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  • 1. Bergquist, Annika
    et al.
    Montgomery, Scott M.
    Örebro University, School of Health and Medical Sciences.
    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 cholangitis2008In: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 6, no 8, p. 939-943Article in journal (Refereed)
    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. 

  • 2.
    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 Disease2012In: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 10, no 1, p. 30-36Article in journal (Refereed)
    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.

  • 3.
    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.
    Örebro University Hospital. 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 Disease2015In: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 13, no 7, p. 1271-1277.e2Article in journal (Refereed)
    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.

  • 4.
    Khalili, Hamed
    et al.
    Gastroenterology Unit, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, 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 University, School of Medical Sciences. Örebro University Hospital. 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, Massachusetts, USA; Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, 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 Colitis2018In: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714Article in journal (Refereed)
    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.

  • 5.
    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 University, School of Medical Sciences. Örebro University Hospital. 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, Brooklyn NY, 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 Diet2018In: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 16, no 2, p. 295-297Article in journal (Refereed)
    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.

  • 6.
    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.
    Örebro University Hospital. 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 Factors2014In: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 12, no 4, p. 632-635Article in journal (Refereed)
  • 7.
    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.
    Örebro University Hospital. 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 Study2015In: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 13, no 6, p. 1111-1117.e2Article in journal (Refereed)
    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.

  • 8.
    Ludvigsson, Jonas F.
    et al.
    Örebro University Hospital. 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 Cholangitis2014In: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 12, no 1, p. 95-100Article in journal (Refereed)
    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.

  • 9. Ludvigsson, Jonas F.
    et al.
    Elfström, Peter
    Örebro University, School of Health and Medical Sciences.
    Broomé, Ulrika
    Ekbom, Anders
    Karolinska Institutet.
    Montgomery, Scott M.
    Örebro University, School of Health and Medical Sciences.
    Celiac disease and risk of liver disease: a general population-based study2007In: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 5, no 1, p. 63-69Article in journal (Refereed)
    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.

  • 10.
    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 Disease2016In: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 14, no 3, p. 410-412Article in journal (Refereed)
  • 11.
    Ludvigsson, Jonas F.
    et al.
    Örebro University, School of Health and Medical Sciences.
    Montgomery, Scott M.
    Örebro University, School of Health and Medical Sciences.
    Ekbom, Anders
    Risk of pancreatitis in 14,000 individuals with celiac disease2007In: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 5, no 11, p. 1347-1353Article in journal (Refereed)
    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.

  • 12.
    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 Pancreatitis2012In: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 10, no 10, p. 1136-1142Article in journal (Refereed)
    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.

  • 13.
    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 University, School of Medical Sciences. Örebro University Hospital. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro, 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 Diseases2017In: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 15, no 4, p. 525-531, article id S1542-3565(16)30371-8Article in journal (Refereed)
    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.

  • 14.
    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 University, School of Science and Technology. 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 Metabolites2016In: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 14, no 10, p. 1463-1472.e6Article in journal (Refereed)
    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.

  • 15.
    Zugna, Daniela
    et al.
    Unita Epidemiol Tumori, Dipartimento Sci Med, Univ Turin, Turin, Italy.
    Ludvigsson, Jonas F.
    Örebro University Hospital. Dept Med Epidemiol & Biostat, Karolinska Inst, Stockholm, Sweden.; Dept Pediat, Örebro Univ Hosp, Örebro, Sweden.
    Improving Our Knowledge on the Risk of Congenital Malformations in Families With Celiac Disease Reply2015In: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 13, no 3, p. 616-616Article in journal (Refereed)
  • 16.
    Zugna, Daniela
    et al.
    Canc Epidemiol Unit, ll Centro di Riferimento per l'Epidemiologia e la Prevenzione Oncologica (CPO) Piemonte, Turin, Italy; Univ Turin, Turin, Italy; Dept Med, Clin Epidemiol Unit, Karolinska Inst, Stockholm, Sweden.
    Richiardi, Lorenzo
    Canc Epidemiol Unit, ll Centro di Riferimento per l'Epidemiologia e la Prevenzione Oncologica (CPO) Piemonte, Turin, Italy; Univ Turin, Turin, Italy.
    Stephansson, Olof
    Dept Med, Clin Epidemiol Unit, Karolinska Inst, Stockholm, Sweden; Div Obstet & Gynecol, Dept Womens & Childrens Hlth, Karolinska Inst, Stockholm, Sweden.
    Pasternak, Bjorn
    Dept Epidemiol Res, Statens Serum Inst, Copenhagen, Denmark.
    Ekbom, Anders
    Dept Med, Clin Epidemiol Unit, Karolinska Inst, Stockholm, Sweden.
    Cnattingius, Sven
    Dept Med, Clin Epidemiol Unit, Karolinska Institutet, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Örebro University Hospital. Dept Med Epidemiol & Biostat, Karolinska Inst, Stockholm, Sweden; Dept Pediat, Örebro Univ Hosp, Örebro, Sweden.
    Risk of Congenital Malformations Among Offspring of Mothers and Fathers With Celiac Disease: A Nationwide Cohort Study2014In: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 12, no 7, p. 1108-+Article in journal (Refereed)
    Abstract [en]

    BACKGROUND & AIMS: Many patients with celiac disease experience malabsorption, weight loss, and anemia; undiagnosed celiac disease during pregnancy has been linked with adverse outcomes. Studies of celiac disease and congenital malformations in offspring have been underpowered. We investigated the risk of congenital malformations among the offspring of parents with celiac disease. METHODS: We performed a nationwide cohort study of data from linked health care registers in Sweden from 1973 through 2009. We collected histopathology data from 28 pathology departments in Sweden to identify individuals with celiac disease (based on the presence of villous atrophy). We estimated the risks of malformations in the offspring of mothers and fathers with and without celiac disease. Logistic regression was used to estimate adjusted prevalence odds ratios (aPORs) with 95% confidence intervals (CIs). RESULTS: Among 11,382 offspring of mothers with celiac disease, there were 672 cases (5.9%) of malformation compared with 2098 cases (5.1%) among 40,922 offspring of mothers without celiac disease. Similarly, 352 (5.9%) of 6002 offspring of fathers with celiac disease and 1009 (5.1%) of 19,600 offspring of fathers without celiac disease had a malformation. In adjusted analyses, the offspring of mothers or fathers with celiac disease had a slightly increased risk of having children with malformations (for those with mothers with celiac disease: aPOR, 1.15; 95% CI, 1.05-1.26; for those with fathers with celiac disease: aPOR, 1.14; 95% CI, 1.00-1.29). However, these excess risks decreased or vanished entirely when we restricted our data to births since 2000 (for those with mothers with celiac disease: aPOR, 1.11; and 95% CI, 0.79-1.56; for those with fathers with celiac disease: aPOR, 1.01; 95% CI, 0.81-1.26). CONCLUSIONS: In a nationwide study, we found an increased risk for malformation among the offspring of mothers or fathers with celiac disease. However, the excess risk is small; the upper limits of the CIs for malformation indicate a 29% maximum relative increase.

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