Crosignani, Paolo
    Tumino, Rosario
    Vineis, Paolo
    Peeters, Petra H. M.
    Gavrilyuk, Oxana
    Skeie, Guri
    Weiderpass, Elisabete
    Duell, Eric J.
    Arguelles, Marcial
    Molina-Montes, Esther
    Navarro, Carmen
    Ardanaz, Eva
    Dorronsoro, Miren
    Lindkvist, Björn
    Wallström, Peter
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Ye, Weimin
    Umeå universitet, Medicinska fakulteten, Enheten för biobanksforskning. Karolinska institutet.
    Khaw, Kay-Tee
    Wareham, Nick
    Key, Timothy J.
    Travis, Ruth C.
    Duarte-Salles, Talita
    Freisling, Heinz
    Licaj, Idlir
    Gallo, Valentina
    Michaud, Dominique S.
    Riboli, Elio
    Bueno-de-Mesquita, H. Bas
    Intake of Coffee, Decaffeinated Coffee, or Tea Does Not Affect Risk for Pancreatic Cancer: Results From the European Prospective Investigation into Nutrition and Cancer Study2013Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 11, nr 11, s. 1486-1492Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND & AIMS: Few modifiable risk factors have been implicated in the etiology of pancreatic cancer. There is little evidence for the effects of caffeinated coffee, decaffeinated coffee, or tea intake on risk of pancreatic cancer. We investigated the association of total coffee, caffeinated coffee, decaffeinated coffee, and tea consumption with risk of pancreatic cancer.

    METHODS: This study was conducted within the European Prospective Investigation into Nutrition and Cancer cohort, comprising male and female participants from 10 European countries. Between 1992 and 2000, there were 477,312 participants without cancer who completed a dietary questionnaire, and were followed up to determine pancreatic cancer incidence. Coffee and tea intake was calibrated with a 24-hour dietary recall. Adjusted hazard ratios (HRs) were computed using multivariable Cox regression.

    RESULTS: During a mean follow-up period of 11.6 y, 865 first incidences of pancreatic cancers were reported. When divided into fourths, neither total intake of coffee (HR, 1.03; 95% confidence interval [CI], 0.83-1.27; high vs low intake), decaffeinated coffee (HR, 1.12; 95% CI, 0.76-1.63; high vs low intake), nor tea were associated with risk of pancreatic cancer (HR, 1.22, 95% CI, 0.95-1.56; high vs low intake). Moderately low intake of caffeinated coffee was associated with an increased risk of pancreatic cancer (HR, 1.33; 95% CI, 1.02-1.74), compared with low intake. However, no graded dose response was observed, and the association attenuated after restriction to histologically confirmed pancreatic cancers.

    CONCLUSIONS: Based on an analysis of data from the European Prospective Investigation into Nutrition and Cancer cohort, total coffee, decaffeinated coffee, and tea consumption are not related to the risk of pancreatic cancer.

  • 11. Efe, Cumali
    et al.
    Hagström, Hannes
    Ytting, Henriette
    Bhanji, Rahima A.
    Müller, Niklas F.
    Wang, Qixia
    Purnak, Tugrul
    Muratori, Luigi
    Werner, Mårten
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Marschall, Hanns-Ulrich
    Muratori, Paolo
    Gunşar, Fulya
    Klintman, Daniel
    Parés, Albert
    Heurgué-Berlot, Alexandra
    Schiano, Thomas D.
    Cengiz, Mustafa
    Tana, Michele May-Sien
    Ma, Xiong
    Montano-Loza, Aldo J.
    Berg, Thomas
    Verma, Sumita
    Larsen, Fin Stolze
    Ozaslan, Ersan
    Heneghan, Michael A.
    Yoshida, Eric M.
    Wahlin, Staffan
    Efficacy and Safety of Mycophenolate Mofetil and Tacrolimus as Second-line Therapy for Patients With Autoimmune Hepatitis2017Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 15, nr 12, s. 1950-1956Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND & AIMS: Predniso(lo) ne, alone or in combination with azathioprine, is the standard-of-care (SOC) therapy for autoimmune hepatitis (AIH). However, the SOC therapy is poorly tolerated or does not control disease activity in up to 20% of patients. We assessed the efficacy of mycophenolate mofetil (MMF) and tacrolimus as second-line therapy for patients with AIH. METHODS: We performed a retrospective study of data (from 19 centers in Europe, the United States, Canada, and China) from 201 patients with AIH who received second-line therapy (121 received MMF and 80 received tacrolimus), for a median of 62 months (range, 6-190 mo). Patients were categorized according to their response to SOC. Patients in group 1 (n = 108) had a complete response to the SOC, but were switched to second-line therapy as a result of side effects of predniso(lo) ne or azathioprine, whereas patients in group 2 (n = 93) had not responded to SOC. RESULTS: There was no significant difference in the proportion of patients with a complete response to MMF (69.4%) vs tacrolimus (72.5%) (P = .639). In group 1, MMF and tacrolimus maintained a biochemical remission in 91.9% and 94.1% of patients, respectively (P = .682). Significantly more group 2 patients given tacrolimus compared with MMF had a complete response (56.5% vs 34%, respectively; P = .029) There were similar proportions of liver-related deaths or liver transplantation among patients given MMF (13.2%) vs tacrolimus (10.3%) (log-rank, P = .472). Ten patients receiving MMF (8.3%) and 10 patients receiving tacrolimus (12.5%) developed side effects that required therapy withdrawal. CONCLUSIONS: Long-term therapy with MMF or tacrolimus generally was well tolerated by patients with AIH. The agents were equally effective in previous complete responders who did not tolerate SOC therapy. Tacrolimus led to a complete response in a greater proportion of previous nonresponder patients compared with MMF.

  • 12.
    Elfström, Peter
    et al.
    Department of Neonatology, Astrid Lindgren Children's Hospital-Danderyd, Karolinska University Hospital, Stockholm, Sweden.
    Granath, Fredrik
    Clinical Epidemiology Unit, Department of Medicine, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
    Ye, Weimin
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Clinical Epidemiology Unit, Department of Medicine, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro, Sweden.
    Low Risk of Gastrointestinal Cancer Among Patients With Celiac Disease, Inflammation, or Latent Celiac Disease2012Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 10, nr 1, s. 30-36Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND & AIMS: Celiac disease has been associated with gastrointestinal (GI) cancers in small studies; risks have not been estimated from large populations or based on histopathology analyses.

    METHODS: We examined the risk of GI cancers by using data from cohorts of patients with celiac disease (villous atrophy, Marsh score of 3; n = 28,882) or inflammation (Marsh score of 1-2; n = 12,860); biopsy samples were evaluated at 28 pathology centers. A third cohort included 3705 individuals with latent celiac disease (normal mucosa, but positive serology results). Data were compared with those from an age-and sex-matched population.

    RESULTS: Of patients with celiac disease, 372 developed incident GI cancers; 347 patients with inflammation and 38 with latent celiac disease developed GI cancers. In the first year after diagnosis and initial biopsy, celiac disease was associated with 5.95-fold increase in risk of incident GI cancer (95% confidence interval [ CI], 4.64-7.64); the hazard ratio [HR] for inflammation was 9.13 (95% CI, 7.19-11.6) and for latent celiac disease was 8.10 (95% CI, 4.69-14.0). After the first year, patients were at no significant increase in risk for GI cancers; the HR for celiac disease was 1.07 (95% CI, 0.93-1.23), for inflammation it was 1.16 (95% CI, 0.98-1.37), and for latent celiac disease it was 0.96 (95% CI, 0.56-1.66). The absolute risk for any GI cancer in patients with celiac disease was 101/100,000 person-years, with an excess risk of 2/100,000 person-years.

    CONCLUSIONS: Although celiac disease, inflammation, and latent disease all increase risk for GI cancers in the first year after diagnosis, there is no increase in risk thereafter.

  • 13.
    Emilsson, Louise
    et al.
    Primary Care Res Unit Vårdctr Värmlands Nysäter, Värmland County, Karlstad, Sweden; Inst Hlth & Soc, Dept Hlth Management & Hlth Econ, Univ Oslo, Oslo, Norway.
    Wijmenga, Cisca
    Dept Genet, Univ Med Ctr Groningen, Univ Groningen, Groningen, Netherlands.
    Murray, Joseph A.
    Dept Internal Med, Div Gastroenterol & Hepatol, Mayo Clin, Rochester MN, USA.
    Ludvigsson, Jonas F.
    Region Örebro län. Dept Med Epidemiol & Biostat, Karolinska Inst, Stockholm, Sweden; Dept Pediat, Örebro University Hospital, Örebro, Sweden.
    Autoimmune Disease in First-Degree Relatives and Spouses of Individuals With Celiac Disease2015Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 13, nr 7, s. 1271-1277.e2Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND & AIMS: First-degree relatives of individuals with celiac disease are at increased risk for this disorder, but little is known about their risk for other autoimmune diseases. We assessed the risk of nonceliac autoimmune disease in first-degree relatives and spouses of people with celiac disease. METHODS: We identified individuals with celiac disease by searching computerized duodenal and jejunal biopsies, collected from 1969 through 2008, at 28 pathology departments in Sweden. Celiac disease was identified based on biopsy reports of villous atrophy (equal to Marsh grade 3; n = 29,096). Individuals with celiac disease were matched with up to 5 controls (people without celiac disease) for sex, age, county, and calendar year (total, 144,522 controls). Through Swedish health care registries, we identified all first-degree relatives (fathers, mothers, siblings, and offspring) and spouses of individuals with celiac disease (n = 84,648) and controls (n = 430,942). We used Cox regression analysis to calculate hazard ratios (HRs) for nonceliac autoimmune disease (Crohn's disease, type 1 diabetes mellitus, hypothyroidism, hyperthyroidism, psoriasis, rheumatoid arthritis, sarcoidosis, systemic lupus erythematosus, or ulcerative colitis) in these groups. RESULTS: During the follow-up period (median, 10.8 y), 3333 of the first-degree relatives of patients with celiac disease (3.9%) and 12,860 relatives of controls (3.0%) had an autoimmune disease other than celiac disease. First-degree relatives of people with celiac disease were at increased risk of nonceliac autoimmune disease, compared with controls (HR, 1.28; 95% confidence interval, 1.23-1.33), as were spouses (HR, 1.20; 95% confidence interval, 1.06-1.35). Risk estimates for nonceliac autoimmune disease did not differ between first-degree relatives and spouses of individuals with celiac disease (interaction test: P =.11). HRs for nonceliac autoimmune disease were highest in the first 2 years of follow-up evaluation. CONCLUSIONS: First-degree relatives and spouses of individuals with celiac disease are at increased risk of nonceliac autoimmune disease. In addition to genetic factors, environmental factors and ascertainment bias might contribute to the increased risk of autoimmunity in first-degree relatives of individuals with celiac disease.

  • 14.
    Flack, Kathryn F.
    et al.
    Icahn Sch Med Mt Sinai, Dept Internal Med, New York, NY 10029 USA..
    Desai, Jay
    Icahn Sch Med Mt Sinai, Dept Internal Med, New York, NY 10029 USA..
    Kolb, Jennifer M.
    Icahn Sch Med Mt Sinai, Dept Internal Med, New York, NY 10029 USA..
    Chatterjee, Prapti
    Icahn Sch Med Mt Sinai, Dept Internal Med, New York, NY 10029 USA..
    Wallentin, Lars C.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Ezekowitz, Michael
    Thomas Jefferson Univ, Sidney Kimmel Med Coll, Philadelphia, PA 19107 USA..
    Yusuf, Salim
    McMaster Univ, Populat Hlth Res Inst, Hamilton, ON, Canada.;Hamilton Hlth Sci, Hamilton, ON, Canada..
    Connolly, Stuart
    McMaster Univ, Populat Hlth Res Inst, Hamilton, ON, Canada.;Hamilton Hlth Sci, Hamilton, ON, Canada..
    Reilly, Paul
    Boehringer Ingelheim Pharmaceut, Ridgefield, CT USA..
    Brueckmann, Martina
    Boehringer Ingelheim GmbH & CoKG, Ingelheim, Germany.;Heidelberg Univ, Fac Med Mannheim, Mannheim, Germany..
    Ilgenfritz, John
    Ilgenfritz Consulting LLC, Conshohocken, PA USA..
    Aisenberg, James
    Icahn Sch Med Mt Sinai, Dept Internal Med, New York, NY 10029 USA..
    Major Gastrointestinal Bleeding Often Is Caused by Occult Malignancy in Patients Receiving Warfarin or Dabigatran to Prevent Stroke and Systemic Embolism From Atrial Fibrillation2017Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 15, nr 5, s. 682-690Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND & AIMS: Gastrointestinal (GI) bleeding in patients receiving anticoagulation agents can be caused by occult malignancies. We investigated the proportions and features of major GI bleeding (MGIB) events related to occult GI cancers in patients receiving anticoagulation therapy.

    METHODS: We analyzed data from the Randomized Evaluation of Long Term Anticoagulant Therapy study (conducted between December 2005 and March 2009 in 951 clinical centers in 44 countries worldwide), which compared the abilities of dabigatran vs warfarin to prevent stroke and systemic embolism in 18,113 patients with atrial fibrillation. Two blinded gastroenterologists independently reviewed source documents of MGIB events (n = 595) that occurred during the study period. We collected data on MGIB events caused by previously unidentified GI malignancies, and compared characteristics of MGIB events in patients who received dabigatran vs warfarin (primary end point), and in patients with bleeding from cancer, vs patients bleeding from a nonmalignant or unidentified source.

    RESULTS: Of 546 unique MGIB events, 44 (8.1%) were found to be from GI cancers (34 of 398 MGIB events in dabigatran users and 10 of 148 MGIB events in warfarin users; P = .60). Colorectal cancer accounted for 35 of 44 of all cancers identified. There were more colorectal cancer-associated MGIB events in the dabigatran group (30 of 34) than in the warfarin group (5 of 10) (P = .02), but more gastric cancer-associated MGIB events in the warfarin group (5 of 10) than in the dabigatran group (1 of 34) (P = .001). There were no differences in the short-term outcomes of cancer-related MGIB events in the dabigatran vs the warfarin group, but 75% of all cancer-related MGIB events required at least 1 blood transfusion and the mean hospital stay was 10.1 days. Compared with MGIB events from a nonmalignant or unidentified source, MGIB from cancer occurred sooner (343.0 vs 223.1 d; P = .003), but the bleeding was more likely to be chronic (for > 7 d) (27.3% vs 63.6%; P < .001).

    CONCLUSIONS: In evaluating data from a study of the effects of anticoagulation therapy, we found approximately 1 of every 12 MGIB events to be related to an occult cancer. Approximately two thirds of cancer-related MGIB presents with chronic bleeding, and morbidity, and resource utilization is high.

  • 15. Garcia-Etxebarria, Koldo
    et al.
    Zheng, Tenghao
    Bonfiglio, Ferdinando
    Bujanda, Luis
    Dlugosz, Aldona
    Lindberg, Greger
    Schmidt, Peter T.
    Karling, Pontus
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Ohlsson, Bodil
    Simren, Magnus
    Walter, Susanna
    Nardone, Gerardo
    Cuomo, Rosario
    Usai-Satta, Paolo
    Galeazzi, Francesca
    Neri, Matteo
    Portincasa, Piero
    Bellini, Massimo
    Barbara, Giovanni
    Jonkers, Daisy
    Eswaran, Shanti
    Chey, William D.
    Kashyap, Purna
    Chang, Lin
    Mayer, Emeran A.
    Wouters, Mira M.
    Boeckxstaens, Guy
    Camilleri, Michael
    Franke, Andre
    D'Amato, Mauro
    Increased Prevalence of Rare Sucrase-isomaltase Pathogenic Variants in Irritable Bowel Syndrome Patients2018Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 16, nr 10, s. 1673-1676Artikkel, forskningsoversikt (Fagfellevurdert)
  • 16.
    Garcia-Etxebarria, Koldo
    et al.
    Biodonostia Hlth Res Inst, Spain; Karolinska Inst, Sweden.
    Zheng, Tenghao
    Karolinska Inst, Sweden; Karolinska Inst, Sweden.
    Bonfiglio, Ferdinando
    Biodonostia Hlth Res Inst, Spain; Karolinska Inst, Sweden.
    Bujanda, Luis
    Biodonostia Hlth Res Inst, Spain; Univ Basque Country, Spain.
    Dlugosz, Aldona
    Karolinska Inst, Sweden.
    Lindberg, Greger
    Karolinska Inst, Sweden.
    Schmidt, Peter T.
    Univ Basque Country, Spain.
    Karling, Pontus
    Umea Univ, Sweden.
    Ohlsson, Bodil
    Lund Univ, Sweden.
    Simren, Magnus
    Univ Gothenburg, Sweden.
    Walter, Susanna
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Hjärt- och Medicincentrum, Magtarmmedicinska kliniken.
    Nardone, Gerardo
    University Federico II, Naples, Italy.
    Cuomo, Rosario
    Federico II Univ Hosp, Italy.
    Usai-Satta, Paolo
    Azienda Osped G Brotzu, Italy.
    Galeazzi, Francesca
    Padova Univ Hosp, Italy.
    Neri, Matteo
    G DAnnunzio Univ and Fdn, Italy.
    Portincasa, Piero
    G DAnnunzio Univ and Fdn, Italy.
    Bellini, Massimo
    Univ Bari, Italy.
    Barbara, Giovanni
    Univ Pisa, Italy.
    Jonkers, Daisy
    Univ Bologna, Italy.
    Eswaran, Shanti
    Univ Michigan, MI USA.
    Chey, William D.
    Univ Michigan, MI USA.
    Kashyap, Purna
    Mayo Clin, MN USA.
    Chang, Lin
    Univ Calif Los Angeles, CA 90095 USA.
    Mayer, Emeran A.
    Univ Calif Los Angeles, CA 90095 USA.
    Wouters, Mira M.
    Katholieke Univ Leuven, Belgium.
    Boeckxstaens, Guy
    Katholieke Univ Leuven, Belgium.
    Camilleri, Michael
    Mayo Clin, MN USA; Mayo Clin, MN USA.
    Franke, Andre
    Maastricht Univ, Netherlands; Christian Albrechts Univ Kiel, Germany.
    DAmato, Mauro
    Biodonostia Hlth Res Inst, Spain; Karolinska Inst, Sweden; Karolinska Inst, Sweden; Basque Sci Fdn, Spain.
    Increased Prevalence of Rare Sucrase-isomaltase Pathogenic Variants in Irritable Bowel Syndrome Patients2018Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 16, nr 10, s. 1673-1676Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    n/a

  • 17.
    Hagstrom, Hannes
    et al.
    Department of Upper GI, Karolinska University Hospital, Stockholm, Sweden; Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.
    Nasr, Patrik
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för kardiovaskulär medicin. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Hjärt- och Medicincentrum, Magtarmmedicinska kliniken.
    Ekstedt, Mattias
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för kardiovaskulär medicin. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Hjärt- och Medicincentrum, Magtarmmedicinska kliniken.
    Stål, Per
    Department of Upper GI, Karolinska University Hospital, Stockholm, Sweden; Department of Medicine, Huddinge, Karolinska Institutet, Stockholm, Sweden.
    Hultcrantz, Rolf
    Department of Upper GI, Karolinska University Hospital, Stockholm, Sweden; Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.
    Kechagias, Stergios
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för kardiovaskulär medicin. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Hjärt- och Medicincentrum, Magtarmmedicinska kliniken.
    Accuracy of Noninvasive Scoring Systems in Assessing Risk of Death and Liver-Related Endpoints in Patients With Nonalcoholic Fatty Liver Disease2019Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 17, nr 6, s. 1148-1156.e4Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background and Aims

    Several non-invasive scoring systems have been developed to determine risk of advanced fibrosis in non-alcoholic fatty liver disease (NAFLD). We examined the association between 4 scoring systems and incident severe liver disease and overall mortality in a large cohort of patients with biopsy-proven NAFLD.

    Methods

    We performed a retrospective analysis of data from 646 patients with biopsy-proven NAFLD, recruited from 2 hospitals in Sweden, from 1971 through 2009. The NAFLD fibrosis score (NFS), FIB-4, APRI, and BARD scores were calculated at the time of the liver biopsy. Based on each score, patients were assigned to categories of low, intermediate, or high risk for advanced fibrosis. Overall mortality and severe liver disease (cirrhosis, decompensated liver disease, liver failure, or hepatocellular carcinoma) were ascertained through linkage with national registers until the end of 2014. Cox regression, area under the receiver operating characteristic (AUROC) curve, and C-statistic analyses were used to study the predictive capacity of each scoring system.

    Results

    During a mean follow-up time of 19.9±8.7 years, there were 214 deaths and 76 cases of severe liver disease. For overall mortality, AUROC curve values were: NFS, 0.72 (95% CI, 0.68–0.76); FIB-4, 0.72 (95% CI, 0.68–0.76); BARD, 0.62 (95% CI, 0.58–0.66); and APRI, 0.52 (95% CI, 0.47–0.57). For severe liver disease, AUROC curve values were: NFS, 0.72 (95% CI, 0.66–0.78); FIB-4, 0.72 (95% CI, 0.66–0.79); BARD, 0.62 (95% CI, 0.55–0.69); APRI, 0.69 (95% CI, 0.63–0.76). C-statistics for all scores were of moderate capacity to predict outcomes.

    Conclusions

    In a retrospective analysis of data from 646 patients with biopsy-proven NAFLD, we found the NFS and the FIB-4 scores to most accurately determine risk of overall death or severe liver disease. However, the AUROC values for these scoring systems are not high enough for use in the clinic; new systems are needed to determine prognoses of patients with NAFLD.

  • 18.
    Hirten, Robert P.
    et al.
    The Dr. Henry D. Janowitz Division of Gastroenterology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
    Lakatos, Peter L.
    Division of Gastroenterology, McGill University Health Centre Montreal Canada; 1st Department of Medicine Semmelweis University Budapest, Hungary.
    Halfvarson, Jonas
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Gastroenterology.
    Colombel, Jean Frederic
    The Dr. Henry D. Janowitz Division of Gastroenterology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
    A Users Guide to De-escalating Immunomodulator and Biologic Therapy in Inflammatory Bowel Disease2019Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    De-escalation of immunomodulators and biologic agents in inflammatory bowel disease is frequently discussed with patients and must weigh the risk of continued medical therapy with the risk of disease recurrence. Risk factors for disease flare after withdrawal of inflammatory bowel disease medications such as disease activity at de-escalation, disease prognostic features and prior course of disease have been identified predominately in retrospective studies allowing for risk stratification of patients. This review evaluates the published literature regarding therapeutic de-escalation and provides a framework for physicians to apply this to clinical practice. Prospective trials are underway and planned which should provide further insight into this treatment paradigm and better inform patient selection for this strategy.

  • 19. Jansson, C
    et al.
    Nordenstedt, H
    Johansson, Saga
    Wallander, Mari-Ann
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Allmänmedicin och klinisk epidemiologi.
    Johnsen, R
    Hveem, K
    Lagergren, J
    Relation between gastroesophageal reflux symptoms and socioeconomic factors: a population-based study (the HUNT Study)2007Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 5, nr 9, s. 1029-1034Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND & AIMS: Gastroesophageal reflux constitutes a major public health problem in the Western world. Few population-based studies have addressed socioeconomic factors in relation to reflux. METHODS: We conducted a case-control study based on 2 health surveys performed in the Norwegian county of Nord-Trondelag in 1984-1986 and 1995-1997, respectively. Reflux was assessed in the second survey, comprising 65,333 participants representing 70% of the county's adult population. Among 58,596 persons responding to questions regarding reflux symptoms, 3153 persons reporting severe symptoms represented the cases, and 40,210 persons without symptoms represented the controls. Data collected in questionnaires included socioeconomic status (SES) based on occupation, education, and material deprivation; family situation; and potential confounders. Odds ratios (ORs) with 95% confidence intervals (CIs) were estimated from unconditional logistic regression in crude models and models adjusted for age, sex, smoking, and body mass. RESULTS: The risk of reflux increased with decreasing levels of SES based on occupation, education, and material deprivation. Increased risks of reflux were seen among unskilled laborers (OR, 1.6; 95% CI, 1.3-2.0), skilled laborers (OR, 1.4; 95% CI, 1.1-1.7), and self-employed and farmers (OR, 1.3; 95% CI, 1.1-1.6). A 1.9-fold (95% CI, 1.7-2.2) increased risk of reflux was observed among persons with low education, compared with highly educated persons. Reflux was more common among materially deprived persons (OR, 3.4; 95% CI, 2.9-4.1). The results were similar in crude and adjusted models. CONCLUSIONS: This large population-based study reveals a link between low SES and reflux symptoms that is not explained by the known risk factors of smoking or obesity. This finding deserves further research.

  • 20. Jansson, Catarina
    et al.
    Nordenstedt, Helena
    Wallander, Mari-Ann
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Allmänmedicin och klinisk epidemiologi.
    Johansson, Saga
    Johnsen, Roar
    Hveem, Kristian
    Lagergren, Jesper
    A population-based study showing an association between gastroesophageal reflux disease and sleep problems2009Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 7, nr 9, s. 960-965Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND & AIMS: Gastroesophageal reflux disease and sleep problems are common health problems in Western nations. It is important to clarify the association between sleep and gastroesophageal reflux disease, but only a few population-based studies have been conducted. METHODS: A population-based, cross-sectional, case-control study was based on 2 large health surveys performed in the Norwegian county Nord-Trondelag in 1984-1986 and 1995-1997. Gastroesophageal reflux disease was assessed in the second survey, which included 65,333 participants (70% of the county's adult population). The 3153 persons who reported severe reflux symptoms constituted the cases, and the 40,210 persons without reflux symptoms constituted the controls. Data on insomnia, sleep problems, and several potential confounders were collected in questionnaires. Odds ratios (ORs) with 95% confidence intervals (CIs) were estimated by using unconditional logistic regression in crude and multivariable models. RESULTS: In models adjusted for age, sex, tobacco smoking, obesity, and socioeconomic status, positive associations were observed between presence of insomnia (OR, 3.2; 95% CI, 2.7-3.7), sleeplessness (OR, 3.3; 95% CI, 2.9-3.8), problems falling asleep (OR, 3.1; 95% CI, 2.5-3.8), and risk of gastroesophageal reflux disease. These associations were attenuated after further adjustments for anxiety, depression, myocardial infarction, angina pectoris, stroke, and gastrointestinal symptoms, but they remained statistically significant. CONCLUSIONS: A large population-based study indicated a link between sleep problems and gastroesophageal reflux disease that might be bidirectional.

  • 21.
    Jarbrink-Sehgal, M. Ellionore
    et al.
    Dept Med, Solna, Sweden;Baylor Coll Med, Digest Dis Ctr, Michael E DeBakey VA Med Ctr, Houston, TX 77030 USA.
    Schmidt, Peter T.
    Karolinska Univ Hosp, Ctr Digest Dis, Stockholm, Sweden;Dept Med, Solna, Sweden.
    Sköldberg, Filip
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Gastrointestinalkirurgi.
    Hemmingsson, Tomas
    Karolinska Inst, Inst Environm Med, Stockholm, Sweden;Stockholm Univ, Dept Publ Hlth Sci, Stockholm, Sweden.
    Hagstrom, Hannes
    Karolinska Univ Hosp, Ctr Digest Dis, Stockholm, Sweden.
    Andreasson, Anna
    Dept Med, Solna, Sweden;Macquarie Univ, Dept Psychol, N Ryde, NSW, Australia;Stockholm Univ, Stress Res Inst, Stockholm, Sweden.
    Lifestyle Factors in Late Adolescence Associate With Later Development of Diverticular Disease Requiring Hospitalization2018Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 16, nr 9, s. 1474-+Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND & AIMS: The burden of diverticular disease on society is high and is increasing with an aging population. It is therefore important to identify risk factors for disease development or progression. Many lifestyle behaviors during adolescence affect risk for later disease. We searched for adolescent lifestyle factors that affect risk of diverticular disease later in life. METHODS: We performed a retrospective analysis of data from 43,772 men (age, 18-20 y) conscripted to military service in Sweden from 1969 through 1970, with a follow-up period of 39 years. All conscripts underwent an extensive mental and physical health examination and completed questionnaires covering alcohol consumption, smoking, and use of recreational drugs; cardiovascular fitness was assessed using an ergometer cycle at the time of conscription. Outcome data were collected from national registers to identify discharge diagnoses of diverticular disease until the end of 2009. We performed Cox regression analysis to determine whether body mass index, cardiovascular fitness, smoking, use of recreational drugs, alcohol consumption, and risky use of alcohol, at time of conscription are independent risk factors for development of diverticular disease. RESULTS: Overweight and obese men had a 2-fold increased risk of diverticular disease compared to normal-weight men (hazard ratio, 2.00; P < .001). A high level of cardiovascular fitness was associated with a reduced risk of diverticular disease requiring hospitalization (P = .009). Smoking (P = .003), but not use of recreational drugs (P = .11), was associated with an increased risk of diverticular disease requiring hospitalization. Risky use of alcohol, but not alcohol consumption per se, was associated with a 43% increase in risk of diverticular disease requiring hospitalization (P = .007). CONCLUSIONS: In a retrospective analysis of data from 43,772 men in Sweden, we associated being overweight or obese, a smoker, a high-risk user of alcohol, and/or having a low level of cardiovascular fitness in late adolescence with an increased risk of developing diverticular disease requiring hospitalization later in life. Improving lifestyle factors among adolescents might reduce the economic burden of diverticular disease decades later.

  • 22.
    Jones, Michael P.
    et al.
    Macquarie Univ, Australia.
    Olsen Faresjö, Åshild
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för samhällsmedicin. Linköpings universitet, Medicinska fakulteten.
    Beath, Alissa
    Macquarie Univ, Australia.
    Faresjö, Tomas
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för samhällsmedicin. Linköpings universitet, Medicinska fakulteten.
    Ludvigsson, Johnny
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för barns och kvinnors hälsa. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Barn- och kvinnocentrum, H.K.H. Kronprinsessan Victorias barn- och ungdomssjukhus Linköping/Motala.
    Abdominal Pain in Children Develops With Age and Increases With Psychosocial Factors2020Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 18, nr 2, s. 360-+Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND amp; AIMS: Functional gastrointestinal disorders are highly prevalent, cause significant suffering, and are costly to society. Pain is a central feature of 2 of the most common functional gastrointestinal disorders: irritable bowel syndrome and functional dyspepsia. Although these disorders have been well studied in adults, their etiology is poorly understood. We sought to identify early life factors associated with the development of abdominal pain in children (age, 2-12 y). METHODS: We collected data from the All Babies in Southeast Sweden study of 1781 children, born from October 1, 1997, through October 31, 1999, whose families answered questions about abdominal pain and risk factors at birth, 1 year, 2.5 years, 5 years, 8 years, and 10 to 12 years. We used latent growth curve models to evaluate risk factors for development of abdominal pain. The primary outcomes were prevalence of abdominal pain and associated factors. RESULTS: The prevalence of abdominal pain increased linearly with age in the study cohort, increasing by approximately 6% per year. Psychosocial variables associated with slope of the growth curve included lower emotional control at age 2 years (P = .005), parental concern for the child at age 2 years (P = .02), and measures of parental stress (P = .004). Nonvaginal birth was associated with a reduced slope of the growth curve (P = .03). CONCLUSIONS: In a study of children in Sweden, we found early psychosocial environment and mode of delivery at birth was associated with development of childhood abdominal pain. Factors associated with development of the early immune system, identified in previous recall-based research, were not supported by data from this study. These findings have important implications for the prevention of abdominal pain in children and later in life.

  • 23. Järbrink-Sehgal, M. Ellionore
    et al.
    Andreasson, Anna
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Talley, Nicholas J.
    Agréus, Lars
    Song, Jeong-Yeop
    Schmidt, Peter T.
    Symptomatic Diverticulosis Is Characterized By Loose Stools2016Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 14, nr 12, s. 1763-1770Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND & AIMS: Symptomatic uncomplicated diverticular disease is considered to be a discreet clinical entity distinct from irritable bowel syndrome (IBS), but population-based data are unavailable. We aimed to investigate the prevalence and location of diverticulosis in the general population, and its association with colonic symptoms and mental health. We propose that individuals with diverticulosis would report more constipation and IBS.

    METHODS: We performed a population-based study of randomly selected adults born in Sweden (age, 18-70 y; 57.2% women); 745 received a gastroenterology consultation, completed validated abdominal symptom and mental health questionnaires, and were examined by colonoscopy. Logistic regression was used to calculate the associations between diverticulosis and age, sex, gastrointestinal symptoms, anxiety, depression, and self-rated health.

    RESULTS: Among the 742 participants (54.6% women), 130 (17.5%) had diverticulosis. Age was the strongest predictor of diverticulosis (P < .001), and diverticulosis was rare in participants younger than 40 years (0.7%). All participants with diverticulosis had sigmoid involvement. Participants with diverticulosis were more likely to report loose stools (odds ratio [OR], 1.88; 95% confidence interval [CI], 1.20-2.96), urgency (OR, 1.64; 95% CI, 1.02-2.63), passing mucus (OR, 2.26; 95% CI, 1.08-4.72), and a high stool frequency (OR, 2.02; 95% CI, 1.11-3.65). Diverticulosis was associated with abdominal pain (OR, 2.10; 95% CI, 1.01-4.36; P = .047) and diarrhea-predominant IBS (OR, 9.55; 95% CI, 1.08-84.08; P = .04) in participants older than 60 years. The presence of anxiety and depression and self-rated health were similar in participants with and without diverticulosis.

    CONCLUSIONS: The prevalence of diverticulosis is age-dependent. Diverticulosis is associated with diarrhea in subjects across all age ranges. In subjects older than age 60, diverticulosis is associated with abdominal pain and diarrhea-predominant IBS.

  • 24. Järbrink-Sehgal, M. Ellionore
    et al.
    Schmidt, Peter T.
    Sköldberg, Filip
    Hemmingsson, Tomas
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Institutionen för folkhälsovetenskap. Karolinska Institutet, Sweden.
    Hagström, Hannes
    Andreasson, Anna
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden; Macquarie University, Australia.
    Lifestyle Factors in Late Adolescence Associate With Later Development of Diverticular Disease Requiring Hospitalization2018Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 16, nr 9, s. 1474-1480Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND & AIMS: The burden of diverticular disease on society is high and is increasing with an aging population. It is therefore important to identify risk factors for disease development or progression. Many lifestyle behaviors during adolescence affect risk for later disease. We searched for adolescent lifestyle factors that affect risk of diverticular disease later in life. METHODS: We performed a retrospective analysis of data from 43,772 men (age, 18-20 y) conscripted to military service in Sweden from 1969 through 1970, with a follow-up period of 39 years. All conscripts underwent an extensive mental and physical health examination and completed questionnaires covering alcohol consumption, smoking, and use of recreational drugs; cardiovascular fitness was assessed using an ergometer cycle at the time of conscription. Outcome data were collected from national registers to identify discharge diagnoses of diverticular disease until the end of 2009. We performed Cox regression analysis to determine whether body mass index, cardiovascular fitness, smoking, use of recreational drugs, alcohol consumption, and risky use of alcohol, at time of conscription are independent risk factors for development of diverticular disease. RESULTS: Overweight and obese men had a 2-fold increased risk of diverticular disease compared to normal-weight men (hazard ratio, 2.00; P < .001). A high level of cardiovascular fitness was associated with a reduced risk of diverticular disease requiring hospitalization (P = .009). Smoking (P = .003), but not use of recreational drugs (P = .11), was associated with an increased risk of diverticular disease requiring hospitalization. Risky use of alcohol, but not alcohol consumption per se, was associated with a 43% increase in risk of diverticular disease requiring hospitalization (P = .007). CONCLUSIONS: In a retrospective analysis of data from 43,772 men in Sweden, we associated being overweight or obese, a smoker, a high-risk user of alcohol, and/or having a low level of cardiovascular fitness in late adolescence with an increased risk of developing diverticular disease requiring hospitalization later in life. Improving lifestyle factors among adolescents might reduce the economic burden of diverticular disease decades later.

  • 25.
    Khalili, Hamed
    et al.
    Gastroenterology Unit, Massachusetts General Hospital, Harvard Medical School, Boston, USA; Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Hakansson, Niclas
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Chan, Simon S.
    Department of Medicine, Norwich Medical School, University of East Anglia, Norwich, United Kingdom; Department of Gastroenterology, Norfolk and Norwich University Hospital NHS Trust, Norwich, United Kingdom.
    Ludvigsson, Jonas F.
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län. Department of Pediatrics.
    Olen, Ola
    Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden; Pediatric Gastroenterology and Nutrition Unit, Sachs’ Children’s Hospital, Stockholm, Sweden.
    Chan, Andrew T.
    Gastroenterology Unit, Massachusetts General Hospital, Harvard Medical School, Boston, USA; Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Harvard Medical School, Boston, USA.
    Hart, Andrew R.
    Department of Medicine, Norwich Medical School, University of East Anglia, Norwich, United Kingdom; Department of Gastroenterology, Norfolk and Norwich University Hospital NHS Trust, Norwich, United Kingdom.
    Wolk, Alicja
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Surgical Sciences, Uppsala University, Uppsala, Sweden.
    No Association Between Consumption of Sweetened Beverages and Later Risk of Crohn's Disease or Ulcerative Colitis2019Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 17, nr 1, s. 123-129Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND & AIMS: Consumption of sweetened beverages has been associated with inflammation, based on measurements of C-reactive protein and tumor necrosis factor, as well as immune-mediated disorders including rheumatoid arthritis. We investigated associations with Crohn's disease (CD) or ulcerative colitis (UC).

    METHODS: We conducted a prospective cohort study of 83,042 participants (44-83 years old) enrolled in the Cohort of Swedish Men or the Swedish Mammography Study. Dietary and lifestyle data were collected using a validated food frequency questionnaire at baseline in 1997. Diagnoses of CD and UC were ascertained from the Swedish Patient Register. We used Cox proportional hazards modeling to calculate hazard ratios (HR) and 95% CIs.

    RESULTS: Through December of 2014, we confirmed 143 incident cases of CD (incidence; rate = 11 cases/100,000 person-years) and 349 incident cases of UC (incidence rate = 28 cases/100,000 person-years) over 1,264,345 person-years of follow up. Consumption of sweetened beverages was not associated with increased risk of CD (Ptrend = 0.34) or UC (Ptrend = 0.40). Compared to participants who reported no consumption of sweetened beverages, the multivariable-adjusted HRs for 1 or more servings per day were 1.02 for CD (95% CI, 0.60-1.73) and 1.14 for UC (95% CI, 0.83-1.57). The association between consumption of sugar-sweetened beverages and risk of CD or UC were not modified by age, sex (cohort), body mass index, or smoking (all Pinteraction ≥ 0.12).

    CONCLUSION: In analyses of data from 2 large prospective cohort studies from Sweden, we observed no evidence for associations between consumption of sweetened beverages and later risk of CD or UC.

  • 26. Khalili, Hamed
    et al.
    Hakansson, Niclas
    Chan, Simon S
    Ludvigsson, Jonas F
    Olen, Ola
    Chan, Andrew T
    Hart, Andrew R
    Wolk, Alicja
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    No Association Between Consumption of Sweetened Beverages and Risk of Later-Onset Crohn's Disease or Ulcerative Colitis.2019Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 17, nr 1, s. 123-129Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND & AIMS: Consumption of sweetened beverages has been associated with inflammation based on measurements of C-reactive protein and tumor necrosis factor, as well as immune-mediated disorders including rheumatoid arthritis. We investigated associations with Crohn's disease (CD) or ulcerative colitis (UC).

    METHODS: We conducted a prospective cohort study of 83,042 participants (age, 44-83 y) enrolled in the Cohort of Swedish Men or the Swedish Mammography Study. Dietary and lifestyle data were collected using a validated food frequency questionnaire at baseline in 1997. Diagnoses of CD and UC were ascertained from the Swedish Patient Register. We used Cox proportional hazards modeling to calculate hazard ratios and 95% CIs.

    RESULTS: Through December of 2014, we confirmed 143 incident cases of CD (incidence rate, 11 cases/100,000 person-years) and 349 incident cases of UC (incidence rate, 28 cases/100,000 person-years) over 1,264,345 person-years of follow-up evaluation. Consumption of sweetened beverages was not associated with increased risk of CD (Ptrend = .34) or UC (Ptrend = .40). Compared with participants who reported no consumption of sweetened beverages, the multivariable-adjusted hazard ratios for 1 or more servings per day were 1.02 for CD (95% CI, 0.60-1.73) and 1.14 for UC (95% CI, 0.83-1.57). The association between consumption of sugar-sweetened beverages and risk of CD or UC were not modified by age, sex (cohort), body mass index, or smoking (all Pinteraction ≥ .12).

    CONCLUSIONS: In analyses of data from 2 large prospective cohort studies from Sweden, we observed no evidence for associations between consumption of sweetened beverages and later risk of CD or UC.

  • 27.
    Khalili, Hamed
    et al.
    Harvard Med Sch, Gastroenterol Unit, Clin & Translat Epidemiol Unit, Massachusetts Gen Hosp, Boston, MA 02115 USA;Karolinska Inst, Clin Epidemiol Unit, Dept Med Solna, Inst Environm Med, Stockholm, Sweden.
    Wolk, Alicja
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi. Karolinska Inst, Dept Med Epidemiol & Biostat, Inst Environm Med, Stockholm, Sweden.
    Reply to: The Association Between Consumption of Sweetened Beverages and the Risk of Inflammatory Bowel Disease2018Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 16, nr 10, s. 1682-1682Artikkel i tidsskrift (Annet vitenskapelig)
  • 28. Lalouni, Maria
    et al.
    Ljótsson, Brjánn
    Bonnert, Marianne
    Ssegonja, Richard
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Socialmedicin/CHAP.
    Benninga, Marc
    Bjureberg, Johan
    Högström, Jens
    Sahlin, Hanna
    Simrén, Magnus
    Feldman, Inna
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Socialmedicin/CHAP.
    Hedman-Lagerlöf, Erik
    Serlachius, Eva
    Olén, Ola
    Clinical and Cost Effectiveness of Online Cognitive Behavioral Therapy in Children with Functional Abdominal Pain Disorders2019Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 17, nr 11, s. 2236-2244Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND & AIMS: Scalable and effective treatments are needed for children with functional abdominal pain disorders (FAPDs). We performed a randomized controlled trial of the efficacy and cost effectiveness of cognitive behavioral therapy delivered online (internet CBT) compared to usual therapy.

    METHODS: We studied children (8-12 years old) diagnosed with FAPDs, based on the Rome IV criteria, in Sweden from September 2016 through April 2017. The patients were randomly assigned to groups that received 10 weeks of therapist-guided, internet-delivered cognitive behavioral therapy (internet CBT, n=46) or usual treatment (treatments within the healthcare and school systems, including medications and visits to doctors and other healthcare professionals; n=44). The primary outcome was Global child-rated gastrointestinal symptom severity assessed using the Pediatric Quality of Life Gastrointestinal Symptom scale. All outcomes were collected from September 2016 through January 2018. Secondary outcomes included quality of life, gastrointestinal-specific anxiety, avoidance behaviors, and parental responses to children's symptoms. Societal costs and costs for healthcare consumption were collected during the treatment.

    RESULTS: Children who received internet CBT had a significantly larger improvement in gastrointestinal symptom severity with a medium effect size (Cohen's d=0.46; 95% CI, 0.05-0.88; number needed to treat, 3.8) compared with children who received the usual treatment. The children's quality of life, gastrointestinal-specific anxiety, avoidance behaviors, and parental responses to children's symptoms also improved significantly in the internet CBT group compared with the usual treatment group. The effects of internet CBT persisted through 36 weeks of follow up. Children who received internet CBT had significantly less healthcare use than children who received usual treatment, with an average cost difference of US $137 (P=.011). We calculated a cost saving of US $1050 for every child treated with internet CBT compared with usual treatment.

    CONCLUSION: In a randomized trial of pediatric patients with FAPDs, we found internet CBT to be clinically and cost effective compared with usual treatment. Internet CBT has the potential to increase the availability of treatment for a number of patients and reduce healthcare costs. ClinicalTrials.gov no.: NCT02873078.

  • 29.
    Laszkowska, Monika
    et al.
    Celiac Disease Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York NY, USA.
    Shiwani, Henna
    Celiac Disease Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York NY, USA.
    Belluz, Julia
    Vox Media, Washington DC, USA.
    Ludvigsson, Jonas F.
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län. Celiac Disease Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York NY, USA; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro, Sweden; Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham, United Kingdom.
    Green, Peter H. R.
    Celiac Disease Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York NY, USA.
    Sheehan, Daniel
    Carto, New York, USA.
    Rundle, Andrew
    Department of Epidemiology, Mailman School of Public Health, Columbia University, New York NY, USA.
    Lebwohl, Benjamin
    Celiac Disease Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York NY, USA; Department of Epidemiology, Mailman School of Public Health, Columbia University, New York NY, USA.
    Socioeconomic vs Health-related Factors Associated With Google Searches for Gluten-Free Diet2018Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 16, nr 2, s. 295-297Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    In a systematic review and meta-analysis, we found risk of major GI bleeding to be similar between NOACs and conventional anticoagulation. Dabigatran and rivaroxaban, however, may be associated with increased odds of major GI bleeding. Further high-quality studies are needed to characterize GI bleeding risk among NOACs.

  • 30.
    Le Nevé, Boris
    et al.
    Danone Nutricia Research, Life Sciences Department, Palaiseau, France.
    Brazeilles, Rémi
    Danone Nutricia Research, Life Sciences Department, Palaiseau, France.
    Derrien, Muriel
    Danone Nutricia Research, Life Sciences Department, Palaiseau, France.
    Tap, Julien
    Danone Nutricia Research, Life Sciences Department, Palaiseau, France / INRA (Institut National de la Recherche Agronomique) MetaGenoPolis, Jouy en Josas, France.
    Guyonnet, Denis
    Danone Nutricia Research, Life Sciences Department, Palaiseau, France.
    Öhman, Lena
    Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Törnblom, Hans
    Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, 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.
    Lactulose Challenge Determines Visceral Sensitivity and Severity of Symptoms in Patients With Irritable Bowel Syndrome2016Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 14, nr 2, s. 226.e1-233.e3Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND & AIMS: Patients with irritable bowel syndrome (IBS) can be assigned to groups with different gastrointestinal (GI) symptoms based on results from a combined nutrient and lactulose challenge. We aimed to identify factors that predict outcomes to this challenge and to determine whether this can be used in noninvasive assessment of visceral sensitivity in patients with IBS.

    METHODS: We performed a prospective study of 100 patients with IBS diagnosed according to Rome III criteria (all subtypes) and seen at a secondary or tertiary care center. After an overnight fast, subjects were given a liquid breakfast (400 mL; Nutridrink) that contained 25 g lactulose. Before the challenge, we assessed visceral sensitivity (via rectal barostat), oro-anal transit time, and fecal microbiota composition (via 16S ribosomal RNA pyrosequencing); we determined IBS severity using questionnaires. The intensity of 8 GI symptoms, the level of digestive comfort, and the amount of exhaled H2 and CH4 in breath were measured before and during a 4-hour period after the liquid breakfast.

    RESULTS: Based on the intensity of 8 GI symptoms and level of digestive comfort during the challenge, patients were assigned to groups with high-intensity GI symptoms (HGS; n = 39) or low-intensity GI symptoms (LGS; n = 61); patients with HGS had more severe IBS (P < .0001), higher somatization (P < .01), and lower quality of life (P < .05-.01) than patients with LGS. Patients with HGS also had significantly higher rectal sensitivity to random phasic distensions (P < .05-.001, compared with patients with LGS). There were no significant differences between groups in fecal microbiota composition, exhaled gas in breath, or oro-anal transit time.

    CONCLUSIONS: We found, in a prospective study, that results from a lactulose challenge test could be used to determine visceral sensitivity and severity of IBS. The intensity of patient symptoms did not correlate with the composition of the fecal microbiota. The lactulose challenge test may help better characterize patients with IBS and evaluate the efficacy of new treatments. ClinicalTrial.gov no: NCT01252550.

  • 31.
    Lebwohl, Benjamin
    et al.
    Celiac Disease Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York NY, United States; Department of Epidemiology, Mailman School of Public Health, Columbia University, New York NY, United States.
    Ludvigsson, Jonas F.
    Region Örebro län. Medical Epidemiology and Biostatistics Unit, Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro, Sweden.
    Green, Peter H. R.
    Celiac Disease Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York NY, United States.
    The Unfolding Story of Celiac Disease Risk Factors2014Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 12, nr 4, s. 632-635Artikkel i tidsskrift (Fagfellevurdert)
  • 32.
    Lebwohl, Benjamin
    et al.
    Celiac Disease Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York NY, United States; Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden.
    Stephansson, Olof
    Clinical Epidemiology Unit, Department of Medicine, Solna, Karolinska Institute, Stockholm, Sweden; Division of Obstetrics and Gynecology, Department of Women's and Children's Health, Karolinska Institute, Stockholm, Sweden.
    Green, Peter H. R.
    Celiac Disease Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York NY, United States; Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Region Örebro län. Celiac Disease Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York NY, United States; Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro, Sweden.
    Mucosal Healing in Patients With Celiac Disease and Outcomes of Pregnancy: A Nationwide Population-Based Study2015Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 13, nr 6, s. 1111-1117.e2Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND & AIMS: Studies have associated undiagnosed celiac disease with adverse outcomes of pregnancy. We investigated the association between persistent villous atrophy and outcomes of pregnancy in women with celiac disease.

    METHODS: We collected data on 337 women with celiac disease who gave birth (to 460 infants) within 5 years of a follow-up biopsy, from 28 pathology departments in Sweden. We compared birth outcomes from women whose follow-up biopsy showed persistent villous atrophy (Marsh score, 3; n = 142; 31% of study population) with those of women with mucosal recovery (n = 318; 69%). We used multivariable logistic regression (adjusted for maternal age, parity, country of birth, smoking, infant sex, and calendar year of birth) to evaluate the association between persistent villous atrophy and pregnancy outcomes.

    RESULTS: Intrauterine growth restriction occurred during 3.5% of pregnancies in women with persistent villous atrophy vs 3.8% of those with mucosal healing (adjusted odds ratio [OR], 0.61; 95% confidence interval [CI], 0.19-1.99). There was no significant association between persistent villous atrophy and low birth weight (OR, 0.98; 95% CI, 0.41-2.39), preterm birth (OR, 1.66; 95% CI, 0.72-3.83), or cesarean section (OR, 0.86; 95% CI, 0.51-1.46).

    CONCLUSIONS: Although undiagnosed celiac disease has been associated with adverse outcomes of pregnancy, we found no evidence from a nationwide population-based study that persistent villous atrophy, based on analysis of follow-up biopsies, increases risk compared with mucosal healing.

  • 33. Leufkens, Anke M
    et al.
    Van Duijnhoven, Fränzel J B
    Siersema, Peter D
    Boshuizen, Hendriek C
    Vrieling, Alina
    Agudo, Antonio
    Gram, Inger T
    Weiderpass, Elisabete
    Dahm, Christina
    Overvad, Kim
    Tjønneland, Anne
    Olsen, Anja
    Boutron-Ruault, Marie-Christine
    Clavel-Chapelon, Françoise
    Morois, Sophie
    Palli, Domenico
    Grioni, Sara
    Tumino, Rosario
    Sacerdote, Charlotta
    Mattiello, Amalia
    Herman, Silke
    Kaaks, Rudolf
    Steffen, Annika
    Boeing, Heiner
    Trichopoulou, Antonia
    Lagiou, Pagona
    Trichopoulos, Dimitrios
    Peeters, Petra H
    van Gils, Carla H
    van Kranen, Henk
    Lund, Eliv
    Dumeaux, Vanessa
    Engeset, Dagrun
    Rodríguez, Laudina
    Sánchez, Maria-José
    Chirlaque, Maria-Dolores
    Barricarte, Aurelio
    Manjer, Jonas
    Almquist, Martin
    van Guelpen, Bethany
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Patologi.
    Hallmans, Göran
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Näringsforskning.
    Khaw, Kay-Tee
    Wareham, Nick
    Tsilidis, Konstantinos K
    Straif, Kurt
    Leon-Roux, Maria
    Vineis, Paul
    Norat, Teresa
    Riboli, Elio
    Bueno-de-Mesquita, H Bas
    Cigarette smoking and colorectal cancer risk in the European prospective investigation into cancer and nutrition study2011Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 9, nr 2, s. 137-144Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Ever smokers have an increased risk of colon cancer, which appeared to be more pronounced in the proximal than the distal colon location.

  • 34.
    Liu, Po-Hong
    et al.
    Clinical and Translational Epidemiology Unit, Massachusetts General Hospital and Harvard Medical School, Boston Massachusetts, USA.
    Burke, Kristin E.
    Clinical and Translational Epidemiology Unit, Massachusetts General Hospital and Harvard Medical School, Boston Massachusetts, USA; Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston Massachusetts, USA.
    Ananthakrishnan, Ashwin N.
    Clinical and Translational Epidemiology Unit, Massachusetts General Hospital and Harvard Medical School, Boston Massachusetts, USA; Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston Massachusetts, USA.
    Lochhead, Paul
    Clinical and Translational Epidemiology Unit, Massachusetts General Hospital and Harvard Medical School, Boston Massachusetts, USA; Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston Massachusetts, USA.
    Olen, Ola
    Department of Medicine, Clinical Epidemiology Unit, 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 University, Örebro, Sweden.
    Richter, James M.
    Clinical and Translational Epidemiology Unit, Massachusetts General Hospital and Harvard Medical School, Boston Massachusetts, USA; Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston Massachusetts, USA.
    Chan, Andrew T.
    Clinical and Translational Epidemiology Unit, Massachusetts General Hospital and Harvard Medical School, Boston Massachusetts, USA; Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston Massachusetts, USA; Broad Institute of Massachusetts Institute of Technology and Harvard, Cambridge, Massachusetts, USA; Department of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Massachusetts, USA; Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston Massachusetts, USA.
    Khalili, Hamed
    Clinical and Translational Epidemiology Unit, Massachusetts General Hospital and Harvard Medical School, Boston Massachusetts, USA; Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston Massachusetts, USA; Department of Medicine, Clinical Epidemiology Unit, Karolinska Institutet, Stockholm, Sweden.
    Obesity and Weight Gain Since Early Adulthood Are Associated With a Lower Risk of Microscopic Colitis2019Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 17, nr 12, s. 2523-2532Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND & AIMS: Obesity promotes intestinal inflammation and might contribute to the pathogenesis of inflammatory bowel disease. We examined the association between obesity and risk of microscopic colitis in a prospective cohort study.

    METHODS: We collected data from 192,101 women enrolled in the Nurses' Health Study (NHS) (from 1986 through 2014) or the NHSII (from 1991 through 2015). Anthropomorphic and lifestyle information were self-reported biennially. Obesity was defined using body mass index (BMI). Microscopic colitis was confirmed by review of medical records. We used Cox proportional hazard models to estimate adjusted hazard ratios (aHRs) and 95% CIs.

    RESULTS: Among the participants in the NHS and NHSII, we confirmed 244 cases of microscopic colitis during 4,223,868 person-years of follow-up evaluation. Higher BMI was associated inversely with risk of microscopic colitis (Ptrend < .001). Compared with women with BMIs ranging from 18.5 to 20.9 kg/m(2), the aHRs were 0.61 (95% CI, 0.41-0.91) for overweight women (BMI, 2529.9 kg/m(2)) and 0.50 (95% CI, 0.32-0.79) for obese women (BMI >= 30 kg/m(2)). The aHR for each 5-kg/m(2) increase in BMI was 0.79 (95% CI, 0.69-0.90). Weight gain since early adulthood (age, 18 y) also was associated inversely with risk of microscopic colitis (Ptrend = .001). The aHR for each 10-kg weight gain since early adulthood was 0.85 (95% CI, 0.77-0.94). The associations were not modified by age, cohort, physical activity, or smoking status (all Pinteraction >= .26).

    CONCLUSIONS: Unlike many other immune- and metabolic-related disorders, obesity and weight gain since early adulthood were associated with a lower risk of microscopic colitis, based on an analysis of participants in the NHS and NHSII.

  • 35.
    Ludvigsson, Johnny F
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn- och ungdomskliniken i Linköping.
    Montgomery, S.M.
    Clinical Epidemiology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden, Clinical Research Centre, Örebro University Hospital, Linkoping, Sweden, Department of Primary Care and Social Medicine, Imperial College, London, United Kingdom.
    Ekbom, A.
    Clinical Epidemiology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden, Harvard School of Public Health, Boston, MA, United States.
    Risk of Pancreatitis in 14,000 Individuals With Celiac Disease2007Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 5, nr 11Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background & Aims: The aim of this study was to examine the risk of pancreatitis in patients with celiac disease (CD) from a general population cohort. Methods: By using Swedish national registers, we identified 14,239 individuals with a diagnosis of CD (1964-2003) and 69,381 reference individuals matched for age, sex, calendar year, and county of residence at the time of diagnosis. Cox regression estimated the hazard ratios (HRs) for a subsequent diagnosis of pancreatitis. We restricted analyses to individuals with more than 1 year of follow-up and no diagnosis of pancreatitis before or within 1 year after study entry. Conditional logistic regression estimated the association of pancreatitis with subsequent CD. Results: CD was associated with an increased risk of subsequent pancreatitis of any type (HR, 3.3, 95% confidence interval [CI], 2.6-4.4, P < .001, on the basis of 95 positive events in individuals with CD vs 163 positive events in reference individuals) and chronic pancreatitis (HR, 19.8, 95% CI, 9.2-42.8, P < .001, on the basis of 37 and 13 positive events, respectively). Adjustment for socioeconomic index, diabetes mellitus, alcohol-related disorders, or gallstone disease had no notable effect on the risk estimates. The risk increase for pancreatitis was only found among individuals with CD diagnosed in adulthood. Pancreatitis of any type (odds ratio, 3.2, 95% CI, 2.5-4.3, P < .001) and chronic pancreatitis (odds ratio, 7.3, 95% CI, 4.0-13.5, P < .001) were associated with subsequent CD. Conclusions: This study suggests that individuals with CD are at increased risk of pancreatitis. © 2007 AGA Institute.

  • 36.
    Ludvigsson, Jonas F.
    et al.
    Region Örebro län. Clinical Epidemiology Unit, Department of Medicine, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro, Sweden; Division of Gastroenterology and Hepatology, Department of Medicine, Mayo Clinic College of Medicine, Rochester NY, United States.
    Bergquist, Annika
    Dept Gastroenterol & Hepatol, Karolinska Univ Hosp, Stockholm, Sweden.
    Ajne, Gunilla
    Dept Womens & Childrens Hlth, Karolinska Univ Hosp, Karolinska Inst, Stockholm, Sweden.
    Kane, Sunanda
    Div Gastroenterol & Hepatol, Dept Med, Coll Med, Mayo Clin, Rochester NY, USA.
    Ekbom, Anders
    Clin Epidemiol Unit, Dept Med, Karolinska Univ Hosp, Stockholm, Sweden.
    Stephansson, Olof
    Clin Epidemiol Unit, Dept Med, Karolinska Univ Hosp, Stockholm, Sweden; Dept Gastroenterol & Hepatol, Karolinska Univ Hosp, Stockholm, Sweden.
    A Population-based Cohort Study of Pregnancy Outcomes Among Women With Primary Sclerosing Cholangitis2014Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 12, nr 1, s. 95-100Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND & AIMS: Studies of primary sclerosing cholangitis (PSC) and pregnancy outcomes have been limited in size and have been inadequate to rule out excess risks. We examined pregnancy outcomes among women with PSC.

    METHODS: Women with PSC were identified from inpatient and hospital-based outpatient data in the Swedish National Patient Register. Through linkage with the Medical Birth Register, we identified 229 singleton births, from 1987 through 2009, to women with PSC before delivery. These were compared with 2,304,863 births to women without a diagnosis of PSC. We used logistic regression, adjusted for maternal age, smoking, education, parity, and year of birth, to calculate adjusted prevalence odds ratios (aPORs) for adverse pregnancy outcomes.

    RESULTS: Maternal PSC was associated with a 3.63-fold increase in preterm birth (95% confidence interval [CI] for aPOR, 2.35-5.61) as well as an increased risk of cesarean section (aPOR, 2.18; 95% CI, 1.50-3.17). We found no increased risk based on analyses of the 5-minute Apgar score, small for gestational age, stillbirths, or neonatal deaths. Maternal PSC was not a risk factor for congenital abnormalities (aPOR, 1.12; 95% CI, 0.56-2.22). Stratification by inflammatory bowel disease status did not affect the risk estimates more than marginally.

    CONCLUSIONS: Maternal PSC is associated with both preterm birth and cesarean section but not with congenital malformation or other adverse outcomes of pregnancy. Pregnancy should not be discouraged in women with PSC.

  • 37. Ludvigsson, Jonas F.
    et al.
    Elfström, Peter
    Örebro universitet, Hälsoakademin.
    Broomé, Ulrika
    Ekbom, Anders
    Karolinska Institutet.
    Montgomery, Scott M.
    Örebro universitet, Hälsoakademin.
    Celiac disease and risk of liver disease: a general population-based study2007Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 5, nr 1, s. 63-69Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background & aims: Celiac disease (CD) is an important cause of hypertransaminasemia. CD may also be associated with severe forms of liver disease. We investigated the risk of liver disease in 13,818 patients with CD (1964-2003) and 66,584 age- and sex-matched reference individuals from a general population cohort.Methods: We used Cox regression to estimate hazard ratios (HRs) for later liver disease and conditional logistic regression to estimate the risk of CD in individuals with liver disease prior to study entry.Results: CD was associated with an increased risk of acute hepatitis (HR = 5.21; 95% CI = 1.88-14.40; P = .001), chronic hepatitis (HR = 5.84; 95% CI = 2.89-11.79; P < .001), primary sclerosing cholangitis (PSC)(HR = 4.46; 95% CI = 2.50-7.98; P < .001), fatty liver (HR = 6.06; 95% CI = 1.35-27.16; P = .018), liver failure (HR = 3.30; 95% CI = 2.22-4.88; P < .001), liver cirrhosis or liver fibrosis (HR = 2.23; 95% CI = 1.34-3.72; P < .001) and primary biliary cirrhosis (HR = 10.16; 95% CI = 2.61-39.49; P < .001). There was no increased risk of liver transplantation (HR = 1.07; 95% CI = 0.12-9.62; P = .954). Adjustment for socioeconomic index or diabetes mellitus had no notable effect on the risk estimates.Prior liver disease was associated with a statistically significant 4-6 fold increased risk of later CD.Conclusion: This study suggests that individuals with CD are at increased risk of both prior and subsequent liver disease.

  • 38.
    Ludvigsson, Jonas F.
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska University Hospital and Karolinska Institute, Stockholm, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro, Sweden; Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham, United Kingdom.
    Lebwohl, Benjamin
    Department of Medical Epidemiology and Biostatistics, Karolinska University Hospital and Karolinska Institute, Stockholm, Sweden; Celiac Disease Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, USA; Department of Epidemiology, Mailman School of Public Health, Columbia University Medical Center, New York, USA.
    Green, Peter H. R.
    Celiac Disease Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, USA.
    Amount May Beat Timing: Gluten Intake and Risk of Childhood Celiac Disease2016Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 14, nr 3, s. 410-412Artikkel i tidsskrift (Fagfellevurdert)
  • 39.
    Ludvigsson, Jonas F.
    et al.
    Örebro universitet, Hälsoakademin.
    Montgomery, Scott M.
    Örebro universitet, Hälsoakademin.
    Ekbom, Anders
    Risk of pancreatitis in 14,000 individuals with celiac disease2007Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 5, nr 11, s. 1347-1353Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background & Aims: The aim of this study was to examine the risk of pancreatitis in patients with celiac disease (CD) from a general population cohort. Methods: By using Swedish national registers, we identified 14,239 individuals with a diagnosis of CD (1964–2003) and 69,381 reference individuals matched for age, sex, calendar year, and county of residence at the time of diagnosis. Cox regression estimated the hazard ratios (HRs) for a subsequent diagnosis of pancreatitis. We restricted analyses to individuals with more than 1 year of follow-up and no diagnosis of pancreatitis before or within 1 year after study entry. Conditional logistic regression estimated the association of pancreatitis with subsequent CD. Results: CD was associated with an increased risk of subsequent pancreatitis of any type (HR, 3.3; 95% confidence interval [CI], 2.6–4.4; P < .001; on the basis of 95 positive events in individuals with CD vs 163 positive events in reference individuals) and chronic pancreatitis (HR, 19.8; 95% CI, 9.2–42.8; P < .001; on the basis of 37 and 13 positive events, respectively). Adjustment for socioeconomic index, diabetes mellitus, alcohol-related disorders, or gallstone disease had no notable effect on the risk estimates. The risk increase for pancreatitis was only found among individuals with CD diagnosed in adulthood. Pancreatitis of any type (odds ratio, 3.2; 95% CI, 2.5–4.3; P < .001) and chronic pancreatitis (odds ratio, 7.3; 95% CI, 4.0–13.5; P < .001) were associated with subsequent CD. Conclusions: This study suggests that individuals with CD are at increased risk of pancreatitis.

  • 40.
    Morgan, David M.
    et al.
    Department of Ecology and Evolutionary Biology, Brown University, Providence, USA.
    Cao, Yueming
    Division of Gastroenterology, Massachusetts General Hospital, Boston, MA, USA.
    Miller, Kaia
    Division of Gastroenterology, Massachusetts General Hospital, Boston, MA, USA.
    McGoldrick, Jessica
    Division of Gastroenterology, Massachusetts General Hospital, Boston, MA, USA.
    Bellavance, Danielle
    Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA, USA.
    Chin, Samantha M.
    Washington University School of Medicine in St. Louis, St. Louis, MO, USA.
    Halvorsen, Stefan
    Center for Computational and Integrative Biology, Massachusetts General Hospital, Boston, MA, USA.
    Maxner, Benjamin
    University of Massachusetts Medical School, Worcester, MA, USA.
    Richter, James M.
    Division of Gastroenterology, Massachusetts General Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USA.
    Sassi, Slim
    Center for Computational and Integrative Biology, Massachusetts General Hospital, Boston, MA 02114, USA; Harvard Medical School, Boston, MA 02115, USA; Orthopedics Oncology Service, Massachusetts General Hospital, Boston, MA, USA.
    Burke, Kristin E.
    Division of Gastroenterology, Massachusetts General Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USA.
    Yarze, Joseph C.
    Division of Gastroenterology, Massachusetts General Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USA.
    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.
    Staller, Kyle
    Division of Gastroenterology, Massachusetts General Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USA; Clinical Epidemiology Unit, Massachusetts General Hospital, Boston, MA, USA; Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Chung, Daniel C.
    Division of Gastroenterology, Massachusetts General Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USA.
    Khalili, Hamed
    Division of Gastroenterology, Massachusetts General Hospital, Boston, MA 02114, USA; Harvard Medical School, Boston, MA, USA; Clinical Epidemiology Unit, Massachusetts General Hospital, Boston, MA, USA; Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Microscopic Colitis is Characterized by Intestinal Dysbiosis2019Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714Artikkel i tidsskrift (Fagfellevurdert)
  • 41. Murphy, Neil
    et al.
    Ward, Heather A.
    Jenab, Mazda
    Rothwell, Joseph A.
    Boutron-Ruault, Marie-Christine
    Carbonnel, Franck
    Kvaskoff, Marina
    Kaaks, Rudolf
    Kühn, Tilman
    Boeing, Heiner
    Aleksandrova, Krasimira
    Weiderpass, Elisabete
    Skeie, Guri
    Borch, Kristin Benjaminsen
    Tjønneland, Anne
    Kyrø, Cecilie
    Overvad, Kim
    Dahm, Christina C.
    Jakszyn, Paula
    Sánchez, Maria-Jose
    Gil, Leire
    Huerta, José M.
    Barricarte, Aurelio
    Ramón Quirós, J.
    Khaw, Kay-Tee
    Wareham, Nick
    Bradbury, Kathryn E.
    Trichopoulou, Antonia
    La Vecchia, Carlo
    Karakatsani, Anna
    Palli, Domenico
    Grioni, Sara
    Tumino, Rosario
    Fasanelli, Francesca
    Panico, Salvatore
    Bueno-de-Mesquita, Bas
    Peeters, Petra H.
    Gylling, Björn
    Myte, Robin
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Jirström, Karin
    Berntsson, Jonna
    Xue, Xiaonan
    Riboli, Elio
    Cross, Amanda J.
    Gunter, Marc J.
    Heterogeneity of Colorectal Cancer Risk Factors by Anatomical Subsite in 10 European Countries: A Multinational Cohort Study2019Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 17, nr 7, s. 1323-1331Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background & Aims: Colorectal cancer located at different anatomical subsites may have distinct etiologies and risk factors. Previous studies that have examined this hypothesis have yielded inconsistent results, possibly because most studies have been of insufficient size to identify heterogeneous associations with precision.

    Methods: In the European Prospective Investigation into Cancer and Nutrition study, we used multivariable joint Cox proportional hazards models, which accounted for tumorsat different anatomical sites (proximal colon, distal colon, and rectum) as competing risks, to examine the relationships between 14 established/suspected lifestyle, anthropometric, and reproductive/menstrual risk factors with colorectal cancer risk. Heterogeneity across sites was tested using Wald tests.

    Results: After a median of 14.9 years of follow-up of 521,330 men and women, 6291 colorectal cancer cases occurred. Physical activity was related inversely to proximal colon and distal colon cancer, but not to rectal cancer (P heterogeneity = .03). Height was associated positively with proximal and distal colon cancer only, but not rectal cancer (P heterogeneity = .0001). For men, but not women, heterogeneous relationships were observed for body mass index (P heterogeneity = .008) and waist circumference (P heterogeneity = .03), with weaker positive associations found for rectal cancer, compared with proximal and distal colon cancer. Current smoking was associated with a greater risk of rectal and proximal colon cancer, but not distal colon cancer (P heterogeneity = .05). No heterogeneity by anatomical site was found for alcohol consumption, diabetes, nonsteroidal anti-inflammatory drug use, and reproductive/menstrual factors.

    Conclusions: The relationships between physical activity, anthropometry, and smoking with colorectal cancer risk differed by subsite, supporting the hypothesis that tumors in different anatomical regions may have distinct etiologies.

  • 42.
    Myléus, Anna
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Allmänmedicin. Umeå universitet, Medicinska fakulteten, Institutionen för epidemiologi och global hälsa.
    Reilly, Norelle R.
    Green, Peter H.R.
    Rate, Risk Factors and Outcomes of Non-adherence in Pediatric Patients with Celiac Disease: a Systematic Review2019Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, artikkel-id 31173891Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND AND AIMS: The only treatment for celiac disease is strict adherence to a gluten-free diet (GFD). We performed a systematic review to investigate the rate of adherence to a GFD in children with celiac disease, risk factors that affect adherence, and outcomes of non-adherence.

    METHODS: We searched PubMed, Cochrane Library, EBSCO, and Scopus for studies through January 2019. We included observational studies of ≥50 children diagnosed with celiac disease and recommended for placement on a GFD. We collected data on adherence assessment (self-report, serology tests, structured dietary interview, biopsies, or assays for gluten immunogenic peptides), risk factors, and outcomes related to adherence. Findings were presented with medians, range, and a narrative synthesis.

    RESULTS: We identified 703 studies; of these, 167 were eligible for full-text assessment and 49 were included in the final analysis, comprising 7850 children. Rates of adherence to a GFD ranged from 23% to 98%. Comparable rates (median rates of adherence, 75%-87%) were found irrespective of how assessments were performed. Adolescents were at risk of non-adherence and children whose parents had good knowledge about celiac disease adhered more strictly. Non-adherence associated with patient growth, symptoms, and quality of life.

    CONCLUSION: In a systematic review of 49 studies of children with celiac disease, we found substantial variation in adherence to a GFD among patients. Rate of adherence was not associated with method of adherence measurement, so all methods appear to be useful, with lack of consensus on the ideal metric. Studies are needed to determine the best method to ensure adherence and effects on long-term health.

  • 43.
    Myrelid, Pär
    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.
    Abdalla, Maie
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för Kirurgi, Ortopedi och Onkologi. Linköpings universitet, Medicinska fakulteten. Suez Canal University, Egypt.
    Landerholm, Kalle
    Ryhov County Hospital, Sweden.
    Efficacy of a Surveillance Endoscopy After an Ileorectal Anastomosis in Patients With Ulcerative Colitis Reply2018Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 16, nr 1, s. 151-153Artikkel i tidsskrift (Annet vitenskapelig)
    Abstract [en]

    n/a

  • 44.
    Münch, Andreas
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Hjärt- och Medicincentrum, Magtarmmedicinska kliniken.
    Langner, Cord
    Medical University of Graz, Austria .
    Microscopic Colitis: Clinical and Pathologic Perspectives2015Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 13, nr 2, s. 228-236Artikkel, forskningsoversikt (Fagfellevurdert)
    Abstract [en]

    Microscopic colitis is a chronic inflammatory bowel disease characterized by chronic nonbloody diarrhea and specific histopathology features. Active disease, defined as 3 or more stools or 1 or more watery stools per day, significantly reduces quality of life. Epidemiologic studies have found the incidence and prevalence of microscopic colitis to be comparable with those of Crohn's disease and ulcerative colitis. Nevertheless, microscopic colitis is still under-recognized in clinical practice-most health care workers know little about its etiology and pathophysiology. Furthermore, there are many challenges to the diagnosis and treatment of patients. We review the epidemiologic and clinical features of this disorder and discuss its pathogenesis. We also outline the criteria for histopathologic evaluation of microscopic colitis, recently published by the European Consensus on Inflammatory Bowel Disease, and discuss a treatment algorithm created by the European Microscopic Colitis Group. Treatment options for patients with budesonide-refractory disease are discussed.

  • 45.
    Sadr-Azodi, Omid
    et al.
    Upper Gastrointestinal Research, Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
    Sanders, David S.
    Gastroenterology and Liver Unit, Royal Hallamshire Hospital, University of Sheffield, Sheffield, United Kingdom.
    Murray, Joseph A.
    Division of Gastroenterology and Hepatology, Departments of Medicine and Immunology, Mayo Clinic College of Medicine, Rochester MN, United States.
    Ludvigsson, Jonas F.
    Clinical Epidemiology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden; Division of Gastroenterology and Hepatology, Departments of Medicine and Immunology, Mayo Clinic College of Medicine, Rochester MN, United States; Department of Pediatrics, Örebro University Hospital, Örebro, Sweden.
    Patients With Celiac Disease Have an Increased Risk for Pancreatitis2012Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 10, nr 10, s. 1136-1142Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND & AIMS: Patients with celiac disease have been reported to be at increased risk for pancreatitis and pancreatic insufficiency, but the risk might have been overestimated because of patient selection and limited numbers of patients for analysis. Furthermore, no distinction has been made between patients with gallstone-related and non-gallstone-related pancreatitis. We performed a nationwide study to determine the risk for any pancreatitis or subtype of pancreatitis among patients with biopsy-verified celiac disease.

    METHODS: We analyzed data from patients in Sweden with celiac disease (n = 28,908) who were identified on the basis of small intestinal biopsy records from 28 pathology departments (those with villous atrophy, Marsh 3). Biopsies were performed from 1969 to 2008, and biopsy report data were collected from 2006 to 2008. Patients with pancreatitis were identified on the basis of diagnostic codes in the Swedish Patient Register and records of pancreatic enzyme use in the Swedish Prescribed Drug Register. Data were matched with those from 143,746 individuals in the general population; Cox regression was used to estimate hazard ratios (HRs) for pancreatitis.

    RESULTS: We identified 406 patients with celiac disease who were later diagnosed with pancreatitis (and 143 with expected pancreatitis) (HR, 2.85; 95% confidence interval [CI], 2.53-3.21). The absolute risk of any pancreatitis among patients with celiac disease was 126/100,000 person-years, with an excess risk of 81/100,000 person-years. The HR for gallstone-related acute pancreatitis was 1.59 (95% CI, 1.06-2.40), for non-gallstone-related acute pancreatitis HR was 1.86 (95% CI, 1.52-2.26), for chronic pancreatitis HR was 3.33 (95% CI, 2.33-4.76), and for supplementation with pancreatic enzymes HR was 5.34 (95% CI, 2.99-9.53). The risk of any pancreatitis within 5 years of diagnosis was 2.76 (95% CI, 2.36-3.22).

    CONCLUSIONS: Based on an analysis of medical records from Sweden, patients with celiac disease have an almost 3-fold increase in risk of developing pancreatitis, compared with the general population.

  • 46.
    Song, Huan
    et al.
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Held, Maria
    Hallands Sjukhus Halmstad, Dept Clin Chem, Halmstad, Sweden..
    Sandin, Sven
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Rautelin, Hilpi
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Klinisk mikrobiologi och infektionsmedicin, Klinisk bakteriologi.
    Eliasson, Mats
    Umea Univ, Sunderby Res Unit, Umea, Sweden..
    Soderberg, Stefan
    Umea Univ, Cardiol & Heart Ctr, Umea, Sweden..
    Hallmans, Goran
    Umea Univ, Dept Publ Hlth & Clin Med, Nutr Res, Umea, Sweden..
    Engstrand, Lars
    Karolinska Inst, Dept Microbiol Tumor & Cell Biol, SE-17177 Stockholm, Sweden..
    Nyren, Olof
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Ye, Weimin
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Increase in the Prevalence of Atrophic Gastritis Among Adults Age 35 to 44 Years Old in Northern Sweden Between 1990 and 20092015Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 13, nr 9, s. 1592-+Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND & AIMS: Atrophic corpus gastritis (ACG) is believed to be an early precursor of gastric adenocarcinoma. We aimed to investigate trends of ACG in Northern Sweden, from 1990 through 2009, and to identify possible risk factors. METHODS: We randomly selected serum samples collected from 5284 participants in 1990, 1994, 1999, 2004, and 2009, as part of the population-based, cross-sectional Northern Sweden Multinational Monitoring of Trends and Determinants in Cardiovascular Disease study (ages, 35-64 y). Information was collected on sociodemographic, anthropometric, lifestyle, and medical factors using questionnaires. Serum samples were analyzed for levels of pepsinogen I to identify participants with functional ACG; data from participants with ACG were compared with those from frequency-matched individuals without ACG (controls). Blood samples were analyzed for antibodies against Helicobacter pylori and Cag pathogenicity island protein A. Associations were estimated with unconditional logistic regression models. RESULTS: Overall, 305 subjects tested positive for functional ACG, based on their level of pepsinogen I. The prevalence of ACG in participants age 55 to 64 years old decreased from 124 per 1000 to 49 per 1000 individuals between 1990 and 2009. However, the prevalence of ACG increased from 22 per 1000 to 64 per 1000 individuals among participants age 35 to 44 years old during this time period. Cag pathogenicity island protein A seropositivity was associated with risk for ACG (odds ratio, 2.29; 95% confidence interval, 1.69-3.12). Other risk factors included diabetes, low level of education, and high body mass index. The association between body mass index and ACG was confined to individuals age 35 to 44 years old; in this group, overweight and obesity were associated with a 2.8-fold and a 4.7-fold increased risk of ACG, respectively. CONCLUSIONS: Among residents of Northern Sweden, the prevalence of ACG increased from 1990 through 2009, specifically among adults age 35 to 44 years old. The stabilizing seroprevalence of H pylori and the increasing prevalence of overweight and obesity might contribute to this unexpected trend. Studies are needed to determine whether these changes have affected the incidence of gastric cancer.

  • 47. Song, Huan
    et al.
    Held, Maria
    Sandin, Sven
    Rautelin, Hilpi
    Eliasson, Mats
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Söderberg, Stefan
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Kardiologi.
    Hallmans, Göran
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Näringsforskning. Umeå universitet, Medicinska fakulteten, Enheten för biobanksforskning.
    Engstrand, Lars
    Nyrén, Olof
    Ye, Weimin
    Increase in the Prevalence of Atrophic Gastritis Among Adults Age 35 to 44 Years Old in Northern Sweden Between 1990 and 20092015Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 13, nr 9, s. 1592-1600Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND & AIMS: Atrophic corpus gastritis (ACG) is believed to be an early precursor of gastric adenocarcinoma. We aimed to investigate trends of ACG in Northern Sweden, from 1990 through 2009, and to identify possible risk factors.

    METHODS: We randomly selected serum samples collected from 5284 participants in 1990, 1994, 1999, 2004, and 2009, as part of the population-based, cross-sectional Northern Sweden Multinational Monitoring of Trends and Determinants in Cardiovascular Disease study (ages 35-64 y). Information was collected on sociodemographic, anthropometric, lifestyle, and medical factors using questionnaires. Serum samples were analyzed for levels of pepsinogen I, to identify participants with functional ACG; data from participants with ACG were compared with those from frequency-matched individuals without ACG (controls). Blood samples were analyzed for antibodies against H pylori and CagA. Associations were estimated with unconditional logistic regression models.

    RESULTS: Overall, 305 subjects tested positive for functional ACG, based on level of pepsinogen I. The prevalence of ACG in participants 55-64 y old decreased, from 124/1000 to 49/1000 individuals, between 1990 and 2009. However, the prevalence of ACG increased, from 22/1000 to 64/1000 individuals among participants 35-44 y old during this time period. CagA seropositivity was associated with risk for ACG (odds ratio, 2.29; 95% confidence interval, 1.69-3.12). Other risk factors included diabetes, low level of education, and high body mass index. The association between body mass index and ACG was confined to individuals 35-44 y old; in this group, overweight and obesity were associated with a 2.8-fold and 4.7-fold increased risk of ACG, respectively.

    CONCLUSIONS: Among residents of Northern Sweden, the prevalence of ACG increased from 1990 through 2009 specifically among adults 35-44 y old. The stabilizing seroprevalence of H pylori and increasing prevalence of overweight and obesity might contribute to this unexpected trend; studies are needed to determine whether these changes have affected the incidence of gastric cancer.

  • 48.
    Sänger, Andreas
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Hjärt- och Medicincentrum, Endokrinmedicinska kliniken.
    Langner, Cord
    Medical University of Graz, Austria.
    Letter: Diagnosing Microscopic Colitis: Is Flexible Sigmoidoscopy a Reliable Alternative to Colonoscopy? Reply in CLINICAL GASTROENTEROLOGY AND HEPATOLOGY, vol 13, issue 3, pp 618-6192015Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 13, nr 3, s. 618-619Artikkel i tidsskrift (Annet vitenskapelig)
    Abstract [en]

    n/a

  • 49.
    Yin, Weiyao
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Reproductive Endocrinology, West China Second University Hospital, Sichuan University, Chengdu, China.
    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.
    Liu, Zhiwei
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Roosaar, Ann
    Department of Dental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Axéll, Tony
    Maxillofacial Unit, Halmstad Hospital Halland, Halmstad, Sweden.
    Ye, Weimin
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Inverse Association Between Poor Oral Health and Inflammatory Bowel Diseases2017Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 15, nr 4, s. 525-531, artikkel-id S1542-3565(16)30371-8Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND & AIMS: The hygiene hypothesis (a lack of childhood exposure to microorganisms increases susceptibility to allergic diseases by altering immune development) has been proposed as an explanation for the increasing incidence of inflammatory bowel disease (IBD). However, there are few data on the relationship between oral hygiene and development of IBD, and study results have been inconsistent. We investigated the association between poor oral health and risks of IBD, ulcerative colitis (UC), and Crohn's disease (CD).

    METHODS: We performed a population-based cohort study of 20,162 individuals followed for 40 years (from 1973 to 2012). Residents of 2 municipalities of Uppsala County, Sweden (N = 30,118), 15 years or older, were invited, and among them 20,333 were examined for tooth loss, dental plaques, and oral mucosal lesions at the time of study entry. Other exposure data were collected from questionnaires. Patients who later developed IBD (UC or CD) were identified by international classification codes from Swedish National Patient and Cause of Death Registers. Cox proportional hazards regression was used to estimate hazard ratios for IBD, UC, and CD.

    RESULTS: From National Patient and Cause of Death Registers, we identified 209 individuals who developed IBD (142 developed UC and 67 developed CD), with an incidence rate of 37.3 per 100,000 person-years. We found an inverse relationship between poor oral health and IBD, especially in individuals with severe oral problems. Loss of 5-6 teeth of the 6 teeth examined was associated with a lower risk of IBD (hazard ratio, 0.56; 95% confidence interval, 0.32-0.98). Having dental plaques that covered more than 33% of tooth surface was negatively associated with CD (hazard ratio, 0.32; 95% confidence interval, 0.10-0.97).

    CONCLUSIONS: In a population-based cohort study of more than 20,000 people in Sweden, we associated poor oral health with reduced risk of future IBD.

  • 50.
    Zhou, You
    et al.
    Minerva Foundation Institute for Medical Research, Helsinki, Finland; Systems Immunity University Research Institute and Division of Infection and Immunity, School of Medicine, Cardiff University, Cardiff, United Kingdom.
    Oresic, Matej
    Steno Diabetes Center, Gentofte, Denmark.
    Leivonen, Marja
    Department of Surgery, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
    Gopalacharyulu, Peddinti
    Institute for Molecular Medicine Finland, University of Helsinki, Helsinki, Finland.
    Hyysalo, Jenni
    Minerva Foundation Institute for Medical Research, Helsinki, Finland; Department of Medicine, University of Helsinki, Helsinki, Finland.
    Arola, Johanna
    Minerva Foundation Institute for Medical Research, Helsinki, Finland; Department of Medicine, University of Helsinki, Helsinki, Finland.
    Verrijken, An
    Department of Endocrinology, Diabetology and Metabolism, Antwerp University Hospital, University of Antwerp, Antwerp, Belgium.
    Francque, Sven
    Department of Gastroenterology and Hepatology, Antwerp University Hospital, University of Antwerp, Antwerp, Belgium.
    Van Gaal, Luc
    Department of Endocrinology, Diabetology and Metabolism, Antwerp University Hospital, University of Antwerp, Antwerp, Belgium.
    Hyötyläinen, Tuulia
    Örebro universitet, Institutionen för naturvetenskap och teknik. Steno Diabetes Center, Gentofte, Denmark.
    Yki-Järvinen, Hannele
    Minerva Foundation Institute for Medical Research, Helsinki, Finland; Department of Medicine, University of Helsinki, Helsinki, Finland.
    Noninvasive Detection of Nonalcoholic Steatohepatitis Using Clinical Markers and Circulating Levels of Lipids and Metabolites2016Inngår i: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 14, nr 10, s. 1463-1472.e6Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND & AIMS: Use of targeted mass spectrometry (MS)-based methods is increasing in clinical chemistry laboratories. We investigate whether MS-based profiling of plasma improves noninvasive risk estimates of nonalcoholic steatohepatitis (NASH) compared with routinely available clinical parameters and patatin-like phospholipase domain-containing protein 3 (PNPLA3) genotype at rs738409.

    METHODS: We used MS-based analytic platforms to measure levels of lipids and metabolites in blood samples from 318 subjects who underwent a liver biopsy because of suspected NASH. The subjects were divided randomly into estimation (n = 223) and validation (n = 95) groups to build and validate the model. Gibbs sampling and stepwise logistic regression, which fulfilled the Bayesian information criterion, were used for variable selection and modeling.

    RESULTS: Features of the metabolic syndrome and the variant in PNPLA3 encoding I148M were significantly more common among subjects with than without NASH. We developed a model to identify subjects with NASH based on clinical data and PNPLA3 genotype (NASH Clin Score), which included aspartate aminotransferase (AST), fasting insulin, and PNPLA3 genotype. This model identified subjects with NASH with an area under the receiver operating characteristic of 0.778 (95% confidence interval, 0.709-0.846). We then used backward stepwise logistic regression analyses of variables from the NASH Clin Score and MS-based factors associated with NASH to develop the NASH ClinLipMet Score. This included glutamate, isoleucine, glycine, lysophosphatidylcholine 16:0, phosphoethanolamine 40:6, AST, and fasting insulin, along with PNPLA3 genotype. It identified patients with NASH with an area under the receiver operating characteristic of 0.866 (95% confidence interval, 0.820-0.913). The NASH ClinLipMet score identified patients with NASH with significantly higher accuracy than the NASH Clin Score or MS-based profiling alone.

    CONCLUSIONS: A score based on MS (glutamate, isoleucine, glycine, lysophosphatidylcholine 16:0, phosphoethanolamine 40:6) and knowledge of AST, fasting insulin, and PNPLA3 genotype is significantly better than a score based on clinical or metabolic profiles alone in determining the risk of NASH.

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