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  • 1.
    Ahlberg, Rickard
    et al.
    Örebro University, School of Medical Sciences.
    Garcia-Argibay, Miguel
    Örebro University, School of Medical Sciences.
    Du Rietz, Ebba
    Karolinska Institutet, Stockholm, Sweden.
    Butwicka, Agnieszka
    Karolinska Institutet, Stockholm, Sweden; Child and Adolescent Psychiatry Stockholm, Stockholm Health Care Services, Region Stockholm, Sweden.
    Cortese, Samuele
    Centre for Innovation in Mental Health, School of Psychology, Faculty of Environmental and Life sciences, University of Southampton, Southampton, United Kingdom; Solent NHS Trust, Southampton, United Kingdom; Division of Psychiatry and Applied Psychology, School of Medicine, University of Nottingham, Nottingham, United Kingdom; Clinical and Experimental Sciences (CNS and Psychiatry), Faculty of Medicine, University of Southampton, Southampton, United Kingdom; Hassenfeld Children´s Hospital at NYU Langone, New York University Child Study Center, New York City, New York; The Division of Psychiatry and Applied Psychology, School of Medicine, University of Nottingham, Nottingham, United Kingdom.
    D'Onofrio, Brian M.
    Karolinska Institutet, Stockholm, Sweden; Indiana University, Bloomington, Indiana, USA.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Karolinska Institutet, Stockholm, Sweden; Örebro University Hospital, Örebro University, Örebro, Sweden.
    Larsson, Henrik
    Örebro University, School of Medical Sciences.
    Associations Between Attention-Deficit/Hyperactivity Disorder (ADHD), ADHD Medication and Shorter Height: A Quasi-Experimental and Family-based Study2023In: Journal of the American Academy of Child and Adolescent Psychiatry, ISSN 0890-8567, E-ISSN 1527-5418, Vol. 62, no 12, p. 1316-1325Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: The association between attention-deficit/hyperactivity disorder (ADHD) and shorter height is unclear. This study examined the risk of shorter height in individuals with ADHD, and the influence of prenatal factors, ADHD medication, psychiatric comorbidity, socioeconomic factors and familial liability.

    METHOD: We draw on Swedish National Registers for two different study designs. First, height data for 14,268 individuals with ADHD and 71,339 controls were stratified into two groups: 1: Before and 2: After stimulant treatment were introduced in Sweden. Second, we used a family-based design including 833,172 relatives without ADHD with different levels of relatedness to the individuals with ADHD and matched controls.

    RESULTS: ADHD was associated with shorter height both before (below average height: OR=1.31, 95 % CI=1.22-1.41) and after (below average height: OR=1.21, 95 % CI=1.13-1.31) stimulants for ADHD were introduced in Sweden and was of similar magnitude in both cohorts. The association between ADHD and shorter height attenuated after adjustment for prenatal factors, psychiatric disorders and SES. Relatives of individuals with ADHD had an increased risk of shorter height (below average height in full siblings: OR=1.14, 95 % CI=1.09-1.19; maternal half siblings: OR=1.10, 95 % CI=1.01-1.20; paternal half siblings: OR=1.15, 95 % CI=1.07-1.24, first full cousins: OR=1.10, 95 % CI=1.08-1.12).

    CONCLUSION: Our findings suggest that ADHD is associated with shorter height. On a population level, this association was present both before and after ADHD-medications were available in Sweden. The association between ADHD and height was partly explained by prenatal factors, psychiatric comorbidity, low SES and a shared familial liability for ADHD.

  • 2.
    Alaedini, Armin
    et al.
    Institute of Human Nutrition, Columbia University Medical Center, New York NY, USA; Department of Medicine, Celiac Disease Center, Columbia University Medical Center, New York NY, USA .
    Lebwohl, Benjamin
    Department of Medicine, Celiac Disease Center, Columbia University Medical Center, New York NY, USA; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Wormser, Gary P.
    Division of Infectious Diseases, Department of Medicine, New York Medical College, Valhalla NY, United States.
    Green, Peter H.
    Department of Medicine, Celiac Disease Center, Columbia University Medical Center, Columbia University, New York NY, USA.
    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; School of Medicine, Division of Epidemiology and Public Health, University of Nottingham, Nottingham, United Kingdom.
    Borrelia infection and risk of celiac disease2017In: BMC Medicine, E-ISSN 1741-7015, Vol. 15, article id 169Article in journal (Refereed)
    Abstract [en]

    Background: Environmental factors, including infectious agents, are speculated to play a role in the rising prevalence and the geographic distribution of celiac disease, an autoimmune disorder. In the USA and Sweden where the regional variation in the frequency of celiac disease has been studied, a similarity with the geographic distribution of Lyme disease, an emerging multisystemic infection caused by Borrelia burgdorferi spirochetes, has been found, thus raising the possibility of a link. We aimed to determine if infection with Borrelia contributes to an increased risk of celiac disease.

    Methods: Biopsy reports from all of Sweden's pathology departments were used to identify 15,769 individuals with celiac disease. Through linkage to the nationwide Patient Register, we compared the rate of earlier occurrence of Lyme disease in the patients with celiac disease to that in 78,331 matched controls. To further assess the temporal relationship between Borrelia infection and celiac disease, we also examined the risk of subsequent Lyme disease in patients with a diagnosis of celiac disease.

    Results: Twenty-five individuals (0.16%) with celiac disease had a prior diagnosis of Lyme disease, whereas 79 (0.5%) had a subsequent diagnosis of Lyme disease. A modest association between Lyme disease and celiac disease was seen both before (odds ratio, 1.61; 95% confidence interval (CI), 1.06-2.47) and after the diagnosis of celiac disease (hazard ratio, 1.82; 95% CI, 1.40-2.35), with the risk of disease being highest in the first year of follow-up.

    Conclusions: Only a minor fraction of the celiac disease patient population had a prior diagnosis of Lyme disease. The similar association between Lyme disease and celiac disease both before and after the diagnosis of celiac disease is strongly suggestive of surveillance bias as a likely contributor. Taken together, the data indicate that Borrelia infection is not a substantive risk factor in the development of celiac disease.

  • 3.
    Axelrad, J.
    et al.
    Department of Gastroenterology, New York University School of Medicine, New York, NY, USA.
    Olén, O.
    Department of Medicine, Karolinska Institute, Stockholm, Sweden.
    Sachs, M.
    Department of Medicine, Karolinska Institute, Stockholm, Sweden.
    Erichsen, R.
    Department of Clinical Epidemiology, Aarhus University, Aarhus, Denmark.
    Pedersen, L.
    Department of Clinical Epidemiology, Aarhus University, Aarhus, Denmark.
    Halfvarson, Jonas
    Örebro University, School of Medical Sciences. Department of Gastroenterology.
    Askling, J.
    Department of Medicine, Karolinska Institute, Stockholm, Sweden.
    Ekbom, A.
    Karolinska Inst, Dept Med, Stockholm, Sweden..
    Sørensen, H. T.
    Department of Clinical Epidemiology, Aarhus University, Aarhus, Denmark.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Medical Epidemiology and Biostatistics.
    Inflammatory bowel disease and risk of small bowel cancer: A binational population-based cohort study from Denmark and Sweden2020In: Journal of Crohn's & Colitis, ISSN 1873-9946, E-ISSN 1876-4479, Vol. 14, no Suppl. 1, p. S007-S009Article in journal (Other academic)
  • 4.
    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 University, School of Medical Sciences. Örebro University Hospital. 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 Study2019In: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 17, no 7, p. 1311-1322Article in journal (Refereed)
    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.

  • 5.
    Axelrad, Jordan E.
    et al.
    Inflammatory Bowel Disease Center at NYU Langone Health, Division of Gastroenterology, Department of Medicine, New York University School of Medicine, New York, New York, USA .
    Olén, Ola
    Clinical Epidemiology Division, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden; Sachs' Children and Youth Hospital, Stockholm South General Hospital, Stockholm, Sweden; Department of Clinical Science and Education, Södersjukhuset, Karolinska Institutet, Stockholm, Sweden.
    Sachs, Michael C.
    Clinical Epidemiology Division, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.
    Erichsen, Rune
    Department of Clinical Epidemiology, Aarhus University Hospital, Aarhus, Denmark; Department of Surgery, Randers Regional Hospital, Randers, Denmark.
    Pedersen, Lars
    Department of Clinical Epidemiology, Aarhus University Hospital, Aarhus, Denmark.
    Halfvarson, Jonas
    Örebro University, School of Medical Sciences. Department of Gastroenterology.
    Askling, Johan
    Clinical Epidemiology Division, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.
    Ekbom, Anders
    Clinical Epidemiology Division, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.
    Sørensen, Henrik Toft
    Department of Clinical Epidemiology, Aarhus University Hospital, Aarhus, Denmark.
    Ludvigsson, Jonas F.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, Orebro University Hospital, Örebro, Sweden; Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham, United Kingdom; Department of Medicine, Columbia University College of Physicians and Surgeons, New York, United States.
    Inflammatory bowel disease and risk of small bowel cancer: a binational population-based cohort study from Denmark and Sweden2021In: Gut, ISSN 0017-5749, E-ISSN 1468-3288, Vol. 70, no 2, p. 297-308Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: Crohn's disease (CD) is associated with increased risk of small bowel cancer (SBC), but previous studies have been small. We aimed to examine the risk of incident SBC and death from SBC in patients with inflammatory bowel disease (IBD).

    DESIGN: In a binational, population-based cohort study from Sweden and Denmark of patients with IBD during 1969-2017 and matched reference individuals from the general population, we evaluated the risk of incident SBC and death from SBC. Cox regression was used to estimate adjusted hazard ratios (aHRs).

    RESULTS: We identified 161 896 individuals with IBD (CD: 47 370; UC: 97 515; unclassified IBD: 17 011). During follow-up, 237 cases of SBC were diagnosed in patients with IBD (CD: 24.4/100 000 person-years; UC: 5.88/100 000 person-years), compared with 640 cases in reference individuals (2.81/100 000 person-years and 3.32/100 000 person-years, respectively). This corresponded to one extra case of SBC in 385 patients with CD and one extra case in 500 patients with UC, followed up for 10 years. The aHR for incident SBC was 9.09 (95% CI 7.34 to 11.3) in CD and 1.85 (95% CI 1.43 to 2.39) in UC. Excluding the first year after an IBD diagnosis, the aHRs for incident SBC decreased to 4.96 in CD and 1.69 in UC. Among patients with CD, HRs were independently highest for recently diagnosed, childhood-onset, ileal and stricturing CD. The relative hazard of SBC-related death was increased in both patients with CD (aHR 6.59, 95% CI 4.74 to 9.15) and patients with UC (aHR 1.57; 95% CI 1.07 to 2.32).

    CONCLUSION: SBC and death from SBC were more common in patients with IBD, particularly among patients with CD, although absolute risks were low.

  • 6.
    Axelrad, Jordan E.
    et al.
    Inflammatory Bowel Disease Center at NYU Langone Health, Division of Gastroenterology, Department of Medicine, New York University School of Medicine, New York, New York, USA.
    Olén, Ola
    Clinical Epidemiology Division, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden; Sachs' Children and Youth Hospital, Stockholm South General Hospital, Stockholm, Sweden; Department of Clinical Science and Education, Södersjukhuset, Karolinska Institutet, Stockholm, Sweden.
    Sachs, Michael C.
    Clinical Epidemiology Division, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.
    Erichsen, Rune
    Department of Clinical Epidemiology, Aarhus University Hospital, Aarhus, Denmark; Department of Surgery, Randers Regional Hospital, Randers, Denmark.
    Pedersen, Lars
    Department of Clinical Epidemiology, Aarhus University Hospital, Aarhus, Denmark.
    Halfvarson, Jonas
    Örebro University, School of Medical Sciences. Department of Gastroenterology.
    Askling, Johan
    Clinical Epidemiology Division, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.
    Ekbom, Anders
    Clinical Epidemiology Division, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.
    Sørensen, Henrik Toft
    Department of Clinical Epidemiology, Aarhus University Hospital, Aarhus, Denmark.
    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; Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham, United Kingdom; Department of Medicine, Columbia University College of Physicians and Surgeons, New York, United States.
    Reply: Survival in Crohn's disease-associated small bowel adenocarcinoma2021In: Gut, ISSN 0017-5749, E-ISSN 1468-3288, Vol. 70, no 5, p. 998-998Article in journal (Refereed)
  • 7.
    Axelrad, Jordan E.
    et al.
    Division of Gastroenterology, Department of Medicine, NYU School of Medicine, New York NY, USA.
    Sachs, Michael C.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro, Sweden; Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham, UK; Department of Medicine, Columbia University College of Physicians and Surgeons, New York NY, USA.
    Olén, Ola
    Clinical Epidemiology Division, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden; Sachs’ Children and Youth Hospital, Stockholm South General Hospital, Stockholm, Sweden; Department of Clinical Science and Education Södersjukhuset, Karolinska Institutet, Stockholm, Sweden.
    A Novel Method for Quantifying Intestinal Inflammatory Burden in Inflammatory Bowel Disease Using Register Data2020In: Clinical Epidemiology, ISSN 1179-1349, E-ISSN 1179-1349, Vol. 12, p. 1059-1072Article in journal (Refereed)
    Abstract [en]

    Background: The Swedish Quality Register for Inflammatory Bowel Disease (SWIBREG) contains clinical data for the study of inflammatory bowel disease (IBD). The Epidemiology Strengthened by histoPathology Reports in Sweden (ESPRESSO) cohort was recently established for the study of gastrointestinal histopathology. We aimed to develop and validate a histology score from ESPRESSO using clinical information from SWIBREG, and secondarily, to evaluate the association of the score on IBD-related hospitalization.

    Methods: In a nationwide, population-based cohort study of patients with IBD during 1969-2017, we linked endoscopic inflammation in SWIBREG with histologic inflammation in ESPRESSO. We established a clinically interpretable model for predicting the endoscopic score from histology using scalable Bayesian rule lists to define a SNOMED-based histology score applicable to the ESPRESSO cohort. We also assessed the impact of baseline endoscopic and histology scores on time to IBD-related hospitalization.

    Results: We identified 5225 individuals with IBD comprising 11,051 endoscopic assessments in SWIBREG linked to a histopathology record in ESPRESSO. We created predictive models to calculate a SNOMED-based histology score which predicted the endoscopic score. Split-sample validated areas under the ROC curves for the score predicting a non-zero endoscopic score were 0.80 (0.78-0.81) in UC, 0.70 (0.68-0.72) in CD, and 0.76 (0.73-0.78) in IBD-U. In a subset of 2741 individuals with an initial IBD diagnosis and a corresponding record in ESPRESSO with an endoscopic assessment in SWIBREG, the baseline endoscopic and histology scores were associated with time to IBD-related hospitalization (endoscopy log-rank UC p<0.001, CD p=0.020, IBD-U p<0.001; histology log-rank UC p=0.018, CD p=0.960, IBD-U p=0.034).

    Conclusion: Histopathology data in ESPRESSO accurately predict endoscopic scores in SWIBREG. Baseline endoscopic and histologic scores were associated with time to IBD-related hospitalization, particularly in UC. The SNOMED-based histology score can be used as a measure of disease activity in future register-based IBD studies.

  • 8.
    Axelrad, Jordan
    et al.
    Inflammatory Bowel Disease Center at NYU Langone Health, Division of Gastroenterology, Department of Medicine, NYU School of Medicine, New York, New York, USA.
    Olén, Ola
    Clinical Epidemiology Division, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden; Sachs' Children and Youth Hospital, Stockholm South General Hospital, Stockholm, Sweden; Department of Clinical Science and Education Södersjukhuset, Karolinska Institutet, Stockholm, Sweden.
    Söderling, Jonas
    Clinical Epidemiology Division, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Roelstraete, Bjorn
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Khalili, Hamed
    Division of Gastroenterology, Department of Medicine, Massachusetts General Hospital, Boston, MA, USA.
    Song, Mingyang
    Division of Gastroenterology, Department of Medicine, Massachusetts General Hospital, Boston, MA, USA.
    Faye, Adam
    Inflammatory Bowel Disease Center at NYU Langone Health, Division of Gastroenterology, Department of Medicine, NYU School of Medicine, New York, New York, USA.
    Eberhardson, Michael
    Department of Gastroenterology and Hepatology, Linköping University Hospital, Linköping University, Linköping, Sweden; Karolinska Institutet, Stockholm, Sweden.
    Halfvarson, Jonas
    Örebro University, School of Medical Sciences. Department of Gastroenterology, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
    Ludvigsson, Jonas F.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro, Sweden; Department of Medicine, Columbia University College of Physicians and Surgeons, New York, New York, USA.
    Inflammatory Bowel Disease and Risk of Colorectal Polyps: A nationwide population-based cohort study from Sweden2023In: Journal of Crohn's & Colitis, ISSN 1873-9946, E-ISSN 1876-4479, Vol. 17, no 9, p. 1395-1409Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Inflammatory bowel disease (IBD) has been linked to an increased risk of colorectal neoplasia. However, the types and risks of specific polyp types in IBD are less clear.

    METHODS: We identified 41,880 individuals with IBD [Crohn's disease (CD: n=12,850); Ulcerative colitis (UC): n=29,030)] from Sweden matched with 41,880 reference individuals. Using Cox regression, we calculated adjusted hazard ratios (aHRs) for neoplastic colorectal polyps (Tubular, Serrated/Sessile, Advanced and Villous) defined by histopathology codes.

    RESULTS: During follow-up, 1648 (3.9%) IBD patients and 1143 (2.7%) reference individuals had an incident neoplastic colorectal polyp, corresponding to an incidence rate of 46.1 and 34.2 per 10,000 person-years, respectively. This correlated to an aHR of 1.23 (95% CI 1.12-1.35) with the highest HRs seen for sessile serrated polyps (8.50, 95% CI 1.10-65.90) and traditional serrated adenomas (1.72, 95% CI 1.02-2.91). aHRs for colorectal polyps were particularly elevated in those diagnosed with IBD at a young age and after 10 years after diagnosis. Both absolute and relative risks of colorectal polyps were higher in UC than in CD (aHRs 1.31 vs. 1.06, respectively), with a 20-year cumulative risk differences of 4.4% in UC and 1.5% in CD, corresponding to one extra polyp in 23 patients with UC and one in 67 CD patients during the first 20 years after IBD diagnosis.

    CONCLUSIONS: In this nationwide population-based study, there was an increased risk of neoplastic colorectal polyps in IBD patients. Colonoscopic surveillance in IBD appears important, especially in UC and after 10 years of disease.

  • 9.
    Ban, L.
    et al.
    Division of Epidemiology and Public Health, School of Medicine, Nottingham City Hospital, University of Nottingham, Nottingham, United Kingdom.
    West, J.
    Division of Epidemiology and Public Health, School of Medicine, Nottingham City Hospital, University of Nottingham, Nottingham, United Kingdom.
    Sultan, A. Abdul
    Division of Epidemiology and Public Health, School of Medicine, Nottingham City Hospital, University of Nottingham, Nottingham, United Kingdom.
    Dhalwani, N. N.
    Division of Epidemiology and Public Health, School of Medicine, Nottingham City Hospital, University of Nottingham, Nottingham, United Kingdom.
    Ludvigsson, Jonas F.
    Örebro University Hospital.
    Tata, L. J.
    Division of Epidemiology and Public Health, School of Medicine, Nottingham City Hospital, University of Nottingham, Nottingham, United Kingdom.
    Limited risks of major congenital anomalies in children of mothers with coeliac disease: a population-based cohort study2015In: British Journal of Obstetrics and Gynecology, ISSN 1470-0328, E-ISSN 1471-0528, Vol. 122, no 13, p. 1833-1841Article in journal (Refereed)
    Abstract [en]

    Objective: To examine major congenital anomaly (CA) risks in children of mothers with coeliac disease (CD) compared with mothers without CD.

    Design: Population-based cohort study.

    Setting: Linked maternal-child medical records from a large primary care database from the UK.

    Population: A total of 562332 live singletons of mothers with and without CD in 1990-2013.

    Methods: We calculated the absolute major CA risks in children whose mothers had CD, and whether this was diagnosed or undiagnosed before childbirth. Logistic regression with a generalised estimating equation was used to estimate adjusted odds ratios (aORs) with 95% confidence intervals (95% CIs) for CAs associated with CD.

    Main outcome measures: Fourteen system-specific major CA groups classified according to the European Surveillance of Congenital Anomalies and neural tube defects (NTDs).

    Results: Major CA risk in 1880 children of mothers with CD was 293 per 10000 liveborn singletons, similar to the risk in those without CD (282; aOR 0.98, 95% CI 0.74-1.30). The risk was slightly higher in 971 children, whose mothers were undiagnosed (350; aOR 1.14, 95% CI 0.79-1.64), than in 909 children whose mothers were diagnosed (231; aOR 0.80, 95% CI 0.52-1.24). There was a three-fold increase in nervous system anomalies in the children of mothers with undiagnosed CD (aOR 2.98, 95%CI 1.06-8.33, based on five exposed cases and one had an NTD), and these women were all diagnosed with CD at least 4years after their children were born.

    Conclusions: There was no statistically significant increase in risk of major CAs in children of mothers with coeliac disease overall, compared with the general population.

  • 10.
    Ban, Lu
    et al.
    Division of Epidemiology & Public Health, University of Nottingham, Nottingham, United Kingdom; Division of Rheumatology, Orthopaedics and Dermatology, Centre of Evidence Based Dermatology, University of Nottingham, Nottingham, United Kingdom.
    Sprigg, Nikola
    Stroke, Division of Neuroscience, University of Nottingham, Nottingham, United Kingdom.
    Abdul Sultan, Alyshah
    Division of Epidemiology & Public Health, University of Nottingham, Nottingham, United Kingdom; Arthritis Research UK Primary Care Centre, Research Institute for Primary Care & Health Sciences, Keele University, Keele, United Kingdom.
    Nelson-Piercy, Catherine
    Women's Health Academic Centre, Guy's and St. Thomas' NHS Foundation Trust, London, United Kingdom.
    Bath, Philip M
    Women's Health Academic Centre, Guy's and St. Thomas' NHS Foundation Trust, London, United Kingdom.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Paediatrics, Örebro University Hospital, Örebro, Sweden.
    Stephansson, Olof
    Department of Medicine, Karolinska Institutet, Stockholm, Sweden; Department of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden.
    Tata, Laila J
    Division of Epidemiology & Public Health, University of Nottingham, Nottingham, United Kingdom.
    Incidence of First Stroke in Pregnant and Nonpregnant Women of Childbearing Age: A Population-Based Cohort Study From England2017In: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, ISSN 2047-9980, E-ISSN 2047-9980, Vol. 6, no 4, article id e004601Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Pregnant women may have an increased risk of stroke compared with nonpregnant women of similar age, but the magnitude and the timing of such risk are unclear. We examined the risk of a first stroke event in women of childbearing age and compared the risk during pregnancy and in the early postpartum period with the background risk outside these periods.

    METHODS AND RESULTS: We conducted an open cohort study of 2 046 048 women aged 15 to 49 years between April 1, 1997, and March 31, 2014, using linked primary (Clinical Practice Research Datalink) and secondary (Hospital Episode Statistics) care records in England. Risk of first stroke was assessed by calculating the incidence rate of stroke in antepartum, peripartum (2 days before until 1 day after delivery), and early (first 6 weeks) and late (second 6 weeks) postpartum periods compared with nonpregnant time using a Poisson regression model with adjustment for maternal age, socioeconomic group, and calendar time. A total of 2511 women had a first stroke. The incidence rate of stroke was 25.0 per 100 000 person-years (95% CI 24.0-26.0) in nonpregnant time. The rate was lower antepartum (10.7 per 100 000 person-years, 95% CI 7.6-15.1) but 9-fold higher peripartum (161.1 per 100 000 person-years, 95% CI 80.6-322.1) and 3-fold higher early postpartum (47.1 per 100 000 person-years, 95% CI 31.3-70.9). Rates of ischemic and hemorrhagic stroke both increased peripartum and early postpartum.

    CONCLUSIONS: Although the absolute risk of first stroke is low in women of childbearing age, healthcare professionals should be aware of a considerable increase in relative risk during the peripartum and early postpartum periods.

  • 11.
    Bengtsson, Bonnie
    et al.
    Division of Hepatology, Department of Upper GI, Karolinska University Hospital, Stockholm, Sweden; Unit of Gastroenterology andnRheumatology, Department of Medicine, Huddinge, Karolinska Institutet, Stockholm, Sweden.
    Askling, Johan
    Rheumatology, Theme Inflammation and Infection, Karolinska University Hospital, Stockholm, Sweden; Clinical Epidemiology Division, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro, Sweden; Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham, UK; Department of Medicine, Columbia University College of Physicians and Surgeons, New York NY, USA.
    Hagström, Hannes
    Division of Hepatology, Department of Upper GI, Karolinska University Hospital, Stockholm, Sweden; Unit of Gastroenterology andnRheumatology, Department of Medicine, Huddinge, Karolinska Institutet, Stockholm, Sweden; Clinical Epidemiology Division, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.
    Validity of administrative codes associated with cirrhosis in Sweden2020In: Scandinavian Journal of Gastroenterology, ISSN 0036-5521, E-ISSN 1502-7708, Vol. 55, no 10, p. 1205-1210Article in journal (Refereed)
    Abstract [en]

    Objectives: Although cirrhosisis a major cause of liver-related mortality globally, validation studies of the administrative coding for diagnoses associated with cirrhosis are scarce. We aimed to determine the validity of the International Classification of Diseases, 10th revision (ICD-10) codes corresponding to cirrhosis and its complications in the Swedish National Patient Register (NPR).

    Methods: We randomly selected 750 patients with ICD codes for either alcohol-related cirrhosis (K70.3), unspecified cirrhosis (K74.6) oesophageal varices (I85.0/I85.9), hepatocellular carcinoma (HCC, C22.0) or ascites (R18.9) registered in the NPR from 72 healthcare centres in 2000-2016. Hospitalisation events and outpatient visits in specialised care were included. Positive predictive values (PPVs) were calculated using the information in the patient charts as the gold standard.

    Results: Complete data were obtained for 630 (of 750) patients (84%). For alcohol-related cirrhosis, 126/136 cases were correctly coded, corresponding to a PPV of 93% (95% confidence interval, 95%CI: 87-96). The PPV for cirrhosis with unspecified aetiology was 91% (121/133, 95%CI: 85-95) and 96% for oesophageal varices (118/123, 95%CI: 91-99). The PPV was lower for HCC, 84% (91/109, 95%CI: 75-90). The PPV for liver-related ascites was low, 43% (56/129, 95%CI: 35-52), as this category often consisted of non-hepatic ascites. When combining the ascites code with a code for chronic liver disease, the PPV for liver-related ascites increased to 93% (50/54, 95%CI: 82-98).

    Conclusions: The validity of ICD-10 codes for cirrhosis, oesophageal varices and HCC is high. However, coding for ascites should be combined with a code of chronic liver disease to have an acceptable validity.

  • 12.
    Bergman, David
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Brommaplans Primary Health Care Center, Stockholm, Sweden.
    Clemente, Mark S.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Khalili, Flamed
    Division of Gastroenterology, Massachusetts General Hospital, Boston Massachusetts, USA; Harvard Medical School, Boston Massachusetts, USA.
    Agréus, Lars
    Division for Family Medicine and Primary Care, Karolinska Institutet, Huddinge, Sweden.
    Hultcrantz, Rolf
    Unit of Hepatology, Centre for Digestive Diseases, Karolinska University Hospital, Stockholm, Sweden; Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro, Sweden.
    A nationwide cohort study of the incidence of microscopic colitis in Sweden2019In: Alimentary Pharmacology and Therapeutics, ISSN 0269-2813, E-ISSN 1365-2036, Vol. 49, no 11, p. 1395-1400Article in journal (Refereed)
    Abstract [en]

    Background: Epidemiological studies of microscopic colitis have shown varying but increasing incidence rates. Aim To assess the incidence of microscopic colitis in Sweden.

    Methods: Nationwide cohort study performed in 1995-2015 based on biopsy reports. Age-specific and age-standardised incidence rates were calculated.

    Results: We identified 13 844 patients with an incident diagnosis of microscopic colitis. Lymphocytic colitis (n = 9238) constituted 67% and collagenous colitis (n = 4606) 33% of microscopic colitis. The mean age at time of diagnosis of microscopic colitis was 60.2 years (58.6 for lymphocytic colitis, 63.3 for collagenous colitis). The lifetime risk of developing microscopic colitis was 0.87% in women (95% confidence interval, CI: 0.85-0.88) and 0.35% in men (95% CI: 0.34-0.36). From 2006, the overall incidence of microscopic colitis was approximately 10.5 cases per 100 000 person-years (95% CI: 9.8-11.3) with higher rates in women (72% of cases, incidence rate ratio = 2.4 (95% CI: 2.3-2.5) and the elderly with increasing rates up to 75-79 years. From 2006-2015, there was a significant increase of 1% per year (P = 0.02) in the overall microscopic colitis incidence rate in women; the estimated annual percent change was similar, although not statistically significant, in men (P = 0.15).

    Conclusions: In Sweden, the incidence of microscopic colitis is still increasing in women, although the rate appears to be stabilising. The incidence is particularly high in women and the elderly up to age 75-79 years. Finally, across a lifetime, 1 in 115 females and 1 in 286 males are expected to be diagnosed with microscopic colitis and thus posing a considerable disease burden.

  • 13.
    Bergman, David
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Hagström, Hannes
    Division of Hepatology, Department of Upper GI Diseases, Karolinska University Hospital, Stockholm, Sweden; Clinical Epidemiology Unit, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden; Department of Medicine, Huddinge, Karolinska Institutet, Stockholm, Sweden.
    Capusan, Andrea Johansson
    Center for Social and Affective Neuroscience, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden; Department of Psychiatry in Linköping, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
    Mårild, Karl
    Department of Pediatrics, Institute of Clinical Sciences, Sahlgrenska Academy, Gothenburg, Sweden; Department of Pediatric Gastroenterology, Queen Silvia Children’s Hospital, Gothenburg, Sweden.
    Nyberg, Fredrik
    School of Public Health and Community Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Sundquist, Kristina
    Center for Primary Health Care Research, Department of Clinical Sciences, Lund University, Malmö, Sweden.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro, Sweden; Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham, UK; Department of Medicine, Columbia University College of Physicians and Surgeons, New York NY, USA .
    Incidence of ICD-Based Diagnoses of Alcohol-Related Disorders and Diseases from Swedish Nationwide Registers and Suggestions for Coding2020In: Clinical Epidemiology, ISSN 1179-1349, E-ISSN 1179-1349, Vol. 12, p. 1433-1442Article in journal (Refereed)
    Abstract [en]

    Aim: To improve consistency between register studies in Sweden and ensure valid comparisons of possible changes in alcohol-related disorders and diseases (ARDDs) over time, we propose a definition of ARDDs. Based on this definition, we examined Sweden's incidence rates of ARDDs from 1970 to 2018 in non-primary healthcare settings (inpatient and outpatient).

    Methods: Swedish Society of Epidemiology members were invited to give feedback on the International Classification of Disease (ICD) codes with a potential link to alcohol use. We then calculated age-standardised and age-specific incidence of ARDDs over time according to the National Patient Register, and the lifetime prevalence of ARDDs diagnosed in adults alive in Sweden on Dec 31, 2018.

    Results: Sweden's estimated incidence of ARDDs increased substantially after introducing the new ICD-9 codes in 1987. In the past 10 years (2009-2018), the incidence of ARDDs has been stable (males: 110/100,000 person-years, females: 49/100,000 person-years). Requiring at least two ICD records for diagnosed ARDDs led to a somewhat lower incidence of ARDDs (males: 71 per 100,000 person-years, females: 29 per 100,000 person-years). In Sweden, the lifetime prevalence of diagnosed ARDDs in adults on Dec 31, 2018, was 1.9% (95% CI=1.9-1.9). Conclusion: In this nationwide study, we found an incidence of ARDDs of 50-100/100,000 person-years. In 2018, 1 in 52 adults in Sweden had been diagnosed with ARDDs in the National Patient Register.

  • 14.
    Bergman, David
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Khalili, Hamed
    Massachusetts General Hospital, Crohn’s and Colitis Center and Harvard Medical School, Boston MA, USA; Division of Clinical Epidemiology, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Roelstraete, Bjorn
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro, Sweden; Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham, UK; Department of Medicine, Columbia University College of Physicians and Surgeons, New York NY, USA.
    Microscopic Colitis and Risk Of Cancer-AA Population-Based Cohort Study2021In: Journal of Crohn's & Colitis, ISSN 1873-9946, E-ISSN 1876-4479, Vol. 15, no 2, p. 212-221Article in journal (Refereed)
    Abstract [en]

    Background and Aims: The association between microscopic colitis [MC] and cancer risk is unclear. Large, population-based studies are lacking.

    Methods: We conducted a nationwide cohort study of 11 758 patients with incident MC [diagnosed 1990-2016 in Sweden], 50 828 matched reference individuals, and 11 614 siblings to MC patients. Data were obtained through Sweden's pathology departments and from the Swedish Cancer Register. Adjusted hazard ratios [aHRs] were calculated using Cox proportional hazards models.

    Results: At the end of follow-up [mean: 6.7 years], 1239 [10.5%] of MC patients had received a cancer diagnosis, compared with 4815 [9.5%] of reference individuals (aHR 1.08 [95% confidence interval1.02-1.16]). The risk of cancer was highest during the first year of follow up. The absolute excess risks for cancer at 5, 10, and 20 years after MC diagnosis were + 1.0% (95% confidence interval [C1]0.4%-1.6%), +1.5% [0.4%-2.6%], and + 3.7% [-2.3-9.6%], respectively, equivalent to one extra cancer event in every 55 individuals with MC followed for 10 years. MC was associated with an increased risk of lymphoma (aHR 1.43 [1.06-1.92]) and lung cancer (aHR 1.32 [1.04-1.68]) but with decreased risks of colorectal (aHR 0.52 [0.40-0.66]) and gastrointestinal cancers (aHR 0.72 [0.60-0.85]). We found no association with breast or bladder cancer. Using siblings as reference group to minimise the impact of shared genetic and early environmental factors, patients with MC were still at an increased risk of cancer (HR 1.20 [1.06-1.36]).

    Conclusions: This nationwide cohort study demonstrated an 8% increased risk of cancer in MC patients. The risk was highest during the first year of follow-up.

  • 15.
    Bergman, David
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden; Brommaplans Primary Health Care Center, Stockholm County, Stockholm, Sweden.
    King, James
    Centre for health informatics, University of Calgary Cumming School of Medicine, Calgary Alberta, Canada.
    Lebwohl, Benjamin
    Department of Medicine, Celiac Disease Center, Columbia University College of Physicians and Surgeons, New York NY, USA.
    Clements, Mark S.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden.
    Roelstraete, Bjorn
    Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden.
    Kaplan, Gilaad G.
    Department of Medicine, University of Calgary, Calgary Alberta, Canada.
    Green, Peter Hr
    Department of Medicine, Celiac Disease Center, Columbia University College of Physicians and Surgeons, New York NY, USA.
    Murray, Joseph A.
    Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester Minnesota, USA.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro, Sweden.
    Two waves of coeliac disease incidence in Sweden: a nationwide population-based cohort study from 1990 to 20152022In: Gut, ISSN 0017-5749, E-ISSN 1468-3288, Vol. 71, no 6, p. 1088-1094Article in journal (Refereed)
    Abstract [en]

    Objectives: To assess the incidence of biopsy-verified coeliac disease (CD) in Sweden and examine the incidence of duodenal/jejunal biopsies with normal mucosa over time as a proxy for CD awareness and investigation.

    Design: Nationwide population-based cohort study 1990-2015 based on biopsy reports indicating villous atrophy (VA) or normal mucosa in the duodenum/jejunum.

    Results: We identified 44 771 individuals (63% females) with a biopsy report specifying VA and 412 279 (62% females) with a biopsy report indicating normal mucosa (without a prior biopsy indicating VA). The median age at diagnosis of CD was 28 years. The mean age-standardised incidence rate during the study period was 19.0 per 100 000 person-years (95% CI 17.3 to 20.8). The incidence reached a peak in 1994 for both sexes and a second higher peak in 2002-2003 for females and in 2006 for males. The lifetime risk of developing CD was 1.8% (2.3% in females and 1.4% in males). Prior to 2015, there was a parallel rise in rates for biopsies showing normal duodenal/jejunal mucosa.

    Conclusions: In Sweden, the incidence of CD increased until 2002-2003 in females and until 2006 in males. Since then, the incidence of CD has declined despite increasing duodenal/jejunal biopsies, suggesting that increased awareness and investigation are unlikely to elevate the incidence of the disease in Sweden. Across a lifetime, 1 in 44 females and 1 in 72 males are expected to be diagnosed with CD in Sweden, indicating a relatively high societal burden of disease.

  • 16.
    Bjornsdottir, Sigridur
    et al.
    Dept Mol Med & Surg, Karolinska Inst, Stockholm, Sweden.
    Sundstrom, Anders
    Dept Clin Epidemiol Unit, Dept Med, Karolinska Inst, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Örebro University Hospital. Dept Clin Epidemiol Unit, Dept Med, Karolinska Inst, Stockholm, Sweden.
    Blomqvist, Paul
    Dept Clin Epidemiol Unit, Dept Med, Karolinska Inst, Stockholm, Sweden.
    Kampe, Olle
    Dept Med Sci, Uppsala Univ, Uppsala, Sweden.
    Bensing, Sophie
    Dept Mol Med & Surg, Karolinska Inst, Stockholm, Sweden; Dept Med Sci, Uppsala Univ, Uppsala, Sweden.
    Drug Prescription Patterns in Patients With Addison's Disease: A Swedish Population-Based Cohort Study2013In: Journal of Clinical Endocrinology and Metabolism, ISSN 0021-972X, E-ISSN 1945-7197, Vol. 98, no 5, p. 2009-2018Article in journal (Refereed)
    Abstract [en]

    Context: There are no published data on drug prescription in patients with Addison's disease ( AD). Objective: Our objective was to describe the drug prescription patterns in Swedish AD patients before and after diagnosis compared with population controls. Design and Setting: We conducted a population-based cohort study in Sweden. Patients: Through the Swedish National Patient Register and the Swedish Prescribed Drug Register, we identified 1305 patients with both a diagnosis of AD and on combination treatment with hydrocortisone/cortisone acetate and fludrocortisone. Direct evidence of the AD diagnosis from patient charts was not available. We identified 11 996 matched controls by the Register of Population. Main Outcome Measure: We determined the ratio of observed to expected number of patients treated with prescribed drugs. Results: Overall, Swedish AD patients received more prescribed drugs than controls, and 59.3% of the AD patients had medications indicating concomitant autoimmune disease. Interestingly, both before and after the diagnosis of AD, patients used more gastrointestinal medications, antianemic preparations, lipid-modifying agents, antibiotics for systemic use, hypnotics and sedatives, and drugs for obstructive airway disease (all P values < .05). Notably, an increased prescription of several antihypertensive drugs and high-ceiling diuretics was observed after the diagnosis of AD. Conclusion: Gastrointestinal symptoms and anemia, especially in conjunction with autoimmune disorders, should alert the physician about the possibility of AD. The higher use of drugs for cardiovascular disorders after diagnosis in patients with AD raises concerns about the replacement therapy.

  • 17.
    Bledsoe, Adam C.
    et al.
    Department of Internal Medicine, University of South Dakota Sanford School of Medicine, Sioux Falls SD, USA.
    Garber, John J.
    Gastrointestinal Unit, Massachusetts General Hospital, Harvard Medical School, Boston MA, USA.
    Ye, Weimin
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Roelstraete, Bjorn
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Murray, Joseph A.
    Celiac Disease Program, Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester MN, USA.
    Ludvigsson, Jonas F.
    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, Clinical Sciences Building 2, City Hospital, Nottingham, UK; Celiac Disease Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York NY, USA.
    Mortality and cancer in eosinophilic gastrointestinal disorders distal to the esophagus: nationwide cohort study 1990-20172022In: Journal of gastroenterology, ISSN 0944-1174, E-ISSN 1435-5922, Vol. 57, p. 735-747Article in journal (Refereed)
    Abstract [en]

    Background: Eosinophilic gastrointestinal disorders (EGIDs) include inflammatory conditions with enteric infiltration of eosinophils and resulting symptoms. This study aims to examine a population-based sample of patients for prevalence, mortality, and cancer risk in EGIDs distal to the esophagus.

    Methods: Nationwide, population-based cohort study. EGID was identified through relevant biopsy codes from Sweden's all 28 pathology departments through the ESPRESSO cohort. Individuals with EGID were then matched to general population reference individuals with similar age and sex. Study participants were linked to Swedish healthcare registers. Through Cox regression, we calculated adjusted hazard ratios (aHRs) adjusting for sex, age, county, calendar period, and education.

    Results: In total, 2429 patients (56% female) were found to have EGID distal to the esophagus, representing a prevalence of about 1/4800 in the Swedish population. Mean age was 44 years with 11% children at the time of diagnosis. Mortality was increased 17% in patients with EGIDs compared to reference individuals (aHR = 1.17; 95%CI = 1.04-1.33). Excess mortality was seen in gastric and small bowel eosinophilic disease, but not colonic disease (aHR = 1.81; 95%CI = 1.32-2.48, aHR = 1.50; 95%CI = 1.18-1.89, and aHR = 0.99; 95%CI = 0.85-1.16, respectively). Cause specific mortality was driven by cancer-related death (aHR = 1.33; 95%CI = 1.05-1.69). However, this study failed to show an increase in incident cancers (aHR = 1.14; 95%CI = 0.96-1.35). Comparison of EGID individuals with their siblings yielded similar aHRs.

    Conclusions: This study found an increased risk of death in patients with EGIDs distal to the esophagus, with cancer death driving the increase. Proximal gut disease seems to confer the greatest risk. There was no increase in incident cancers.

  • 18. Bonamy, Anna-Karin E
    et al.
    Holmström, Gerd
    Stephansson, Olof
    Ludvigsson, Jonas F
    Örebro University Hospital.
    Cnattingius, Sven
    Preterm birth and later retinal detachment: a population-based cohort study of more than 3 million children and young adults2013In: Ophthalmology, ISSN 0161-6420, E-ISSN 1549-4713, Vol. 120, no 11, p. 2278-2285Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: Ophthalmologic complications after preterm birth are common. Small studies show an association between retinopathy of prematurity and later retinal detachment. There are no population-based studies of preterm birth and risk of retinal detachment, which was the objective of the current investigation.

    DESIGN: Nationwide Swedish cohort study based on population registries.

    PARTICIPANTS: Of 3 423 697 subjects born in Sweden, 1 271 725 were born between 1973 and 1986 (i.e., before the national screening program for retinopathy of prematurity started), and 2 151 972 were born between 1987 and 2008. The participants were followed up from 1 year of age until 2009.

    METHODS: Unadjusted and adjusted hazard ratios (HRs) for retinal detachment were calculated using Cox proportional hazards regression.

    MAIN OUTCOME MEASURES: Incident retinal detachment, as defined by a diagnosis in the Swedish Patient Register (both inpatient and hospital-based outpatient data).

    RESULTS: During follow-up (median follow-up, 17.4 years), 1749 subjects were diagnosed with retinal detachment. Among the 188 852 subjects born prematurely (i.e., at <37 weeks of gestation), there were 124 cases of retinal detachment, of which 42 occurred in the 20 470 subjects born before 32 weeks of gestation. Compared with subjects born at term (37-41 weeks), the adjusted HR for retinal detachment after extremely preterm birth (<28 weeks of gestation) was 19.2 (95% confidence interval [CI], 10.3-35.8) for births between 1973 and 1986 and 8.95 (95% CI, 3.98-20.1) for births between 1987 and 2008. The corresponding HRs in subjects born very prematurely (28-31 weeks) were 4.32 (95% CI, 2.70-6.90) and 2.80 (95% CI, 1.38-5.69), respectively. Moderately preterm birth (32-36 weeks) was not associated with an increased risk of retinal detachment.

    CONCLUSIONS: Birth before 32 weeks of gestation is associated with a substantially increased relative risk of retinal detachment. These findings may have implications for ophthalmologic follow-up of children and adults born very prematurely.

  • 19.
    Bozorg, Soran R.
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden.
    Song, Mingyang
    Department of Epidemiology and Nutrition, Harvard T.H. Chan School of Public Health, Boston MA, United States; Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Harvard Medical School, Boston MA, United States; Division of Gastroenterology, Massachusetts General Hospital, Harvard Medical School, Boston MA, United States.
    Emilsson, Louise
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden; Department of Epidemiology and Nutrition, Harvard T.H. Chan School of Public Health, Boston MA, United States; Institute of Health and Society, University of Oslo, Oslo, Norway; Vårdcentralen Värmlands Nysäter, Centre for Clinical Research, County Council of Värmland, Sweden.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden; Department of Paediatrics, Örebro University Hospital, Örebro, Sweden; Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham, United Kingdom; Department of Medicine, Columbia University College of Physicians and Surgeons, New York NY, United States.
    Validation of serrated polyps (SPs) in Swedish pathology registers2019In: BMC Gastroenterology, ISSN 1471-230X, E-ISSN 1471-230X, Vol. 20, no 1, article id 3Article in journal (Refereed)
    Abstract [en]

    Background: Little is known about the natural history of serrated polyps (SPs), partly due to the lack of large-scale epidemiologic data. In this study, we examined the validity of SP identification according to SNOMED (Systematised Nomenclature of Medicine) codes and free text from colorectal histopathology reports.

    Methods: Through the ESPRESSO (Epidemiology Strengthened by histoPathology Reports in Sweden) study, we retrieved data on SPs from all pathology departments in Sweden in 2015-2017 by using SNOMED codes and free-text search in colorectal histopathology reports. Randomly selected individuals with a histopathology report of SPs were validated against patient charts using a structured, retrospective review.

    Results: SPs were confirmed in 101/106 individuals with a histopathology report of SPs, yielding a positive predictive value (PPV) of 95% (95%CI = 89-98%). By year of diagnosis, the PPV was 89% (95%CI = 69-97%), 96% (95%CI = 81-99%) and 97% (95%CI = 89-99%) for individuals diagnosed before 2001 (n = 19), between 2001 and 2010 (n = 26) and after 2010 (n = 61), respectively. According to search method, the PPV for individuals identified by SNOMED codes was 100% (95%CI = 93-100%), and 93% (95%CI = 86-97%) using free-text search. Recorded location (colon vs. rectum) was correct in 94% of all SP histopathology reports (95%CI = 84-98%) identified by SNOMED codes. Individuals with SPs were classified into hyperplastic polyps (n = 34; 32%), traditional serrated adenomas (n = 3; 3%), sessile serrated adenomas/polyps (SSA/Ps) (n = 70; 66%), unspecified SPs (n = 3, 3%), and false positive SPs (n = 5, 5%). For individuals identified by SNOMED codes, SSA/Ps were confirmed in 49/52 individuals, resulting in a PPV of 94% (95%CI: 84-98%). In total, 57% had >= 2 polyps (1: n = 44, 2-3: n = 33 and >= 4: n = 27). Some 46% of SPs (n = 71) originated from the proximal colon and 24% were >= 10 mm in size (n = 37). Heredity for colorectal cancer, intestinal polyposis syndromes, or both was reported in seven individuals (7%). Common comorbidities included diverticulosis (n = 45, 42%), colorectal cancer (n = 19, 18%), and inflammatory bowel disease (n = 10, 9%).

    Conclusion: Colorectal histopathology reports are a reliable data source to identify individuals with SPs.

  • 20.
    Bozorg, Soran R.
    et al.
    Örebro University, School of Medical Sciences. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm Sweden; University Health Care Research Center, Örebro University Hospital, Örebro, Sweden.
    Söderling, Jonas
    Clinical Epidemiology Division, Department of Medicine, Karolinska Institutet, Sweden.
    Everhov, Åsa H.
    Clinical Epidemiology Division, Department of Medicine, Karolinska Institutet, Sweden; Department of Clinical Science and Education, Södersjukhuset, Karolinska Institutet, Stockholm, Sweden.
    Lebwohl, Benjamin
    Celiac Disease Center, Department of Medicine, Columbia University Medical Centre, Columbia University, New York, USA.
    Green, Peter Hr.
    Celiac Disease Center, Department of Medicine, Columbia University Medical Centre, Columbia University, New York, USA.
    Neovius, Martin
    Clinical Epidemiology Division, Department of Medicine, Karolinska Institutet, Sweden.
    Ludvigsson, Jonas F.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm Sweden; Celiac Disease Center, Department of Medicine, Columbia University Medical Centre, Columbia University, New York, USA; Department of Pediatrics, Örebro University Hospital, Örebro, Sweden.
    Mårild, Karl
    Department of Pediatrics, Institute of Clinical Sciences, Sahlgrenska Academy, Gothenburg, Sweden; Department of Pediatric Gastroenterology, Queen Silvia Children's Hospital, Gothenburg, Sweden.
    Work loss in patients with celiac disease: A population-based longitudinal study2022In: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 20, no 5, p. 1068-1076.e6Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Celiac disease (CD) affects around 1% of the population worldwide. Data on work disability in celiac patients remain scarce. We estimated work loss in celiac patients including its temporal relationship to diagnosis.

    METHODS: Through biopsy reports from Sweden's 28 pathology departments, we identified 16,005 working-aged patients with prevalent CD (villus atrophy) as of January 1, 2015, and 4,936 incident patients diagnosed with CD in 2008-2015. Each patient was matched to up to 5 general-population comparators. Using nationwide social insurance registers, we retrieved prospectively-recorded data on compensation for sick leave and disability leave to assess work loss in patients and comparators.

    RESULTS: In 2015, patients with prevalent CD had a mean of 42.5 lost work days as compared with 28.6 in comparators (mean difference: 14.7, 95%CI: 13.2-16.2), corresponding to a relative increase of 49%. More than half of the work loss (60.1%) in celiac patients was derived from a small subgroup (7%) while 75.4% had no work loss. Among incident patients, the annual mean difference between patients and comparators was 8.0 (5.4-10.6) lost work days 5 years before CD diagnosis, which grew to 13.7 (9.1-18.3) days 5 years after diagnosis. No difference in work loss was observed between patients with or without mucosal healing at follow-up.

    CONCLUSIONS: Celiac patients lost more work days than comparators before their diagnosis, and this loss increased after diagnosis. Identifying patients with an increased risk of work loss may serve as a target to mitigate work disability, and thereby reduce work loss, in CD.

  • 21.
    Bozorg, Soran Rabin
    et al.
    Örebro University, School of Medical Sciences. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm Sweden.
    Söderling, Jonas
    Clinical Epidemiology Division, Department of Medicine, Karolinska Institutet, Sweden.
    Everhiv, Åsa H.
    Clinical Epidemiology Division, Department of Medicine, Karolinska Institutet, Sweden; Department of Clinical Science and Education, Södersjukhuset, Karolinska Institutet, Stockholm, Sweden.
    Lebwohl, Benjamin
    Celiac Disease Center, Department of Medicine, Columbia University Medical Centre, Columbia University, New York, USA.
    Green, Peter H. R.
    Celiac Disease Center, Department of Medicine, Columbia University Medical Centre, Columbia University, New York, USA.
    Neovius, Martin
    Clinical Epidemiology Division, Department of Medicine, Karolinska Institutet, Sweden.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm Sweden; Celiac Disease Center, Department of Medicine, Columbia University Medical Centre, Columbia University, New York, USA; Department of Pediatrics, Örebro University Hospital, Örebro, Sweden.
    Mårild, Karl
    Department of Pediatrics, Institute of Clinical Sciences, Sahlgrenska Academy, Gothenburg, Sweden; Department of Pediatric Gastroenterology, Queen Silvia Children’s Hospital, Gothenburg, Sweden.
    Work loss before and after diagnosis in patients with celiac disease2021In: European Journal of Immunology, ISSN 0014-2980, E-ISSN 1521-4141, Vol. 51, no Suppl. 1, p. 286-286Article in journal (Other academic)
    Abstract [en]

    Celiac disease (CD) is an immune‐mediated disease triggered by gluten intake and affects around 1% of the population worldwide. Although patients with CD have an increased use of healthcare, data on work disability remains scarce. To estimate work loss in patients with CD before and after diagnosis. We identified 16,005 working‐age patients with prevalent CD, and 4,936 incident working‐age patients diagnosed in 2008‐2015 through biopsy reports from Sweden’s 28 pathology departments. CD was defined by presence of villus atrophy (Marsh 3) on biopsy (gold standard). Each patient was compared to up to 5 matched general‐population comparators. Using nationwide social insurance registers, we retrieved prospectively‐recorded data on compensation for sick leave and disability. In 2015, patients with prevalent CD had a mean of 42.5 (95%CI: 40.9‐44.1) lost work days as compared with 28.6 (27.9‐29.2) in the general‐population comparators, corresponding to a relative difference of 49%. Among incident patients, the annual mean difference between patients and comparators was 8.0 (5.4‐10.6) lost work days 5 years before CD diagnosis, which grew to 13.7 (9.1‐18.3) days 5 years after diagnosis. In addition to the continuously increasing mean difference in lost work days over time, there was also a transient increase in work loss in patients with CD during the year of diagnosis (mean difference: 15.6 days, 95%CI: 13.1‐18.0). Patients with CD miss more work days than comparators before their diagnosis, and this loss increases and persists after diagnosis despite presumed installation of treatment with gluten‐free diet. 

  • 22.
    Brew, Bronwyn K.
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden; National Perinatal Epidemiology and Statistics Unit, Centre for Big Data Research in Health and School of Clinical Medicine, University of New South Wales, Kensington, New South Wales, Australia.
    Osvald, Emma Caffrey
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden; Pediatric Allergy and Pulmonology Unit, Astrid Lindgren Children's Hospital, Karolinska University Hospital, Stockholm, Sweden.
    Gong, Tong
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden.
    Hedman, Anna M.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden.
    Holmberg, Kirsten
    Child Health and Parenting (CHAP), Department of Public Health and Caring Sciences, Uppsala University, Uppsala, Sweden.
    Larsson, Henrik
    Örebro University, School of Medical Sciences. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden.
    Ludvigsson, Jonas F.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro, Sweden; .
    Mubanga, Mwenya
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden.
    Smew, Awad I.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden.
    Almqvist, Catarina
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden; Pediatric Allergy and Pulmonology Unit, Astrid Lindgren Children's Hospital, Karolinska University Hospital, Stockholm, Sweden.
    Paediatric asthma and non-allergic comorbidities: A review of current risk and proposed mechanisms2022In: Clinical and Experimental Allergy, ISSN 0954-7894, E-ISSN 1365-2222, Vol. 15, no 9, p. 1035-1047Article, review/survey (Refereed)
    Abstract [en]

    It is increasingly recognized that children with asthma are at a higher risk of other non-allergic concurrent diseases than the non-asthma population. A plethora of recent research has reported on these comorbidities and progress has been made in understanding the mechanisms for comorbidity. The goal of this review was to assess the most recent evidence (2016-2021) on the extent of common comorbidities (obesity, depression and anxiety, neurodevelopmental disorders, sleep disorders and autoimmune diseases) and the latest mechanistic research, highlighting knowledge gaps requiring further investigation. We found that the majority of recent studies from around the world demonstrate that children with asthma are at an increased risk of having at least one of the studied comorbidities. A range of potential mechanisms were identified including common early life risk factors, common genetic factors, causal relationships, asthma medication and embryologic origins. Studies varied in their selection of population, asthma definition and outcome definitions. Next, steps in future studies should include using objective measures of asthma, such as lung function and immunological data, as well as investigating asthma phenotypes and endotypes. Larger complex genetic analyses are needed, including genome-wide association studies, gene expression-functional as well as pathway analyses or Mendelian randomization techniques; and identification of gene-environment interactions, such as epi-genetic studies or twin analyses, including omics and early life exposure data. Importantly, research should have relevance to clinical and public health translation including clinical practice, asthma management guidelines and intervention studies aimed at reducing comorbidities.

  • 23.
    Brooke, Hannah Louise
    et al.
    Unit of Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Talback, Mats
    Unit of Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Hörnblad, Jesper
    National Board of Health and Welfare, Stockholm, Sweden.
    Johansson, Lars Age
    Department of Public Health and Caring Sciences, Uppsala University, Uppsala, Sweden.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Paediatrics, Örebro University Hospital, Örebro, Sweden; Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham, United Kingdom; Department of Medicine, Columbia University College of Physicians and Surgeons, New York NY, United States.
    Druid, Henrik
    Department of Oncology and Pathology, Karolinska Institutet, Stockholm, Sweden.
    Feychting, Maria
    Unit of Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Ljung, Rickard
    Unit of Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    The Swedish cause of death register2017In: European Journal of Epidemiology, ISSN 0393-2990, E-ISSN 1573-7284, Vol. 32, no 9, p. 765-773Article in journal (Refereed)
    Abstract [en]

    Sweden has a long tradition of recording cause of death data. The Swedish cause of death register is a high quality virtually complete register of all deaths in Sweden since 1952. Although originally created for official statistics, it is a highly important data source for medical research since it can be linked to many other national registers, which contain data on social and health factors in the Swedish population. For the appropriate use of this register, it is fundamental to understand its origins and composition. In this paper we describe the origins and composition of the Swedish cause of death register, set out the key strengths and weaknesses of the register, and present the main causes of death across age groups and over time in Sweden. This paper provides a guide and reference to individuals and organisations interested in data from the Swedish cause of death register.

  • 24.
    Bröms, Gabriella
    et al.
    Clinical Epidemiology Division, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden; Department of Internal Medicine, Danderyds Hospital, Stockholm, Sweden.
    Söderling, Jonas
    Clinical Epidemiology Division, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden.
    Sachs, Michael C.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden.
    Halfvarson, Jonas
    Örebro University, School of Medical Sciences. Department of Gastroenterology.
    Myrelid, Par
    Department of Surgery, Linköping University Hospital, Linköping, Sweden; Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
    Ludvigsson, Jonas F.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro, Sweden.
    Everhov, Åsa H.
    Clinical Epidemiology Division, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden; Sachs' Children and Youth Hospital, Stockholm South General Hospital, Stockholm, Sweden.
    Olén, Ola
    Clinical Epidemiology Division, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden; Sachs' Children and Youth Hospital, Stockholm South General Hospital, Stockholm, Sweden; Department of Clinical Science and Education Södersjukhuset, Karolinska Institutet, Stockholm, Sweden.
    Capturing biologic treatment for IBD in the Swedish Prescribed Drug Register and the Swedish National Patient Register: a validation study2021In: Scandinavian Journal of Gastroenterology, ISSN 0036-5521, E-ISSN 1502-7708, Vol. 56, no 4, p. 410-421Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: It is not known to what extent biologic treatment for IBD is captured in the Swedish Prescribed Drug Register (PDR) and the National Patient Register (NPR).

    METHODS: A cross-sectional study from July 2005 until 2017, comparing data on biologic treatment in the PDR and the NPR with medical records. We assessed the proportion of started treatment episodes in the medical records that were found in the PDR/NPR ever, within +/- one year and within +/- three months; for any biologic drug, per specific drug (infliximab, adalimumab, golimumab, vedolizumab, ustekinumab), by calendar period (2005-2008, 2009-2012, and 2013-2017) and by study center. For adalimumab, we assessed the validity of end of treatment episodes.

    RESULTS: Medical records of 1361 patients and 2323 treatment episodes with any biologic were reviewed and 80.1% (95% CI: 78.4-81.7) were ever captured in the PDR/NPR in. A time window of +/- one year or +/- three months reduced the sensitivity to 63.3% (95% CI: 61.3-65.3) and 52.6% (95% CI: 50.5-54.6), respectively. The sensitivity was high (>85%) for the prescribed injection drugs adalimumab, golimumab, and ustekinumab for all time windows and for adalimumab end of treatment, while considerably lower for the infusion drugs infliximab and vedolizumab.

    CONCLUSIONS: The PDR and the NPR are reliable data sources on treatment with injection biologics in patients with IBD in Sweden. Infliximab and vedolizumab are poorly captured, why PDR/NPR data should only be used after careful consideration of their limitations or complemented by other data sources, e.g., the disease-specific quality register SWIBREG.

  • 25.
    Burke, Kristin E.
    et al.
    Gastroenterology Unit, Massachusetts General Hospital, Boston Massachusetts, USA; Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Boston Massachusetts, USA; Harvard Medical School, Boston Massachusetts, USA.
    Ananthakrishnan, Ashwin N.
    Gastroenterology Unit, Massachusetts General Hospital, Boston Massachusetts, USA; Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Boston Massachusetts, USA; Harvard Medical School, Boston Massachusetts, USA.
    Lochhead, Paul
    Gastroenterology Unit, Massachusetts General Hospital, Boston Massachusetts, USA; Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Boston Massachusetts, USA; Harvard Medical School, Boston Massachusetts, USA.
    Liu, Po-Hong
    Gastroenterology Unit, Massachusetts General Hospital, Boston Massachusetts, USA; Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Boston Massachusetts, USA; Harvard Medical School, Boston Massachusetts, USA.
    Olen, Ola
    Pediatric Gastroenterology and Nutrition Unit, Sachs’ Children’s Hospital, Stockholm, Sweden; Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro University, Örebro, Sweden.
    Richter, James M.
    Gastroenterology Unit, Massachusetts General Hospital, Boston Massachusetts, USA; Harvard Medical School, Boston Massachusetts, USA.
    Tworoger, Shelley S.
    Moffit Cancer Center, Tampa Florida, USA; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston Massachusetts, USA.
    Chan, Andrew T.
    Gastroenterology Unit, Massachusetts General Hospital, Boston Massachusetts, USA; Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Boston Massachusetts, USA; Harvard Medical School, Boston Massachusetts, USA; Channing Division of Network Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston Massachusetts, USA; Broad Institute, Cambridge Massachusetts, USA; Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston Massachusetts, USA.
    Khalili, Hamed
    Gastroenterology Unit, Massachusetts General Hospital, Boston Massachusetts, USA; Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Boston Massachusetts, USA; Harvard Medical School, Boston Massachusetts, USA; Karolinska Clinical Epidemiology Unit, Karolinska Institutet, Solna, Sweden.
    Identification of Menopausal and Reproductive Risk Factors for Microscopic Colitis-Results From the Nurses' Health Study2018In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 155, no 6, p. 1764-1775Article in journal (Refereed)
    Abstract [en]

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

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

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

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

  • 26.
    Burke, Kristin E.
    et al.
    Gastroenterology Unit, Massachusetts General Hospital, Boston MA, USA; Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Boston MA, USA; Harvard Medical School, Boston MA, USA.
    Ananthakrishnan, Ashwin N.
    Gastroenterology Unit, Massachusetts General Hospital, Boston MA, USA; Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, BostonMA, USA; Harvard Medical School, Boston MA, USA.
    Lochhead, Paul
    Gastroenterology Unit, Massachusetts General Hospital, Boston MA, USA; Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Boston MA, USA; Harvard Medical School, Boston MA, USA.
    Olen, Ola
    Pediatric Gastroenterology and Nutrition Unit, Sachs' Children's Hospital, Stockholm, Sweden; Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Pediatrics, Örebro University Hospital, Örebro, Sweden; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Richter, James M.
    Gastroenterology Unit, Massachusetts General Hospital, Boston MA, USA; Harvard Medical School, Boston MA, USA.
    Chan, Andrew T.
    Gastroenterology Unit, Massachusetts General Hospital, Boston MA, USA; Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Boston MA, USA; Harvard Medical School, Boston MA, USA; Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston MA, USA.
    Khalili, Hamed
    Gastroenterology Unit, Massachusetts General Hospital, Boston MA, USA; Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Boston MA, USA; Harvard Medical School, Boston MA, USA; Karolinska Clinical Epidemiology Unit, Karolinska Institutet, Solna, Sweden.
    Smoking is Associated with an Increased Risk of Microscopic Colitis: Results From Two Large Prospective Cohort Studies of US Women2018In: Journal of Crohn's & Colitis, ISSN 1873-9946, E-ISSN 1876-4479, Vol. 12, no 5, p. 559-567Article in journal (Refereed)
    Abstract [en]

    Introduction: Long-term data on the influence of smoking on risk of microscopic colitis are limited. We therefore sought to examine and characterize the association between smoking and risk of incident microscopic colitis in two large prospective cohorts of women.

    Methods: We conducted a prospective study of 231,015 women enrolled in the Nurses' Health Study (NHS) and NHSII. Information regarding smoking, other lifestyle factors, and medications were collected biennially from 1976 to 2012 in NHS and 1989 to 2013 in NHSII. Incident cases of microscopic colitis were confirmed through physician medical record review. We used Cox proportional hazards modeling to examine the association between smoking and risk of microscopic colitis.

    Results: We documented 166 incident cases of microscopic colitis over 6,122,779 person-years of follow up. Compared to non-smokers, the multivariable-adjusted hazard ratio (HR) for microscopic colitis was 2.52 (95% CI 1.59 - 4.00) amongst current smokers and 1.54 (95% CI 1.09 - 2.17) amongst past smokers. The risk increased with higher pack-years of smoking (Ptrend = 0.001) and diminished following smoking cessation (Ptrend = 0.017). Current smoking appeared to be more strongly associated with risk of collagenous colitis (3.68; 95% CI 1.94 - 6.97) than lymphocytic colitis (HR 1.71; 95% CI 0.83 - 3.53).

    Conclusion: In two large prospective cohort studies, we observed an association between current smoking and risk of microscopic colitis. Risk of microscopic colitis appeared to increase with higher pack-years and diminish following smoking cessation. Future studies focused on characterizing the biologic mechanisms underlying these associations are warranted.

  • 27.
    Burke, Kristin E.
    et al.
    Gastroenterology Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Boston, MA, USA.
    D'Amato, Mauro
    Gastrointestinal Genetics Lab, CIC bioGUNE, Basque Research and Technology Alliance (BRTA), Derio, Spain; Ikerbasque, Basque Foundation for Science, Bilbao, Spain.
    Ng, Siew C.
    Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, LK Institute of Health Science, The Chinese University of Hong Kong, Shatin, NT, Hong Kong, China.
    Pardi, Darrell S.
    Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN, USA.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Paediatrics, Örebro University Hospital, Örebro, Sweden.
    Khalili, Hamed
    Gastroenterology Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Boston, MA, USA; Institute of Environmental Medicine, Nutrition Epidemiology, Karolinska Institutet, Solna, Sweden.
    Microscopic colitis2021In: Nature reviews. Disease primers, E-ISSN 2056-676X, Vol. 7, no 1, article id 39Article, review/survey (Refereed)
    Abstract [en]

    Microscopic colitis (MC) is an inflammatory disease of the large intestine associated with urgent watery diarrhoea. MC may occur in people of all ages, although the disease primarily affects older women. Once believed to be rare, MC is now known to be a common cause of chronic watery diarrhoea in high-income countries, affecting 1 in 115 women and 1 in 286 men during their lifetime in Swedish population-based estimates. An inappropriate immune response to disturbances in the gut microenvironment is implicated in the pathogenesis of MC. Evidence also supports an underlying genetic basis for disease. The diagnosis of MC relies on clinical symptoms and microscopic assessment of colonic biopsy samples. MC is categorized histologically into collagenous colitis, lymphocytic colitis and their incomplete forms. The mainstay of treatment includes the use of budesonide, with or without adjunctive therapies, and withdrawal of offending drugs. Emerging studies suggest a role for biologicals and immunosuppressive therapies for the management of budesonide-refractory or budesonide-dependent disease. MC can have a substantial negative effect on patient quality of life. The outlook for MC includes a better understanding of the immune response, genetics and the microbiome in disease pathogenesis along with progress in disease management through robust clinical trials.

  • 28.
    Busch, K.
    et al.
    Dept Med, Clin Epidemiol Unit, Karolinska Inst, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Örebro University Hospital. Dept Med, Clin Epidemiol Unit, Karolinska Inst, Stockholm, Sweden; Dept Pediat, Örebro University Hospital, Örebro, Sweden.
    Ekstrom-Smedby, K.
    Dept Med, Clin Epidemiol Unit, Karolinska Inst, Stockholm, Sweden.
    Ekbom, A.
    Dept Med, Clin Epidemiol Unit, Karolinska Inst, Stockholm, Sweden.
    Askling, J.
    Dept Med, Clin Epidemiol Unit, Karolinska Inst, Stockholm, Sweden; Dept Rheumatol, Karolinska Univ Hosp, Stockholm, Sweden.
    Neovius, M.
    Dept Med, Clin Epidemiol Unit, Karolinska Inst, Stockholm, Sweden.
    Nationwide prevalence of inflammatory bowel disease in Sweden: a population-based register study2014In: Alimentary Pharmacology and Therapeutics, ISSN 0269-2813, E-ISSN 1365-2036, Vol. 39, no 1, p. 57-68Article in journal (Refereed)
    Abstract [en]

    Background: Regional studies on inflammatory bowel disease (IBD) suggest an increasing prevalence over time, but no nationwide estimate has been published so far.

    Aim: To estimate the IBD prevalence in 2010 in Sweden overall, by disease, and in specific patient segments.

    Methods: Patients were identified according to international classification codes for ulcerative colitis and Crohn's disease in in-patient care (1987-2010), day surgery and nonprimary out-patient care (1997-2010) in the nationwide Swedish Patient Register.

    Results: Requiring two or more diagnoses of IBD in nonprimary care, a total of 61344 individuals with physician-diagnosed IBD were alive in Sweden in 2010 (mean age 50years; 51% men), corresponding to a prevalence of 0.65% (95% CI, 0.65-0.66). The prevalence increased with age, and peaked in women at ages 50-59years and in men at ages 60-69years. Adding the requirement of IBD as main (vs. main or contributory) diagnosis code, or diagnosis from an internal medicine/gastroenterology/surgery department did not change the prevalence estimate. Prevalence of actively treated disease (defined as two or more IBD-related visits, of which one occurred in 2010, plus at least one dispensed prescription of IBD-related drugs in 2010) was 0.27% (95% CI, 0.27-0.28).

    Conclusions: The Swedish nationwide register-based IBD prevalence was higher compared with previous Swedish and international estimates. While prevalence estimates were robust across different case definitions, once two or more visits were required, only about one-third of prevalent patients were drawing resources from specialised care in 2010.

  • 29.
    Busch, Katharina
    et al.
    Dept Med Solna, Clin Epidemiol Unit, Karolinska Inst, Stockholm, Sweden.
    da Silva, Simone A.
    Dept Prevent Med, Univ Sao Paulo, Sao Paulo, Brazil.
    Holton, Michelle
    Lorimer Enterprises Inc, Red Deer AB, Canada.
    Rabacow, Fabiana M.
    Dept Prevent Med, Univ Sao Paulo, Sao Paulo, Brazil.
    Khalili, Named
    Digest Healthcare Ctr, Massachusetts Gen Hosp, Boston, USA.
    Ludvigsson, Jonas F.
    Örebro University Hospital. Dept Pediat, Örebro University Hospital, Örebro, Sweden; Dept Med Epidemiol & Biostat, Karolinska Inst, Stockholm, Sweden.
    Sick leave and disability pension in inflammatory bowel disease: A systematic review2014In: Journal of Crohn's & Colitis, ISSN 1873-9946, E-ISSN 1876-4479, Vol. 8, no 11, p. 1362-1377Article, review/survey (Refereed)
    Abstract [en]

    Background & aims: Inflammatory bowel disease has considerable effects on work-related outcomes and leads to high societal costs due to sick leave and disability pension. The aims of this study were to systematically review evidence on work-related outcomes that are relevant to productivity losses and to evaluate whether medical or surgical interventions have a positive impact on patients work ability.

    Methods: A systematic literature search in PubMed was conducted in June 2013. Abstracts were screened by two independent reviewers, and full-text articles describing the frequency of work-related outcomes were retrieved. Two independent reviewers extracted data according to the PRISMA Statement for Reporting Systematic Reviews and Meta-Analyses. Findings were organized by study design (non-interventional/interventional). Non-interventional studies were structured according to whether they presented data in comparison to control groups or not and interventional studies were summarized according to type of intervention.

    Results: This review included 30 non-interventional (15 with comparison groups and 15 without comparison group) and 17 interventional studies (9 surgical and 8 medical). The majority of the studies reported a high burden of work:related outcomes among inflammatory bowel disease patients regardless of the methodology used. While biologic agents showed positive effect on work absenteeism and presenteeism in randomized clinical trials, the impact of surgical interventions needs further evaluation.

    Conclusions: Inflammatory bowel disease patients experience a high burden in work-related outcomes. Additional data on productivity losses and the long-term impact of interventions is needed to help inform decision-makers about treatment options and their benefits in reducing productivity losses in inflammatory bowel disease patients. (C) 2014 European Crohn's and Colitis Organisation. Published by Elsevier B.V. All rights reserved.

  • 30.
    Butwicka, Agnieszka
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden;.
    Lichtenstein, Paul
    Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden .
    Frisén, Louise
    Child and Adolescent Psychiatry Research Center, Stockholm, Sweden; Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden.
    Almqvist, Catarina
    Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden; Child and Adolescent Psychiatry Research Center, Stockholm, Sweden.
    Larsson, Henrik
    Örebro University, School of Medical Sciences. Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Medical Epidemiology and Biostatistics, 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; Department of Medicine, Columbia University College of Physicians and Surgeons, New York NY, United States.
    Celiac disease is associated with childhood psychiatric disorders: A Population-Based Study2017In: Journal of Pediatrics, ISSN 0022-3476, E-ISSN 1097-6833, Vol. 184, p. 87-93.e1, article id S0022-3476(17)30153-1Article in journal (Refereed)
    Abstract [en]

    OBJECTIVES: To determine the risk of future childhood psychiatric disorders in celiac disease, assess the association between previous psychiatric disorders and celiac disease in children, and investigate the risk of childhood psychiatric disorders in siblings of celiac disease probands.

    STUDY DESIGN: This was a nationwide registry-based matched cohort study in Sweden with 10 903 children (aged <18 years) with celiac disease and 12 710 of their siblings. We assessed the risk of childhood psychiatric disorders (any psychiatric disorder, psychotic disorder, mood disorder, anxiety disorder, eating disorder, psychoactive substance misuse, behavioral disorder, attention-deficit hyperactivity disorder [ADHD], autism spectrum disorder [ASD], and intellectual disability). HRs of future psychiatric disorders in children with celiac disease and their siblings was estimated by Cox regression. The association between previous diagnosis of a psychiatric disorder and current celiac disease was assessed using logistic regression.

    RESULTS: Compared with the general population, children with celiac disease had a 1.4-fold greater risk of future psychiatric disorders. Childhood celiac disease was identified as a risk factor for mood disorders, anxiety disorders, eating disorders, behavioral disorders, ADHD, ASD, and intellectual disability. In addition, a previous diagnosis of a mood, eating, or behavioral disorder was more common before the diagnosis of celiac disease. In contrast, siblings of celiac disease probands were at no increased risk of any of the investigated psychiatric disorders.

    CONCLUSIONS: Children with celiac disease are at increased risk for most psychiatric disorders, apparently owing to the biological and/or psychological effects of celiac disease.

  • 31.
    Butwicka, Agnieszka
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden; Department of Child Psychiatry, Medical University of Warsaw, Warsaw, Poland; Stockholm Health Care Services, Stockholm County Council, Stockholm, Sweden.
    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; Unit of Biostatistics, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Larsson, Henrik
    Örebro University, School of Medical Sciences. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden.
    Halfvarson, Jonas
    Örebro University, School of Medical Sciences. Department of Gastroenterology.
    Almqvist, Catarina
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden; Lung and Allergy Unit, Astrid Lindgren Children's Hospital, Stockholm, Sweden.
    Lichtenstein, Paul
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden.
    Serlachius, Eva
    Stockholm Health Care Services, Stockholm County Council, Stockholm, Sweden; Centre for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Frisén, Louise
    Stockholm Health Care Services, Stockholm County Council, Stockholm, Sweden; Centre for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    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; Department of Medicine, Columbia University College of Physicians and Surgeons, New York, New York.
    Association of Childhood-Onset Inflammatory Bowel Disease With Risk of Psychiatric Disorders and Suicide Attempt2019In: JAMA pediatrics, ISSN 2168-6203, E-ISSN 2168-6211, Vol. 173, no 10, p. 969-978Article in journal (Refereed)
    Abstract [en]

    Importance: Inflammatory bowel disease (IBD) has been associated with psychiatric morbidity in adults, although previous studies have not accounted for familial confounding. In children, IBD has an even more severe course, but the association between childhood-onset IBD and psychiatric morbidity remains unclear.

    Objective: To examine the risk of psychiatric morbidity in individuals with childhood-onset IBD, controlling for potential confounding shared between siblings.

    Design, Setting, and Participants: A population-based cohort study was conducted using data from the Swedish national health care and population registers of all children younger than 18 years born from 1973 to 2013. The study included 6464 individuals with a diagnosis of childhood-onset IBD (3228 with ulcerative colitis, 2536 with Crohn disease, and 700 with IBD unclassified) who were compared with 323 200 matched reference individuals from the general population and 6999 siblings of patients with IBD. Cox proportional hazards regression was used to estimate hazard ratios (HRs) with 95% CIs. Statistical analysis was performed from January 1, 1973, to December 1, 2013.

    Main Outcomes and Measures: The primary outcome was any psychiatric disorder and suicide attempt. Secondary outcomes were the following specific psychiatric disorders: psychotic, mood, anxiety, eating, personality, and behavioral disorders; substance misuse; attention-deficit/hyperactivity disorder; autism spectrum disorders; and intellectual disability.

    Results: The study included 6464 individuals with a diagnosis of childhood-onset IBD (2831 girls and 3633 boys; mean [SD] age at diagnosis of IBD, 13 [4] years). During a median follow-up time of 9 years, 1117 individuals with IBD (17.3%) received a diagnosis of any psychiatric disorder (incidence rate, 17.1 per 1000 person-years), compared with 38 044 of 323 200 individuals (11.8%) in the general population (incidence rate, 11.2 per 1000 person-years), corresponding to an HR of 1.6 (95% CI, 1.5-1.7), equaling 1 extra case of any psychiatric disorder per 170 person-years. Inflammatory bowel disease was significantly associated with suicide attempt (HR, 1.4; 95% CI, 1.2-1.7) as well as mood disorders (HR, 1.6; 95% CI, 1.4-1.7), anxiety disorders (HR, 1.9; 95% CI, 1.7-2.0) eating disorders (HR, 1.6; 95% CI, 1.3-2.0), personality disorders (HR, 1.4; 95% CI, 1.1-1.8), attention-deficit/hyperactivity disorder (HR, 1.2; 95% CI, 1.1-1.4), and autism spectrum disorders (HR, 1.4; 95% CI, 1.1-1.7) Results were similar for boys and girls. Hazard ratios for any psychiatric disorder were highest in the first year of follow-up but remained statistically significant after more than 5 years. Psychiatric disorders were particularly common for patients with very early-onset IBD (<6 years) and for patients with a parental psychiatric history. Results were largely confirmed by sibling comparison, with similar estimates noted for any psychiatric disorder (HR, 1.6; 95% CI, 1.5-1.8) and suicide attempt (HR, 1.7; 95% CI, 1.2-2.3).

    Conclusions and Relevance: Overall, childhood-onset IBD was associated with psychiatric morbidity, confirmed by between-sibling results. Particularly concerning is the increased risk of suicide attempt, suggesting that long-term psychological support be considered for patients with childhood-onset IBD.

  • 32.
    Butwicka, Agnieszka
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Child Psychiatry, Medical University of Warsaw, Warsaw, Poland.
    Sariaslan, Amir
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Larsson, Henrik
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Halfvarson, Jonas
    Örebro University, School of Medical Sciences. Department of Gastroenterology.
    Myrelid, Pär E.
    Division of Surgery, Department of Clinical and Experimental Medicine, Faulty of Health Sciences, Linköping University, Linköping, Sweden; Department of Surgery, County Council of Östergötland, Linköping, Sweden.
    Olén, Ola
    Sachs' Children and Youth Hospital, Stockholm South General Hospital, Stockholm, Sweden; Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Frisen, Louise
    Child and Adolescent Psychiatry Research Center, Stockholm, Sweden; Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden.
    Lichtenstein, Paul
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro University, Örebro, Sweden.
    No association between urbanisation, neighbourhood deprivation and IBD: a population-based study of 4 million individuals2019In: Gut, ISSN 0017-5749, E-ISSN 1468-3288, Vol. 68, no 5, p. 947-948Article in journal (Refereed)
  • 33.
    Cameron, Raquel
    et al.
    College of Health, Medicine and Wellbeing, University of Newcastle, Newcastle, Australia; NHMRC Centre for Research Excellence in Digestive Health, Newcastle, Australia; Hunter Medical Research Institute, Newcastle, Australia.
    Walker, Marjorie M.
    College of Health, Medicine and Wellbeing, University of Newcastle, Newcastle, Australia; NHMRC Centre for Research Excellence in Digestive Health, Newcastle, Australia.
    Thuresson, Marcus
    Statisticon AB, Uppsala, Sweden.
    Roelstraete, Bjorn
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Sköldberg, Filip
    Department of Surgical Sciences, Uppsala University, Uppsala, Sweden.
    Olén, Ola
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Talley, Nicholas J.
    College of Health, Medicine and Wellbeing, University of Newcastle, Newcastle, Australia; NHMRC Centre for Research Excellence in Digestive Health, Newcastle, Australia; Hunter Medical Research Institute, Newcastle, Australia.
    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; Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham, UK; Celiac Disease Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York NY, USA.
    Mortality risk increased in colonic diverticular disease: a nationwide cohort study2022In: Annals of Epidemiology, ISSN 1047-2797, E-ISSN 1873-2585, Vol. 76, p. 39-49Article in journal (Refereed)
    Abstract [en]

    Introduction: There are limited population cohort data on overall and cause-specific mortality in colonic diverticular disease.

    Objective: To measure overall and cause-specific mortality in colonic diverticular disease, compared to matched reference individuals and siblings.

    Methods: Population-based cohort study ("the ESPRESSO study") in Sweden. There were 97,850 cases with a medical diagnosis of diverticular disease (defined by international classification of disease codes) and colorectal histology identified in 1987-2017 from histopathology reports. The mortality risk between individuals with colonic diverticular disease and matched reference individuals ( n = 453/634) from the general population was determined. Cox regression models adjusted for comorbidity estimated hazard ratios (HRs) for all-cause mortality.

  • 34.
    Canova, C.
    et al.
    Unit of Biostatistics, Epidemiology and Public Health, Department of Cardio-Thoraco-Vascular Sciences and Public Health, University of Padua, Padua, Italy.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro University, Örebro, Sweden; Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham, United Kingdom; Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY, United States.
    Di Domenicantonio, R.
    Department of Epidemiology, Lazio Regional Health Service, ASL Rome, Italy.
    Zanier, L.
    Epidemiological Service, Health Directorate, Udine, Italy.
    Amidei, C. B.
    Unit of Biostatistics, Epidemiology and Public Health, Department of Cardio-Thoraco-Vascular Sciences and Public Health, University of Padua, Padua, Italy.
    Zingone, F.
    Department of Surgery, Oncology and Gastroenterology, Gastroenterology Section, University Hospital of Padua, Padua, Italy.
    Perinatal and antibiotic exposures and the risk of developing childhood-onset inflammatory bowel disease: A nested case-control study based on a population-based birth cohort2020In: International Journal of Environmental Research and Public Health, ISSN 1661-7827, E-ISSN 1660-4601, Vol. 17, no 7, article id 2409Article in journal (Refereed)
    Abstract [en]

    The role of early-life environmental exposures on Inflammatory Bowel Disease (IBD) onset remains unclear. We aimed to quantify the impact of perinatal conditions and antibiotic use in the first 6 and 12 months of life, on the risk of childhood-onset IBD, in a birth cohort of the region Friuli-Venezia Giulia (Italy). A nested case-control design on a longitudinal cohort of 213,515 newborns was adopted. Conditional binomial regression models were used to estimate Odds Ratios (OR) with 95% confidence intervals (CI) for all analyzed risk factors. We identified 164 individuals with IBD onset before the age of 18 years and 1640 controls. None of the considered perinatal conditions were associated with IBD. Analyses on antibiotic exposure were based on 70 cases and 700 controls. Risks were significantly higher for children with ≥4 antibiotic prescriptions in the first 6 and 12 months of life (OR = 6.34; 95%CI 1.68–24.02 and OR = 2.91; 95%CI 1.31–6.45, respectively). This association was present only among patients with Crohn’s disease and those with earlier IBD onset. We found that perinatal characteristics were not associated to IBD, while the frequent use of antibiotics during the first year of life was associated to an increased risk of developing subsequent childhood-onset IBD.

  • 35.
    Canova, Cristina
    et al.
    Department of Cardio-Thoraco-Vascular Sciences and Public Health, University of Padua, Padua, Italy.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro, Sweden; Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham, UK; Department of Medicine, Columbia University College of Physicians and Surgeons, New York, USA.
    Baldo, Vincenzo
    Department of Cardio-Thoraco-Vascular Sciences and Public Health, University of Padua, Padua, Italy.
    Amidei, Claudio Barbiellini
    Department of Cardio-Thoraco-Vascular Sciences and Public Health, University of Padua, Padua, Italy.
    Zanier, Loris
    Epidemiological Service, Health Directorate, Udine, Italy.
    Zingone, Fabiana
    Department of Surgery, Oncology and Gastroenterology, Gastroenterology Section, University Hospital of Padua, Padua, Italy.
    Risk of bacterial pneumonia and pneumococcal infection in youths with celiac disease: A population-based study2019In: Digestive and Liver Disease, ISSN 1590-8658, E-ISSN 1878-3562, Vol. 51, no 8, p. 1101-1105Article in journal (Refereed)
    Abstract [en]

    Objective: Assess the risk of hospitalizations for bacterial pneumonia or pneumococcal infections, in a cohort of young individuals with celiac disease (CD) compared to matched references.

    Study design: The cohort consists of 213,635 individuals, born in 1989-2012 and resident in Friuli-Venezia Giulia (Italy). Through pathology reports, hospital discharge records or co-payment exemptions, we identified 1294 CD patients and 6470 reference individuals matched by gender and birth year. We considered hospital admissions for first episodes of bacterial pneumonia and pneumococcal infections. Hazard ratios (HRs) for episodes after CD diagnosis were calculated with Cox regression and odds ratios (OR) for the ones before CD diagnosis with conditional logistic regression. Further analyses were performed on unvaccinated follow-up periods.

    Results: 14 CD patients (in 9450 person-years) and 42 references (in 48,335 person-years) experienced a first episode of bacterial pneumonia, with an increased risk among CD patients (HR 1.82; 95% CI 0.98-3.35). Risks of bacterial pneumonia were significantly increased before CD diagnosis and especially the year before CD diagnosis (OR 6.00, 95% CI 1.83-19.66). Risks of pneumococcal infections showed a non-significant increase in CD patients.

    Conclusions: CD children and youth showed an increased risk of bacterial pneumonia, especially in proximity to CD diagnosis. Anti-pneumococcal vaccination should be recommended to all young CD patients. (C) 2019 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.

  • 36.
    Canova, Cristina
    et al.
    Department of Cardiac, Thoracic and Vascular Sciences and Public Health, University of Padua, Padua, Italy.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro University, Örebro, Sweden; Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham, UK; Department of Medicine, Columbia University College of Physicians and Surgeons, New York, New York, USA.
    Barbiellini Amidei, Claudio
    Department of Cardiac, Thoracic and Vascular Sciences and Public Health, University of Padua, Padua, Italy.
    Zanier, Loris
    Epidemiological Service, Health Directorate, Friuli Venezia-Giulia Region, Udine, Italy.
    Zingone, Fabiana
    Department of Surgery, Oncology and Gastroenterology, Gastroenterology Section, University Hospital of Padua, Italy.
    The risk of epilepsy in children with celiac disease: a population-based cohort study2020In: European Journal of Neurology, ISSN 1351-5101, E-ISSN 1468-1331, Vol. 27, no 6, p. 1089-1095Article in journal (Refereed)
    Abstract [en]

    Background and purpose: The purpose was to estimate the risk of epilepsy in a cohort of young individuals with celiac disease (CD) compared to that of matched references.

    Methods: The cohort consists of 213,635 individuals born during 1989-2011 and residing in Friuli-Venezia Giulia (Italy). We identified 1,215 individuals affected by CD and 6,075 reference individuals matched by sex and age. Epilepsy was defined by means of hospital diagnosis or drug prescriptions. Conditional logistic regression was used to estimate the odds ratios (ORs) of having epilepsy among individuals with CD, before CD diagnosis and in the entire period, compared with those of their matched references. Cox regression was used to calculate the hazard ratios (HRs) for epilepsy diagnosed after CD diagnosis. Different definitions of epilepsy were used for sensitivity analyses.

    Results: Thirty-one (2.6%) individuals with CD and 78 (1.3%) reference individuals had epilepsy (adjusted OR: 2.03 95%CI: 1.33-3.10). The risk of epilepsy was increased prior to CD (adjusted OR: 2.29; 95%CI: 1.33-3.94), with similar estimates after CD diagnosis (adjusted HR 1.96; 95%CI: 0.95-4.02). The increased risk of epilepsy was not explained by a peak in epilepsy diagnosis just around CD diagnosis. Sex stratification found a significantly higher risk of epilepsy among female individuals with CD. Sensitivity analyses confirmed the positive association between CD and epilepsy.

    Conclusion: Children and youths with CD were at increased risk of epilepsy. Patients with epilepsy without a clear etiology should be screened for CD since an early diagnosis and treatment might improve the response to antiepileptic therapies.

  • 37.
    Canova, Cristina
    et al.
    Dept Mol Med, Lab Publ Hlth & Populat Studies, Univ Padua, Padua, Italy.
    Pitter, Gisella
    Dept Mol Med, Lab Publ Hlth & Populat Studies, Univ Padua, Padua, Italy.
    Ludvigsson, Jonas F.
    Örebro University Hospital. Dept Med Epidemiol & Biostat, Karolinska Inst, Stockholm, Sweden.; Dept Pediat, Örebro University Hospital, Örebro, Sweden.
    Romor, Pierantonio
    Reg Hlth Informat Syst, Informat Sistema Enti Locali INSIEL SpA, Udine, Italy.
    Zanier, Loris
    Epidemiol Serv, Hlth Directorate Friuli Venezia Giulia Reg, Udine, Italy.
    Zanotti, Renzo
    Dept Mol Med, Lab Publ Hlth & Populat Studies, Univ Padua, Padua, Italy.
    Simonato, Lorenzo
    Dept Mol Med, Lab Publ Hlth & Populat Studies, Univ Padua, Padua, Italy.
    Coeliac disease and asthma association in children: the role of antibiotic consumption2015In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 46, no 1, p. 115-122Article in journal (Refereed)
    Abstract [en]

    The relationship between coeliac disease and asthma has been scarcely investigated. Infant antibiotic exposure has been linked to both diseases. We evaluated the association between childhood coeliac disease and asthma and the role of antibiotics in the first year of life. We followed a cohort of children born in 1995-2011 in the Friuli-Venezia Giulia region (Italy). Prescriptions for antibiotics in the first year of life and subsequent treated asthma were retrieved from drug prescription records; coeliac disease incident cases were identified from pathology reports, hospital discharges and exemption from prescription charges for clinical tests.We estimated incidence rate ratios (IRRs) using multivariate Poisson regression models. Among the 143 144 children, we identified 717 coeliac children and 34 969 asthmatics. Children with asthma were at increased risk of coeliac disease (IRR 1.46, 95% CI 1.25-1.67). Restricting the analysis to asthma that occurred before the diagnosis of coeliac disease, the excess risk disappeared, except for coeliac disease diagnosed after 5 years of age (IRR 1.37, 95% CI 1.09-1.71). Antibiotics were not a confounding factor in these associations. Childhood treated asthma and coeliac disease are significantly associated. This association is not confounded by antibiotic exposure in the first year of life and may be explained by other shared risk factors.

  • 38.
    Canova, Cristina
    et al.
    Department of Cardiological, Thoracic and Vascular Sciences, University of Padua, Padua, Italy.
    Pitter, Gisella
    Department of Cardiological, Thoracic and Vascular Sciences, University of Padua, Padua, Italy.
    Zanier, Loris
    Epidemiological Service, Health Directorate, Friuli Venezia-Giulia Region, Udine, Italy.
    Simonato, Lorenzo
    Department of Cardiological, Thoracic and Vascular Sciences, University of Padua, Padua, Italy.
    Michaelsson, Karl
    Department of Surgical Sciences, Uppsala University, Uppsala, Sweden.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro University, Örebro, Sweden; Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham, United Kingdom; Department of Medicine, Columbia University College of Physicians and Surgeons, New York NY, USA.
    Risk of Fractures in Youths with Celiac Disease: A Population-Based Study2018In: The Journal of Pediatrics, ISSN 0022-3476, E-ISSN 1097-6833, Vol. 198, p. 117-120Article in journal (Refereed)
    Abstract [en]

    Objective: To assess the risk of any fracture requiring hospital care in a cohort of individuals with celiac disease diagnosed in childhood/adolescence compared with reference individuals matched by age and sex.

    Study design: Our study cohort consisted of 213 635 people born and residing in Friuli-Venezia Giulia Region, Italy, in 1989-2011. We selected, through pathology reports, hospital discharge records, or co-payment exemptions, 1233 individuals with celiac disease (aged 0-17 years at diagnosis) and compared them with 6167 reference individuals matched by sex and year of birth. Fractures were identified through hospital discharge records. We calculated hazard ratios (HRs) for any fracture after celiac disease diagnosis (or index date for reference individuals) with Cox regression and ORs for any fracture before celiac disease diagnosis with conditional logistic regression.

    Results: During the follow-up period (maximum 23 years), 22 individuals with celiac disease (9394 person-years) and 128 reference individuals (47 308 person-years) experienced a fracture. giving an overall HR of 0.87 (95% CI 0.55-1.37). The risk was not modified by sex, age at diagnosis, or calendar period of diagnosis. We obtained similar HRs when excluding fractures occurring after the age of 18 years and adjusting for maternal education or vitamin D supplementation. The odds of previous fracture also did not differ between subjects with celiac disease and reference individuals (22 and 96 cases, respectively: OR 1.15: 95% CI 0.72-1.84).

    Conclusions: We did not find any evidence of an increased risk of fractures during childhood and youth among patients with celiac disease.

  • 39.
    Canova, Cristina
    et al.
    Department of Molecular Medicine, University of Padua, Padua, Italy.
    Pitter, Gisella
    Department of Molecular Medicine, University of Padua, Padua, Italy; School of Specialization in Hygiene and Preventive Medicine, University of Padua, Padua, Italy.
    Zanier, Loris
    Epidemiological Service, Udine, Italy.
    Zanotti, Renzo
    Department of Molecular Medicine, University of Padua, Padua, Italy.
    Simonato, Lorenzo
    Department of Cardiological, Thoracic and Vascular Sciences, University of Padua, Padua, Italy.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden; Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham, United Kingdom; Department of Medicine, College of Physicians and Surgeons, Columbia University, New York NY, USA.
    Inflammatory Bowel Diseases in Children and Young Adults with Celiac Disease: A Multigroup Matched Comparison2017In: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 23, no 11, p. 1996-2000Article in journal (Refereed)
    Abstract [en]

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

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

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

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

  • 40.
    Cantarutti, Anna
    et al.
    National Centre for Healthcare Research and Pharmacoepidemiology, Milan, Italy; Laboratory of Healthcare Research & Pharmacoepidemiology, Department of Statistics and Quantitative Methods, University of Milano-Bicocca, Milan, Italy.
    Barbiellini Amidei, Claudio
    Unit of Biostatistics, Epidemiology and Public Health, Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padova, Padova, Italy.
    Valsecchi, Camilla
    Laboratory of Healthcare Research & Pharmacoepidemiology, Department of Statistics and Quantitative Methods, University of Milano-Bicocca, Milan, Italy.
    Scamarcia, Antonio
    Pedianet Project, Padua, Italy.
    Corrao, Giovanni
    National Centre for Healthcare Research and Pharmacoepidemiology, Milan, Italy; Laboratory of Healthcare Research & Pharmacoepidemiology, Department of Statistics and Quantitative Methods, University of Milano-Bicocca, Milan, Italy.
    Gregori, Dario
    Division of Pediatric Infectious Diseases, Department of Woman’s and Child’s Health, University of Padua, Padua, Italy.
    Giaquinto, Carlo
    Univ Padua, Div Pediat Infect Dis, Dept Womans & Childs Hlth, I-35131 Padua, Italy..
    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; Division of Epidemiology and Public Health, University of Nottingham School of Medicine, Nottingham, UK; Celiac Disease Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York NY, USA.
    Canova, Cristina
    Unit of Biostatistics, Epidemiology and Public Health, Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padova, Padova, Italy.
    Association of Treated and Untreated Gastroesophageal Reflux Disease in the First Year of Life with the Subsequent Development of Asthma2021In: International Journal of Environmental Research and Public Health, ISSN 1661-7827, E-ISSN 1660-4601, Vol. 18, no 18, article id 9633Article in journal (Refereed)
    Abstract [en]

    Introduction: Gastroesophageal reflux disease (GERD) as well as its treatment with acid-suppressive medications have been considered possible risk factors for the development of asthma, but few studies have disentangled the role of GERD with that of its treatment. The present study aimed at estimating the association of treated and untreated GERD in the first year of life with the risk of asthma.

    Methods: Retrospective cohort study including all children born between 2004 and 2015 registered in Pedianet, an Italian primary care database. We analyzed the association of children exposed to GERD (both treated and untreated) in the first year of life with the risk of developing clinically assessed asthma (clinical asthma) after 3 years. Secondary outcomes included asthma identified by anti-asthmatic medications (treated asthma) and wheezing after 3 years. Hazard ratios (HR) and 95% confidence intervals (CI) were estimated comparing children with and without GERD, stratifying by treatment with acid-suppressive medications.

    Results: Out of 86,381 children, 1652 (1.9%) were affected by GERD in the first year of life, of which 871 (53%) were treated with acid-suppressive medications. Compared with controls, children with GERD were at increased risk of clinical asthma (HR: 1.40, 95% CI 1.15-1.70). Risks were similar between treated and untreated GERD (p = 0.41). Comparable results were found for treated asthma, but no risk increase was seen for wheezing.

    Discussion: Early-life GERD was associated with subsequent childhood asthma. Similar risks among children with treated and untreated GERD suggest that acid-suppressive medications are unlikely to play a major role in the development asthma.

  • 41.
    Carr, Hanna
    et al.
    Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Cnattingius, Sven
    Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Granath, Fredrik
    Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Bonamy, Anna-Karin Edstedt
    Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden; Department of Women ’ s and Children’s Health, Karolinska Institutet, Stockholm, Sweden.
    Preterm Birth and Risk of Heart Failure Up to Early Adulthood2017In: Journal of the American College of Cardiology, ISSN 0735-1097, E-ISSN 1558-3597, Vol. 69, no 21, p. 2634-2642Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: In small clinical studies, preterm birth was associated with altered cardiac structure and increased cardiovascular mortality in the young.

    OBJECTIVES: The goal of this study was to determine the association between preterm birth and risk of incident heart failure (HF) in children and young adults.

    METHODS: This register-based cohort study included 2,665,542 individuals born in Sweden from 1987 to 2012 who were followed up from 1 year of age to December 31, 2013. The main study outcome was diagnosis of HF in the National Patient Register or the Cause of Death Register. The association between preterm birth and risk of incident HF was analyzed by using a Poisson regression model. Estimates were adjusted for maternal and pregnancy characteristics, socioeconomic status, and maternal and paternal cardiovascular disease.

    RESULTS: During 34.8 million person-years of follow-up (median 13.1 years), there were 501 cases of HF. After exclusion of 52,512 individuals with malformations (n = 196 cases), 305 cases of HF remained (0.88 per 100,000 person-years). Gestational age was inversely associated with the risk of HF. Compared with individuals born at term (>= 37 weeks' gestation), adjusted incidence relative risks for HF were 17.0 (95% confidence interval [CI]: 7.96 to 36.3) after extremely preterm birth (<28 weeks) and 3.58 (95% CI: 1.57 to 8.14) after very preterm birth (28 to 31 weeks). There was no risk increase after moderately preterm birth (32 to 36 weeks) (relative risk: 1.36; 95% CI: 0.87 to 2.13).

    CONCLUSIONS: There was a strong association between preterm birth before 32 weeks of gestation and HF in childhood and young adulthood. Although the absolute risk of HF is low in young age, our findings indicate that preterm birth may be a previously unknown risk factor for HF. (J Am Coll Cardiol 2017;69:2634-42) (C) 2017 by the American College of Cardiology Foundation.

  • 42.
    Chan, Simon S. M.
    et al.
    Department of Gastroenterology, Norfolk and Norwich University Hospital NHS Trust, Norwich, United Kingdom; Department of Medicine, Bob Champion Research and Education Building, Norwich Medical School, University of East Anglia, Norwich, United Kingdom.
    Chen, Ye
    Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Harvard Medical School, Boston Massachusetts, USA.
    Casey, Kevin
    Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Harvard Medical School, Boston Massachusetts, USA.
    Olen, Ola
    Clinical Epidemiology Division, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden; Department of Clinical Science and Education, Södersjukhuset, Karolinska Institutet, Stockholm, Sweden; Department of Pediatric Gastroenterology and Nutrition, Sachs’ Children and Youth Hospital, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Paediatrics, Örebro University Hospital, Örebro, Sweden.
    Carbonnel, Franck
    Service de Gastroentérologie, Centre hospitalier Universitaire de Bicêtre, Assistance Publique Hôpitaux de Paris, Université Paris Saclay, Le Kremlin Bicêtre, France; INSERM U1018, Villejuif, France.
    Oldenburg, Bas
    Department of Gastroenterology and Hepatology, University Medical Centre Utrecht, Utrecht, The Netherlands.
    Gunter, Marc J.
    Section of Nutrition and Metabolism, International Agency for Research on Cancer - WHO, Lyon, France.
    Tjønneland, Anne
    Grip, Olof
    Department of Gastroenterology, Skåne University Hospital, Malmö, Sweden.
    Lochhead, Paul
    Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Harvard Medical School, Boston Massachusetts, USA; Gastroenterology Unit, Massachusetts General Hospital, Harvard Medical School, Boston Massachusetts, USA.
    Chan, Andrew T.
    Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Harvard Medical School, Boston Massachusetts, USA; Gastroenterology Unit, Massachusetts General Hospital, Harvard Medical School, Boston Massachusetts, USA.
    Wolk, Alicia
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden; Department of Surgical Sciences, Uppsala University, Uppsala, Sweden.
    Khalili, Hamed
    Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Harvard Medical School, Boston Massachusetts, USA; Gastroenterology Unit, Massachusetts General Hospital, Harvard Medical School, Boston Massachusetts, USA; Broad Institute of MIT and Harvard, Cambridge, Massachusetts, USA.
    Obesity is Associated With Increased Risk of Crohn's disease, but not Ulcerative Colitis: A Pooled Analysis of Five Prospective Cohort Studies2022In: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 20, no 5, p. 1048-1058Article in journal (Refereed)
    Abstract [en]

    BACKGROUND AND AIMS: It is unclear whether obesity is associated with the development of inflammatory bowel disease despite compelling data from basic science studies. We therefore examined the association between obesity and risk of Crohn's disease (CD) and ulcerative colitis (UC).

    METHODS: We conducted pooled analyses of 5 prospective cohorts with validated anthropometric measurements for body mass index (BMI) and waist-hip ratio and other lifestyle factors. Diagnoses of CD and UC were confirmed through medical records or ascertained using validated definitions. We used Cox proportional hazards modeling to calculate pooled multivariable-adjusted HRs (aHRs) and 95% confidence intervals (CIs).

    RESULTS: Among 601,009 participants (age range, 18-98 years) with 10,110,018 person-years of follow-up, we confirmed 563 incident cases of CD and 1047 incident cases of UC. Obesity (baseline BMI >= 30 kg/m(2)) was associated with an increased risk of CD (pooled aHR, 1.34; 95% CI, 1.05-1.71, I-2 = 0%) compared with normal BMI (18.5 to <25 kg/m(2)). Each 5 kg/m(2) increment in baseline BMI was associated with a 16% increase in risk of CD (pooled aHR, 1.16; 95% CI, 1.05-1.22; I-2 = 0%). Similarly, with each 5 kg/m(2) increment in early adulthood BMI (age, 18-20 years), there was a 22% increase in risk of CD (pooled aHR, 1.22; 95% CI, 1.05-1.40; I-2 = 13.6%). An increase in waist-hip ratio was associated with an increased risk of CD that did not reach statistical significance (pooled aHR across quartiles, 1.08; 95% CI, 0.97-1.19; I-2 = 0%). No associations were observed between measures of obesity and risk of UC.

    CONCLUSIONS: In an adult population, obesity as measured by BMI was associated with an increased risk of older-onset CD but not UC.

  • 43.
    Chen, Qi
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Larsson, Henrik
    Örebro University, School of Medical Sciences. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Almqvist, Catarina
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Pediatric Allergy and Pulmonology Unit at Astrid Lindgren Children ’ s Hospital, Karolinska University Hospital, Stockholm, Sweden.
    Chang, Zheng
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Lichtenstein, Paul
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    D'Onofrio, Brian M.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Psychological and Brain Sciences, Indiana University, Bloomington, Indiana, USA.
    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; Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Clinical Sciences Building 2, City Hospital, Nottingham, UK; Department of Medicine, Columbia University College of Physicians and Surgeons, New York, USA.
    Association between pharmacotherapy for ADHD in offspring and depression-related specialty care visits by parents with a history of depression2019In: BMC Psychiatry, E-ISSN 1471-244X, Vol. 19, article id 224Article in journal (Refereed)
    Abstract [en]

    Background: Pharmacotherapy is effective in reducing the core symptoms of attention-deficit/hyperactivity disorder (ADHD). We aimed to investigate the concurrent association between pharmacotherapy for ADHD in offspring and depression-related specialty care visits by the parents with a history of depression.

    Methods: Using data from a variety of Swedish national registers, we conducted a cohort study with 8-year follow-up of 5605 parents (3872 mothers and 1733 fathers) who had a history of depression and an offspring diagnosed with ADHD. The hazard rate for parental depression-related specialty care visits during exposed periods when the offspring was on medication for treatment of ADHD was compared with the hazard rate during unexposed periods when the offspring was off medication. Within-individual comparisons were employed to control for time-constant confounding factors.

    Results: Among mothers, the crude rates of depression-related specialty care visits during exposed and unexposed periods were 61.33 and 63.95 per 100 person-years, respectively. The corresponding rates among fathers were 49.23 and 54.65 per 100 person-years. When the same parent was compared with him or herself, fathers showed a decreased hazard rate for depression-related visits during exposed periods when the offspring was on medication for treatment of ADHD as compared to unexposed periods (hazard ratio, 0.79 [95% confidence interval, 0.70 to 0.90]). No statistically significant associations were observed in mothers.

    Conclusions: Among parents with a history of depression, pharmacotherapy for ADHD in offspring is concurrently associated with a decreased rate of depression-related specialty care visits in fathers but not in mothers. Future research with refined measures of parental depression and other time-varying familial factors is needed to better understand the mechanisms underlying the association.

  • 44.
    Ciacci, Carolina
    et al.
    Dept Med & Surg, Gastroenterol, Univ Salerno, Baronissi, Italy.
    Ciclitira, Paul
    Div Diabet & Nutr Sci, Dept Gastroenterol, Kings Coll London, London, England; Rayne Inst, St Thomas Hosp, London, England.
    Hadjivassiliou, Marios
    Acad Dept Neurosci, Sheffield Teaching Hosp NHS Trust, Sheffield, England; Royal Hallamshire Hosp, Sheffield, England.
    Kaukinen, Katri
    Sch Med, Univ Tampere, Tampere, Finland; Dept Internal Med, Tampere Univ Hosp, Tampere, Finland.; Dept Internal Med, Seinajoki Cent Hosp, Seinajoki, Finland.
    Ludvigsson, Jonas F.
    Örebro University Hospital. Dept Med Epidemiol & Biostat, Karolinska Inst, Stockholm, Sweden; Dept Pediat, Örebro University Hospital, Örebro, Sweden.
    McGough, Norma
    Coeliac UK, High Wycombe, England.
    Sanders, David S.
    Gastroenterol & Liver Unit, Royal Hallamshire Hosp, Sheffield, England; Univ Sheffield, Sheffield, England.
    Woodward, Jeremy
    Cambridge Intestinal Unit, Addenbrookes Hosp, Cambridge, England.
    Leonard, Jonathan N.
    St Mary's Hosp, Imperial Coll Healthcare NHS Trust, Dept Dermatol, London, England.
    Swift, Gillian L.
    Dept Gastroenterol, Univ Hosp Llandough, Cardiff, England.
    The gluten-free diet and its current application in coeliac disease and dermatitis herpetiformis2015In: United European Gastroenterology journal, ISSN 2050-6406, E-ISSN 2050-6414, Vol. 3, no 2, p. 121-135Article, review/survey (Refereed)
    Abstract [en]

    Background: A gluten-free diet (GFD) is currently the only available therapy for coeliac disease (CD). Objectives: We aim to review the literature on the GFD, the gluten content in naturally gluten-free (GF) and commercially available GF food, standards and legislation concerning the gluten content of foods, and the vitamins and mineral content of a GFD. Methods: We carried out a PubMed search for the following terms: Gluten, GFD and food, education, vitamins, minerals, calcium, Codex wheat starch and oats. Relevant papers were reviewed and for each topic a consensus among the authors was obtained. Conclusion: Patients with CD should avoid gluten and maintain a balanced diet to ensure an adequate intake of nutrients, vitamins, fibre and calcium. A GFD improves symptoms in most patients with CD. The practicalities of this however, are difficult, as (i) many processed foods are contaminated with gluten, (ii) staple GF foods are not widely available, and (iii) the GF substitutes are often expensive. Furthermore, (iv) the restrictions of the diet may adversely affect social interactions and quality of life. The inclusion of oats and wheat starch in the diet remains controversial.

  • 45.
    Cnattingius, S.
    et al.
    Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Kramer, M. S.
    Department of Pediatrics, McGill University Faculty of Medicine, Montreal QC, Canada; Department of Epidemiology, Biostatistics and Occupational Health, McGill University Faculty of Medicine, Montreal QC, Canada.
    Norman, M.
    Division of Pediatrics, Department of Clinical Science, Intervention and Technology, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden; Department of Neonatology, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro, Sweden.
    Fang, F.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Lu, D.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Centre of Public Health Sciences, Faculty of Medicine, University of Iceland, Reykjavik, Iceland.
    Investigating fetal growth restriction and perinatal risks in appropriate for gestational age infants: using cohort and within-sibling analyses2019In: British Journal of Obstetrics and Gynecology, ISSN 1470-0328, E-ISSN 1471-0528, Vol. 126, no 7, p. 842-850Article in journal (Refereed)
    Abstract [en]

    Objective: Fetal growth restriction refers to fetuses that fail to reach their growth potential. Studies within siblings may be useful to disclose fetal growth restriction in appropriate for gestational age (AGA) infants. We analysed associations between birthweight percentiles and perinatal risks in AGA infants, using both population-based and within-sibling analyses.

    Design: Population-based cohort study. Setting and sample Using nation-wide Swedish registries (1987-2012), we identified 2 134 924 singleton AGA births (10th-90th birthweight percentile for gestational age), of whom 1 377 326 were full siblings.

    Methods: Unconditional Poisson regression was used for population analyses, and conditional (matched) Poisson regression for within-sibling analyses. We estimated associations between birthweight percentiles and stillbirth, neonatal mortality, and morbidity, using incidence rate ratios (IRRs) with 95% confidence intervals (CIs).

    Results: Stillbirth and neonatal mortality risks declined with increasing birthweight percentiles, but the declines were larger in within-sibling analyses. Compared with the reference group (40th to <60th percentile), IRRs (95% CIs) of stillbirth for the lowest and highest percentile groups (10th to <25th and 75th-90th percentiles, respectively) were 1.87 (1.72-2.03) to 0.76 (0.68-0.85) in population analysis and 2.60 (2.27-2.98) and 0.43 (0.36-0.50) in within-sibling analysis. Neonatal morbidity risks in term non-malformed infants with low birthweight percentiles were generally only increased in within-sibling analyses.

    Conclusion: Using birthweight information from siblings may help to define fetal growth restriction in AGA infants.

  • 46.
    Cnattingius, Sven
    et al.
    Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Kramer, Michael S.
    Departments of Pediatrics and of Epidemiology, Biostatistics and Occupational Health, McGill University Faculty of Medicine, Montreal, Canada.
    Norman, Mikael
    Division of Pediatrics, Department of Clinical Science, Intervention and Technology, Stockholm, Sweden; Department of Neonatalogy, Karolinska University Hospital, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro, Sweden.
    Fang, Fang
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Lu, Donghao
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Centre of Public Health Sciences, Faculty of Medicine, University of Iceland, Reykjavik, Iceland .
    Keep it in the family: comparing perinatal risks in small-for-gestational-age infants based on population vs within-sibling designs2019In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 48, no 1, p. 297-306Article in journal (Refereed)
    Abstract [en]

    Background: Small-for-gestational-age (SGA) birth is commonly used as a proxy for fetal growth restriction, but also includes constitutionally small infants. Genetic factors account for almost half of the risk of SGA birth. We estimated perinatal risks of SGA birth using both population-based and within-sibling analyses, where the latter by design controls for shared genetic factors and maternal environmental factors that are constant across pregnancies.

    Methods: This was a prospective nationwide cohort study of 2 616 974 singleton infants born in Sweden between January 1987 and December 2012, of whom 1 885 924 were full siblings. We estimated associations between severe or moderate SGA (<3rd percentile and 3rd to <10th percentiles, respectively) and risks of stillbirth, neonatal mortality and morbidity, using both population-based and within-sibling analyses. Hazard ratios (HRs) with 95% confidence intervals (CIs) were estimated in stillbirth analyses, whereas relative risks (RRs) were used for analyses of neonatal outcomes.

    Results: Compared with non-SGA births (>10th percentile), the HR (95% CI) of stillbirth was 18.5 (95% CI 17.4-19.5) among severe SGA births in the population analysis and 22.5 (95% CI 18.7-27.1) in the within-sibling analysis. In non-malformed infants, RRs for neonatal mortality in moderate and severe SGA infants were similarly increased in both population and within-sibling analyses. In term non-malformed infants (>= 37 weeks), SGA-related RRs of several neonatal morbidities were higher in within-sibling than in population analyses.

    Conclusions: Perinatal risks associated with fetal growth restriction are more accurately estimated from analyses of SGA in which genetic factors are accounted for.

  • 47.
    Cnattingius, Sven
    et al.
    Clinical Epidemiology Division, Department of Medicine, Karolinska Institutet, Solna, Sweden.
    Källén, Karin
    Department of Clinical Sciences, Centre of Reproduction Epidemiology, Tornblad Institute, Lund University, Lund, Sweden.
    Sandström, Anna
    Clinical Epidemiology Division, Department of Medicine, Karolinska Institutet, Solna, Sweden; Department of Women’s Health, Division of Obstetrics, Karolinska University Hospital, Stockholm, Sweden.
    Rydberg, Henny
    Statistics Unit 1, Department of Registers and Statistics, National Board of Health and Welfare, Stockholm, Sweden.
    Månsson, Helena
    Statistics Unit 1, Department of Registers and Statistics, National Board of Health and Welfare, Stockholm, Sweden.
    Stephansson, Olof
    Clinical Epidemiology Division, Department of Medicine, Karolinska Institutet, Solna, Sweden; Department of Women’s Health, Division of Obstetrics, Karolinska University Hospital, Stockholm, Sweden.
    Frisell, Thomas
    Clinical Epidemiology Division, Department of Medicine, Karolinska Institutet, Solna, Sweden.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro, Sweden; Department of Medicine, Columbia University College of Physicians and Surgeons, New York NY, USA.
    The Swedish medical birth register during five decades: documentation of the content and quality of the register2023In: European Journal of Epidemiology, ISSN 0393-2990, E-ISSN 1573-7284, Vol. 38, no 1, p. 109-120Article in journal (Refereed)
    Abstract [en]

    Pregnancy-related factors are important for short- and long-term health in mothers and offspring. The nationwide population-based Swedish Medical Birth Register (MBR) was established in 1973. The present study describes the content and quality of the MBR, using original MBR data, Swedish-language and international publications based on the MBR. The MBR includes around 98% of all births in Sweden. From 1982 onwards, the MBR is based on prospectively recorded information in standardized antenatal, obstetric, and neonatal records. When the mother and infant are discharged from hospital, this information is forwarded to the MBR, which is updated annually. Maternal data include information from first antenatal visit on self-reported obstetric history, infertility, diseases, medication use, cohabitation status, smoking and snuff use, self-reported height and measured weight, allowing calculation of body mass index. Birth and neonatal data include date and time of birth, mode of delivery, singleton or multiple birth, gestational age, stillbirth, birth weight, birth length, head circumference, infant sex, Apgar scores, and maternal and infant diagnoses/procedures, including neonatal care. The overall quality of the MBR is very high, owing to the semi-automated data extraction from the standardized regional electronic health records, Sweden's universal access to antenatal care, and the possibility to compare mothers and offspring to the Total Population Register in order to identify missing records. Through the unique personal identity numbers of mothers and live-born offspring, the MBR can be linked to other health registers. The Swedish MBR contains high-quality pregnancy-related information on more than 5 million births during five decades.

  • 48.
    Dixit, Rohit
    et al.
    Dept Med, Celiac Dis Ctr, Columbia Univ Coll Phys & Surg, Columbia Univ, New York NY, USA..
    Lebwohl, Benjamin
    Dept Med, Celiac Dis Ctr, Columbia Univ Coll Phys & Surg, Columbia Univ, New York NY, USA.
    Ludvigsson, Jonas F.
    Örebro University Hospital. Clinical Epidemiology Unit, Department of Medicine, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro, Sweden.
    Lewis, Suzanne K.
    Dept Med, Celiac Dis Ctr, Columbia Univ Coll Phys & Surg, Columbia Univ, New York NY, USA.
    Rizkalla-Reilly, Norelle
    Dept Pediat, Celiac Dis Ctr, Columbia Univ Coll Phys & Surg, Columbia Univ, New York NY, 10027 USA.
    Green, Peter H. R.
    Dept Med, Celiac Dis Ctr, Columbia Univ Coll Phys & Surg, Columbia Univ, New York USA; NewYork Presbyterian Hosp, New York, USA.
    Celiac Disease Is Diagnosed Less Frequently in Young Adult Males2014In: Digestive Diseases and Sciences, ISSN 0163-2116, E-ISSN 1573-2568, Vol. 59, no 7, p. 1509-1512Article in journal (Refereed)
    Abstract [en]

    The female predominance in celiac disease is difficult to explain because population-based screening studies reveal similar rates for celiac disease-specific autoantibodies in males and females. The aim of this study was to explore the role of age and gender in the presentation of celiac disease. The frequency of presentation according to age, gender and mode of presentation was determined by analysis of a prospectively maintained database of children and adults seen at a tertiary medical center. Of 1,682 patients (68 % female) aged 3 months to 86 years who were diagnosed with celiac disease, age at diagnosis in females peaked at 40-45 years, whereas the age at diagnosis for males had two peaks: 10-15 and 35-40 years. A significantly lower percentage of males in early adulthood were diagnosed compared with males in all other age groups (P < 0.0001). The young and elderly had a more even gender distribution. Based on our analysis, males are diagnosed with celiac disease less frequently than females, especially in early adulthood. There should be more emphasis on the diagnosis of celiac disease among young adult males.

  • 49.
    Dornbusch, Hans Juergen
    et al.
    Department of Paediatrics and Adolescent Medicine, Medical University of Graz, Graz, Austria.
    Hadjipanayis, Adamos
    Department of Paediatrics, Larnaca General Hospital, Derynia, Cyprus; Medical School, European University of Cyprus, Nicosia, Cyprus .
    Del Torso, Stefano
    Dipartimento della Sanità Pubblica, Padova, Italy.
    Mercier, Jean-Christophe
    Service de Pédiatrie-Urgences, Hôpital Louis Mourier, Assistance Publique-Hôpitaux de Paris & Université Paris Diderot, Paris, France .
    Wyder, Corinne
    Paediatric Primary Care Center Kurwerk, Burgdorf, Switzerland.
    Schrier, Lenneke
    Juliana Children’s Hospital, The Hague, Netherlands.
    Ross-Russell, Robert
    Department of Paediatric Respiratory Medicine, Cambridge University Hospitals NHS Foundation Trust, Cambridge, United Kingdom.
    Stiris, Tom
    Department of Neonatology, Oslo University Hospital, Oslo, Norway; Faculty of Medicine, University of Oslo, Oslo, Norway .
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Paediatrics, Örebro University Hospital, Örebro, Sweden.
    We strongly support childhood immunisation-statement from the European Academy of Paediatrics (EAP)2017In: European Journal of Pediatrics, ISSN 0340-6199, E-ISSN 1432-1076, Vol. 176, no 5, p. 679-680Article in journal (Refereed)
    Abstract [en]

    The eradication of smallpox and the elimination of several other infectious diseases from much of the world has provided convincing evidence that vaccines are among the most effective interventions for promoting health. The current scepticism about immunisation among members of the new US administration carries a risk of decreasing immunisation rates also in Europe. While only a small minority of the population are strongly anti-vaccine, their public activities have significantly influenced an uncertainty among the general population about both the safety of and the necessity for vaccination. Therefore, the EAP calls for greater publically available, scientifically supported information on vaccination, particularly targeted at health care providers, for the further development of electronically based immunisation information systems (IIS). We further call on all European countries to work together both in legislative and public health arenas in order to increase vaccination coverage among the paediatric population. In the interest of children and their parents, the EAP expresses its strong support for childhood immunisation and recommended vaccination schedules. We are prepared to work with governments and media and share the extensive evidence demonstrating the effectiveness and safety of vaccines.

  • 50.
    Doyle, John B.
    et al.
    Celiac Disease Center, Department of Medicine, Columbia University Irving Medical Center, New York NY, USA.
    Lebwohl, Benjamin
    Celiac Disease Center, Department of Medicine, Columbia University Irving Medical Center, New York NY, USA.
    Askling, Johan
    Clinical Epidemiology Division, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Forss, Anders
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Green, Peter H. R.
    Celiac Disease Center, Department of Medicine, Columbia University Irving Medical Center, New York NY, USA.
    Roelstraete, Bjorn
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Söderling, Jonas
    Clinical Epidemiology Division, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Celiac Disease Center, Department of Medicine, Columbia University Irving Medical Center, New York NY, USA; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro, Sweden.
    Risk of Juvenile Idiopathic Arthritis and Rheumatoid Arthritis in Patients With Celiac Disease: A Population-Based Cohort Study2022In: American Journal of Gastroenterology, ISSN 0002-9270, E-ISSN 1572-0241, Vol. 117, no 12, p. 1971-1981Article in journal (Refereed)
    Abstract [en]

    INTRODUCTION: Celiac disease (CD) is associated with many immune-mediated conditions, but a definitive epidemiological association between CD and juvenile idiopathic arthritis (JIA) or rheumatoid arthritis (RA) has not been established. We quantified the risk of JIA and RA among patients with CD using a population-based cohort.

    METHODS: We identified patients diagnosed with biopsy-proven CD between 2004 and 2017 using data from a national histopathology cohort in Sweden. Each patient was matched by age, sex, calendar year, and geographic region to reference individuals in the general population. We calculated the incidence and estimated the relative risk, through Cox proportional hazards models, of JIA in individuals with CD aged ≥18.

    RESULTS: We identified 24,014 individuals with CD who were matched to 117,397 reference individuals from the general population. Among individuals aged <18, the incidence rate of JIA was 5.9 per 10,000 person-years in patients with CD and 2.2 per 10,000 person-years in the general population (n events = 40 and 73, respectively; hazard ratio [HR] 2.68, 95% confidence interval 1.82-3.95) over a follow-up of 7.0 years. Among individuals aged >= 18, the incidence of RA was 8.4 per 10,000 person-years in CD and 5.1 per 10,000 person-years in matched comparators (n events = 110 and 322, respectively; HR 1.70, 95% confidence interval 1.36-2.12) over a follow-up of 8.8 years.

    DISCUSSION: Among children with CD, JIA develops nearly 3 times as often as it does in the general population, and among adults with CD, RA occurs nearly 2 times as often. Clinicians caring for patients with CD with joint symptoms should have a low threshold to evaluate for JIA or RA.

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