oru.sePublications
Change search
Refine search result
1 - 10 of 10
CiteExportLink to result list
Permanent link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Rows per page
  • 5
  • 10
  • 20
  • 50
  • 100
  • 250
Sort
  • Standard (Relevance)
  • Author A-Ö
  • Author Ö-A
  • Title A-Ö
  • Title Ö-A
  • Publication type A-Ö
  • Publication type Ö-A
  • Issued (Oldest first)
  • Issued (Newest first)
  • Created (Oldest first)
  • Created (Newest first)
  • Last updated (Oldest first)
  • Last updated (Newest first)
  • Disputation date (earliest first)
  • Disputation date (latest first)
  • Standard (Relevance)
  • Author A-Ö
  • Author Ö-A
  • Title A-Ö
  • Title Ö-A
  • Publication type A-Ö
  • Publication type Ö-A
  • Issued (Oldest first)
  • Issued (Newest first)
  • Created (Oldest first)
  • Created (Newest first)
  • Last updated (Oldest first)
  • Last updated (Newest first)
  • Disputation date (earliest first)
  • Disputation date (latest first)
Select
The maximal number of hits you can export is 250. When you want to export more records please use the Create feeds function.
  • 1.
    Chen, Qi
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden.
    Sjölander, Arvid
    Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden.
    Runeson, Bo
    Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden.
    D'Onofrio, Brian M.
    Department of Psychological and Brain Sciences, Indiana University, Bloomington, USA.
    Lichtenstein, Paul
    Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden.
    Larsson, Henrik
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Drug treatment for attention-deficit/hyperactivity disorder and suicidal behaviour: register based study2014In: BMJ. British Medical Journal, E-ISSN 1756-1833, ISSN 0959-535X, Vol. 348, article id g3769Article in journal (Refereed)
    Abstract [en]

    Objective: To investigate the association between drug treatment for attention-deficit/hyperactivity disorder (ADHD) and risk of concomitant suicidal behaviour among patients with ADHD.

    Design: Register based longitudinal study using within patient design.

    Setting: Linkage of multiple national registers in Sweden.

    Participants: 37,936 patients with ADHD born between 1960 and 1996 and followed from 2006 to 2009 for treatment status by ADHD drug treatment and suicide related events (suicide attempt and completed suicide).

    Main outcome measure: Incidence rate of suicide related events during ADHD drug treatment periods compared with that during non-treatment periods.

    Results: Among 37,936 patients with ADHD, 7019 suicide related events occurred during 150,721 person years of follow-up. At the population level, drug treatment of ADHD was associated with an increased rate of suicide related events (hazard ratio 1.31, 95% confidence interval 1.19 to 1.44). However, the within patient comparison showed a reverse association between ADHD drug treatment and rate of suicide related events (0.89, 0.79 to 1.00). Among stimulant users, a reduced within patient rate of suicide related events was seen during treatment periods (0.81, 0.70 to 0.94). Among non-stimulant/mixed users, no significantly increased within patient rate of suicide related events during non-stimulant treatment periods was seen (0.96, 0.72 to 1.30).

    Conclusions: This study found no evidence for a positive association between the use of drug treatments for ADHD and the risk of concomitant suicidal behaviour among patients with ADHD. If anything, the results pointed to a potential protective effect of drugs for ADHD on suicidal behaviour, particularly for stimulant drugs. The study highlights the importance of using within patient designs to control for confounding in future pharmacoepidemiological studies.

  • 2.
    Johansson, Minna
    et al.
    Department of Public Health and Community Medicine, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; Research Unit and Section for General Practice, FoUU-centrum Fyrbodal, Vänersborg, Sweden.
    Hansson, Anders
    Department of Public Health and Community Medicine, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; Research Unit and Section for General Practice, FoUU-centrum Fyrbodal, Vänersborg, Sweden.
    Brodersen, John
    Research Unit for General Practice and Section of General Practice, Department of Public Health, University of Copenhagen, Copenhagen, Denmark.
    Estimating overdiagnosis in screening for abdominal aortic aneurysm: could a change in smoking habits and lowered aortic diameter tip the balance of screening towards harm?2015In: BMJ. British Medical Journal, E-ISSN 1756-1833, Vol. 350, article id h825Article in journal (Refereed)
    Abstract [en]

    Clinical context—Abdominal aortic aneurysms (AAAs) are often asymptomatic until they rupture, when the death rate is greater than 80%. If diagnosed before rupture, AAA can be treated with surgery, which has a mortality of 4-5% Diagnostic change— Sweden, the UK, and the US have initiated screening programmes for AAA. There are also proposals to change the aortic diameter for diagnosis from ≥30 mm to 25 mm Rationale for change—Early diagnosis by screening allows the opportunity of surgery to prevent ruptures Leap of faith—Detecting asymptomatic aneurysms will reduce AAA mortality and morbidity Impact on prevalence—Our estimates indicate that screening almost doubles AAA prevalence, but most AAAs are small and at low risk of rupture. Changing the definition of an AAA from 30 mm to 25 mm would double prevalence again Evidence of overdiagnosis—We estimate that if 10 000 men are invited to screening, 46 AAA deaths can be prevented over 13-15 years but 176 would have an AAA ≥30 mm detected that remained asymptomatic after 13 years. A recent drop in AAA prevalence reduces the benefits of screening and worsens the benefit:harm ratio Harms of overdiagnosis—Asymptomatic men are labelled at risk of a life threatening condition for which they will be under lifelong surveillance. Of 10 000 men invited to AAA screening, 37 (95% confidence interval 15 to 60) overdiagnosed men had unnecessary preventive surgery, of whom 1.6 (1.4 to 1.7) died Limitations—Figures for exact calculations of overdiagnosis are not available and unlikely to emerge. The psychosocial consequences of living with a screen detected AAA are inadequately investigated. Cost effectiveness data on screening are inconclusive Conclusion— Screening programmes have changed the meaning of an AAA diagnosis from a life threatening condition to a risk factor. AAA screening programmes should be revisited because of reduced benefits in modern populations and because data suggest considerable harm

  • 3.
    Lebwohl, Benjamin
    et al.
    Coll Phys & Surg, Celiac Dis Ctr, Dept Med, Columbia Univ, New York NY, USA; Dept Med Epidemiol & Biostat, Karolinska Univ Hosp, Stockholm, Sweden; Karolinska Inst, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Örebro University Hospital. Dept Med Epidemiol & Biostat, Karolinska Univ Hosp, Stockholm, Sweden; Karolinska Inst, Stockholm, Sweden; Dept Pediat, Örebro Univ Hosp, Örebro, Sweden.
    Green, Peter H. R.
    Coll Phys & Surg, Celiac Dis Ctr, Dept Med, Columbia Univ, New York NY, USA.
    Celiac disease and non-celiac gluten sensitivity2015In: BMJ. British Medical Journal, E-ISSN 1756-1833, Vol. 351, article id h4347Article, review/survey (Refereed)
    Abstract [en]

    Celiac disease is a multisystem immune based disorder that is triggered by the ingestion of gluten in genetically susceptible individuals. The prevalence of celiac disease has risen in recent decades and is currently about 1% in most Western populations. The reason for this rise is unknown, although environmental factors related to the hygiene hypothesis are suspected. The pathophysiology of celiac disease involves both the innate and adaptive immune response to dietary gluten. Clinical features are diverse and include gastrointestinal symptoms, metabolic bone disease, infertility, and many other manifestations. Although a gluten-free diet is effective in most patients, this diet can be burdensome and can limit quality of life; consequently, non-dietary therapies are at various stages of development. This review also covers non-celiac gluten sensitivity. The pathophysiology of this clinical phenotype is poorly understood, but it is a cause of increasing interest in gluten-free diets in the general population.

  • 4.
    Ludvigsson, Jonas F.
    et al.
    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, City Hospital, Nottingham, United Kingdom; Department of Medicine, Columbia University, College of Physicians and Surgeons, New York NY, United States.
    Neovius, Martin
    Clinical Epidemiology Division, Department of Medicine Solna, Karolinska Institutet, Sweden.
    Söderling, Jonas
    Clinical Epidemiology Division, Department of Medicine Solna, Karolinska Institutet, Sweden.
    Gudbjörnsdottir, Soffia
    National Diabetes Register, Centre of Registers Västra Götaland, Sweden; Institute of Medicine, Department of Molecular and Clinical Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Svensson, Ann-Marie
    National Diabetes Register, Centre of Registers Västra Götaland, Sweden.
    Franzén, Stefan
    National Diabetes Register, Centre of Registers Västra Götaland, Sweden.
    Stephansson, Olof
    Clinical Epidemiology Division, Department of Medicine Solna, Karolinska Institutet, Sweden; Department of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden.
    Pasternak, Björn
    Clinical Epidemiology Division, Department of Medicine Solna, Karolinska Institutet, Sweden; Department of Epidemiology Research, Statens Serum Institut, Copenhagen, Denmark.
    Periconception glycaemic control in women with type 1 diabetes and risk of major birth defects: population based cohort study in Sweden2018In: BMJ. British Medical Journal, E-ISSN 1756-1833, Vol. 362, article id k2638Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: To examine the association between maternal type 1 diabetes and the risk of major birth defects according to levels of glycated haemoglobin (HbA1C) within three months before or after estimated conception.

    DESIGN: Population based historical cohort study using nationwide health registers. SETTING Sweden, 2003-15.

    PARTICIPANTS: 2458 singleton liveborn infants of mothers with type 1 diabetes and a glycated haemoglobin measurement within three months before or after estimated conception and 1 159 865 infants of mothers without diabetes.

    MAIN OUTCOME MEASURES: Major cardiac and non-cardiac birth defects according to glycated haemoglobin levels.

    RESULTS: 122 cases of major cardiac defects were observed among 2458 infants of mothers with type 1 diabetes. Compared with 15 cases of major cardiac defects per 1000 infants of mothers without diabetes, the rates among infants of mothers with type 1 diabetes were 33 per 1000 for a glycated haemoglobin level of <6.5% (adjusted risk ratio 2.17, 95% confidence interval 1.37 to 3.42), 49 per 1000 for 6.5% to <7.8% (3.17, 2.45 to 4.11), 44 per 1000 for 7.8% to <9.1% (2.79, 1.90 to 4.12), and 101 per 1000 for >= 9.1% (6.23, 4.32 to 9.00). The corresponding adjusted risk differences were 17 (5 to 36), 32 (21 to 46), 26 (13 to 46), and 77 (49 to 118) cases of major cardiac defects per 1000 infants, respectively. 50 cases of major non-cardiac defects were observed among infants of mothers with type 1 diabetes. Compared with 18 cases of major non-cardiac defects per 1000 infants of mothers without diabetes, the rates among infants of mothers with type 1 diabetes were 22 per 1000 for a glycated haemoglobin level of <6.5% (adjusted risk ratio 1.18, 0.68 to 2.07), 19 per 1000 for 6.5% to <7.8% (1.01, 0.66 to 1.54), 17 per 1000 for 7.8% to <9.1% (0.89, 0.46 to 1.69), and 32 per 1000 for >= 9.1%(1.68, 0.85 to 3.33).

    CONCLUSIONS: Among liveborn infants of mothers with type 1 diabetes, increasingly worse glycaemic control in the three months before or after estimated conception was associated with a progressively increased risk of major cardiac defects. Even with glycated haemoglobin within target levels recommended by guidelines (<6.5%), the risk of major cardiac defects was increased more than twofold. The risk of major non-cardiac defects was not statistically significantly increased at any of the four glycated haemoglobin levels examined; the study had limited statistical power for this outcome and was based on live births only.

  • 5.
    Markt, Sarah C.
    et al.
    Department of Epidemiology, Harvard TH Chan School of Public Health, Boston, USA.
    Nuttall, Elizabeth
    Department of Epidemiology, Harvard TH Chan School of Public Health, Boston, USA.
    Turman, Constance
    Program in Molecular and Genetic Epidemiology, Harvard TH Chan School of Public Health, Boston, USA.
    Sinnott, Jennifer
    Department of Epidemiology, Harvard TH Chan School of Public Health, Boston, USA; Department of Statistics, Ohio State University, Columbus, USA.
    Rimm, Eric B.
    Department of Epidemiology, Harvard TH Chan School of Public Health, Boston, USA; Department of Nutrition, Harvard TH Chan School of Public Health, Boston, USA; Channing Division of Network Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, USA.
    Ecsedy, Ethan
    Cabot School, Newton, USA.
    Unger, Robert H.
    Department of Epidemiology, Harvard TH Chan School of Public Health, Boston, USA.
    Fall, Katja
    Örebro University, School of Medical Sciences. Department of Epidemiology, Harvard TH Chan School of Public Health, Boston, USA; Division of Public Health Sciences, University of Iceland, Reykjavik, Iceland.
    Finn, Stephen
    Department of Pathology, Trinity College, Dublin, Republic of Ireland.
    Jensen, Majken K.
    Department of Nutrition, Harvard TH Chan School of Public Health, Boston, USA; Channing Division of Network Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, USA.
    Rider, Jennifer R.
    Department of Epidemiology, Harvard TH Chan School of Public Health, Boston, USA; Department of Epidemiology, Boston University School of Public Health, Boston, USA.
    Kraft, Peter
    Department of Epidemiology, Harvard TH Chan School of Public Health, Boston, USA; Department of Biostatistics, Harvard TH Chan School of Public Health, Boston, USA; Program in Molecular and Genetic Epidemiology, Harvard TH Chan School of Public Health, Boston, USA.
    Mucci, Lorelei A.
    Department of Epidemiology, Harvard TH Chan School of Public Health, Boston, USA; Channing Division of Network Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, US; Division of Public Health Sciences, University of Iceland, Reykjavik, Iceland.
    Sniffing out significant "Pee values": genome wide association study of asparagus anosmia2016In: BMJ. British Medical Journal, E-ISSN 1756-1833, Vol. 355, article id i6071Article in journal (Refereed)
    Abstract [en]

    Objective: To determine the inherited factors associated with the ability to smell asparagus metabolites in urine.

    Design: Genome wide association study.

    Sstting: Nurses' Health Study and Health Professionals Follow-up Study cohorts.

    Participants: 6909 men and women of European-American descent with available genetic data from genome wide association studies.

    Main outcome measure: Participants were characterized as asparagus smellers if they strongly agreed with the prompt "after eating asparagus, you notice a strong characteristic odor in your urine," and anosmic if otherwise. We calculated per-allele estimates of asparagus anosmia for about nine million single nucleotide polymorphisms using logistic regression. P values <5×10(-8) were considered as genome wide significant.

    Results: 58.0% of men (n=1449/2500) and 61.5% of women (n=2712/4409) had anosmia. 871 single nucleotide polymorphisms reached genome wide significance for asparagus anosmia, all in a region on chromosome 1 (1q44: 248139851-248595299) containing multiple genes in the olfactory receptor 2 (OR2) family. Conditional analyses revealed three independent markers associated with asparagus anosmia: rs13373863, rs71538191, and rs6689553.

    Conclusion: A large proportion of people have asparagus anosmia. Genetic variation near multiple olfactory receptor genes is associated with the ability of an individual to smell the metabolites of asparagus in urine. Future replication studies are necessary before considering targeted therapies to help anosmic people discover what they are missing.

  • 6.
    Mohammad, Moman A
    et al.
    Department of Cardiology, Clinical Sciences, Lund University, Skåne University Hospital, Lund, Sweden.
    Karlsson, Sofia
    Department of Cardiology, Clinical Sciences, Lund University, Skåne University Hospital, Lund, Sweden.
    Haddad, Jonathan
    Department of Cardiology, Clinical Sciences, Lund University, Skåne University Hospital, Lund, Sweden.
    Cederberg, Björn
    Department of Cardiology, Clinical Sciences, Lund University, Skåne University Hospital, Lund, Sweden.
    Jernberg, Tomas
    Department of clinical sciences, Danderyd's University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Lindahl, Bertil
    Department of Medical Sciences and Uppsala Clinical Research Center, Uppsala University, Uppsala, Sweden.
    Fröbert, Ole
    Örebro University, School of Medical Sciences. Department of Cardiology.
    Koul, Sasha
    Department of Cardiology, Clinical Sciences, Lund University, Skåne University Hospital, Lund, Sweden.
    Erlinge, David
    Department of Cardiology, Clinical Sciences, Lund University, Skåne University Hospital, Lund, Sweden.
    Christmas, national holidays, sport events, and time factors as triggers of acute myocardial infarction: SWEDEHEART observational study 1998-20132018In: BMJ. British Medical Journal, E-ISSN 1756-1833, Vol. 363, article id k4811Article in journal (Refereed)
    Abstract [en]

    OBJECTIVES: To study circadian rhythm aspects, national holidays, and major sports events as triggers of myocardial infarction.

    DESIGN: Retrospective observational study using the nationwide coronary care unit registry, SWEDEHEART.

    SETTING: Sweden.

    PARTICIPANTS: 283 014 cases of myocardial infarction reported to SWEDEHEART between 1998 and 2013. Symptom onset date was documented for all cases, and time to the nearest minute for 88%.

    INTERVENTIONS: Myocardial infarctions with symptom onset on Christmas/New Year, Easter, and Midsummer holiday were identified. Similarly, myocardial infarctions that occurred during a FIFA World Cup, UEFA European Championship, and winter and summer Olympic Games were identified. The two weeks before and after a holiday were set as a control period, and for sports events the control period was set to the same time one year before and after the tournament. Circadian and circaseptan analyses were performed with Sunday and 24:00 as the reference day and hour with which all other days and hours were compared. Incidence rate ratios were calculated using a count regression model.

    MAIN OUTCOME MEASURES: Daily count of myocardial infarction.

    RESULTS: Christmas and Midsummer holidays were associated with a higher risk of myocardial infarction (incidence rate ratio 1.15, 95% confidence interval 1.12 to 1.19, P<0.001, and 1.12, 1.07 to 1.18, P<0.001, respectively). The highest associated risk was observed for Christmas Eve (1.37, 1.29 to 1.46, P<0.001). No increased risk was observed during Easter holiday or sports events. A circaseptan and circadian variation in the risk of myocardial infarction was observed, with higher risk during early mornings and on Mondays. Results were more pronounced in patients aged over 75 and those with diabetes and a history of coronary artery disease.

    CONCLUSIONS: In this nationwide real world study covering 16 years of hospital admissions for myocardial infarction with symptom onset documented to the nearest minute, Christmas, and Midsummer holidays were associated with higher risk of myocardial infarction, particularly in older and sicker patients, suggesting a role of external triggers in vulnerable individuals.

  • 7.
    Olén, Ola
    et al.
    Sachs’ Children and Youth Hospital, Stockholm South General Hospital, Stockholm, Sweden; Department of Clinical Science and Education, Södersjukhuset, Karolinska Institutet, Stockholm, Sweden; Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Askling, Johan
    Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Sachs, Michael C.
    Unit of Biostatistics, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Frumento, Paolo
    Unit of Biostatistics, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Neovius, Martin G.
    Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Smedby, Karin Ekström
    Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Ekbom, Anders M.
    Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Malmborg, Petter
    Sachs’ Children and Youth Hospital, Stockholm South General Hospital, Stockholm, Sweden; Department of Women’s and Children’s Health, Karolinska Institutet, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro, Sweden; Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham, UK; Department of Medicine, Columbia University College of Physicians and Surgeons, New York NY, US.
    Childhood onset inflammatory bowel disease and risk of cancer: a Swedish nationwide cohort study 1964-20142017In: BMJ. British Medical Journal, E-ISSN 1756-1833, ISSN 0959-8138, Vol. 358, article id j3951Article in journal (Refereed)
    Abstract [en]

    Objective: To assess risk of cancer in patients with childhood onset inflammatory bowel disease in childhood and adulthood.

    Design: Cohort study with matched general population reference individuals using multivariable Cox regression to estimate hazard ratios.

    Setting: Swedish national patient register (both inpatient and non-primary outpatient care) 1964-2014.

    Participants: Incident cases of childhood onset (<18 years) inflammatory bowel disease (n=9405: ulcerative colitis, n=4648; Crohn's disease, n=3768; unclassified, n=989) compared with 92 870 comparators from the general population matched for sex, age, birth year, and county.

    Main outcome measures: Any cancer and cancer types according to the Swedish Cancer Register.

    Results: During follow-up through adulthood (median age at end of follow-up 27 years), 497 (3.3 per 1000 person years) people with childhood onset inflammatory bowel disease had first cancers, compared with 2256 (1.5 per 1000 person years) in the general population comparators (hazard ratio 2.2, 95% confidence interval 2.0 to 2.5). Hazard ratios for any cancer were 2.6 in ulcerative colitis (2.3 to 3.0) and 1.7 in Crohn's disease (1.5 to 2.1). Patients also had an increased risk of cancer before their 18th birthday (2.7, 1.6 to 4.4; 20 cancers in 9405 patients, 0.6 per1000 person years). Gastrointestinal cancers had the highest relative risks, with a hazard ratio of 18.0 (14.4 to 22.7) corresponding to 202 cancers in patients with inflammatory bowel disease. The increased risk of cancer (before 25th birthday) was similar over time (1964-1989: 1.6, 1.0 to 2.4; 1990-2001: 2.3, 1.5 to 3.3); 2002-06: 2.9, 1.9 to 4.2; 2007-14: 2.2, 1.1 to 4.2).

    Conclusion: Childhood onset inflammatory bowel disease is associated with an increased risk of any cancer, especially gastrointestinal cancers, both in childhood and later in life. The higher risk of cancer has not fallen over time.

  • 8.
    Ortqvist, Anne K.
    et al.
    Dept Med Epidemiol & Biostat, Karolinska Inst, Stockholm, Sweden.
    Lundholm, Cecilia
    Dept Med Epidemiol & Biostat, Karolinska Inst, Stockholm, Sweden.
    Kieler, Helle
    Dept Med, Ctr Pharmacoepidemiol T2, Karolinska Univ Hosp, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Örebro University Hospital. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Paediatrics, Örebro University Hospital, Örebro, Sweden.
    Fall, Tove
    Dept Med Sci, Mol Epidemiol & Sci Life Lab, Uppsala Univ, Uppsala, Sweden.
    Ye, Weimin
    Dept Med Epidemiol & Biostat, Karolinska Inst, Stockholm, Sweden.
    Almqvist, Catarina
    Dept Med Epidemiol & Biostat, Karolinska Inst, Stockholm, Sweden; Lung & Allergy Unit, Astrid Lindgren Childrens Hosp, Karolinska Univ Hosp, Stockholm, Sweden.
    Antibiotics in fetal and early life and subsequent childhood asthma: nationwide population based study with sibling analysis2014In: BMJ. British Medical Journal, E-ISSN 1756-1833, Vol. 349, article id g6979Article in journal (Refereed)
    Abstract [en]

    Objective: To investigate the association between exposure to antibiotics in fetal and early life and asthma in childhood, with adjustment for confounding factors.

    Design: Nationwide prospective population based cohort study, including sibling control design.

    Setting: Swedish population identified from national demographic and health registers.

    Participants: 493 785 children born 2006-10; 180 894 of these were eligible for sibling analyses.

    Main outcome measure: Asthma defined as having both an asthma diagnosis and dispensed asthma drugs. The association between antibiotic exposure and asthma was investigated in the whole cohort with Cox proportional hazard regression. A stratified proportional hazards model conditional on sibling group was used to adjust for shared factors within families. Confounding by respiratory infections was assessed by investigating whether specific groups of antibiotics were associated with asthma.

    Results: Antibiotic exposure in fetal life was associated with an increased risk of asthma in cohort analyses (hazard ratio 1.28, 95% confidence interval 1.25 to 1.32), but not in sibling analyses (0.99, 0.92 to 1.07). In cohort analyses, antibiotics used to treat respiratory infections in childhood were associated with a more pronounced increased risk of asthma (4.12, 3.78 to 4.50) than antibiotics used for urinary tract and skin infections (1.54, 1.24 to 1.92). In sibling analyses, the excess risks after exposure to antibiotics for respiratory infections decreased (2.36, 1.78 to 3.13) and disappeared for antibiotics for urinary tract and skin (0.85, 0.47 to 1.55).

    Conclusions: Previous positive associations between exposure to antibiotics in fetal and early life and subsequent childhood asthma could have been caused by confounding by shared familial factors, in addition to confounding by respiratory infections.

  • 9.
    Steineck, Isabelle
    et al.
    Department of Endocrinology, Aarhus University Hospital, Aarhus, Denmark.
    Cederholm, Jan
    Department of Public Health and Caring Sciences/Family and Preventive Medicine, Uppsala University, Uppsala, Sweden.
    Eliasson, Björn
    Institute of Medicine, Sahlgrenska University Hospital, University of Gothenburg, Gothenburg, Sweden.
    Rawshani, Araz
    National Diabetes Register, Centre of Registers Västra Götaland, Gothenburg, Sweden.
    Eeg-Olofsson, Katarina
    Institute of Medicine, Sahlgrenska University Hospital, University of Gothenburg, Gothenburg, Sweden.
    Svensson, Ann-Marie
    National Diabetes Register, Centre of Registers Västra Götaland, Gothenburg, Sweden.
    Zethelius, Björn
    Department of Public Health and Caring Sciences/Geriatrics, Uppsala University, Uppsala, Sweden; Medical Products Agency, Uppsala, Sweden.
    Avdic, Tarik
    National Diabetes Register, Centre of Registers Västra Götaland, Gothenburg, Sweden.
    Landin-Olsson, Mona
    Department of Clinical Science, Lund University, Lund, Sweden.
    Jendle, Johan
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Gudbjörnsdottir, Soffia
    Institute of Medicine, Sahlgrenska University Hospital, University of Gothenburg, Gothenburg, Sweden; National Diabetes Register, Centre of Registers Västra Götaland, Gothenburg, Sweden.
    Insulin pump therapy, multiple daily injections, and cardiovascular mortality in 18 168 people with type 1 diabetes: observational study2015In: BMJ. British Medical Journal, E-ISSN 1756-1833, Vol. 350, article id h3234Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: To investigate the long term effects of continuous subcutaneous insulin infusion (insulin pump therapy) on cardiovascular diseases and mortality in people with type 1 diabetes. Design Observational study.

    SETTING: Swedish National Diabetes Register, Sweden 2005-12.

    PARTICIPANTS: 18 168 people with type 1 diabetes, 2441 using insulin pump therapy and 15 727 using multiple daily insulin injections.

    MAIN OUTCOME MEASURES: Cox regression analysis was used to estimate hazard ratios for the outcomes, with stratification of propensity scores including clinical characteristics, risk factors for cardiovascular disease, treatments, and previous diseases.

    RESULTS: Follow-up was for a mean of 6.8 years until December 2012, with 114 135 person years. With multiple daily injections as reference, the adjusted hazard ratios for insulin pump treatment were significantly lower: 0.55 (95% confidence interval 0.36 to 0.83) for fatal coronary heart disease, 0.58 (0.40 to 0.85) for fatal cardiovascular disease (coronary heart disease or stroke), and 0.73 (0.58 to 0.92) for all cause mortality. Hazard ratios were lower, but not significantly so, for fatal or non-fatal coronary heart disease and fatal or non-fatal cardiovascular disease. Unadjusted absolute differences were 3.0 events of fatal coronary heart disease per 1000 person years; corresponding figures were 3.3 for fatal cardiovascular disease and 5.7 for all cause mortality. When lower body mass index and previous cardiovascular diseases were excluded, results of subgroup analyses were similar to the results from complete data. A sensitivity analysis of unmeasured confounders in all individuals showed that an unmeasured confounders with hazard ratio of 1.3 would have to be present in > 80% of the individuals treated with multiple daily injections versus not presence in those treated with pump therapy to invalidate the significantly lower hazard ratios for fatal cardiovascular disease. Data on patient education and frequency of blood glucose monitoring were missing, which might have influenced the observed association.

    CONCLUSION: Among people with type 1 diabetes use of insulin pump therapy is associated with lower cardiovascular mortality than treatment with multiple daily insulin injections.

  • 10.
    Sultan, Alyshah Abdul
    et al.
    Research Institute of Primary Care and Health Sciences, Keele University, Keele, United Kingdom; Division of Epidemiology and Public Health, University of Nottingham, City Hospital, Nottingham, United Kingdom; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    West, Joe
    Division of Epidemiology and Public Health, University of Nottingham, City Hospital, Nottingham, United Kingdom.
    Grainge, Matthew J
    Division of Epidemiology and Public Health, University of Nottingham, City Hospital, Nottingham, United Kingdom.
    Riley, Richard D
    Research Institute of Primary Care and Health Sciences, Keele University, Keele, United Kingdom.
    Tata, Laila J
    Division of Epidemiology and Public Health, University of Nottingham, City Hospital, Nottingham, United Kingdom.
    Stephansson, Olof
    Department of Medicine, Solna, Clinical Epidemiology Unit, Karolinska Institutet, Stockholm, Sweden; Department of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden.
    Fleming, Kate M
    Division of Epidemiology and Public Health, University of Nottingham, City Hospital, Nottingham, United Kingdom; Public Health Institute, Liverpool John Moores University, Liverpool, United Kingdom.
    Nelson-Piercy, Catherine
    Women's Health Academic Centre, Guy's and St Thomas' Foundation Trust, St Thomas' Hospital, London, United Kingdom.
    Ludvigsson, Jonas F
    Örebro University, School of Medical Sciences. Division of Epidemiology and Public Health, University of Nottingham, City Hospital, Nottingham, United Kingdom; Department of Paediatrics, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Development and validation of risk prediction model for venous thromboembolism in postpartum women: multinational cohort study2016In: BMJ. British Medical Journal, E-ISSN 1756-1833, Vol. 355, article id i6253Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE:  To develop and validate a risk prediction model for venous thromboembolism in the first six weeks after delivery (early postpartum).

    DESIGN:  Cohort study.

    SETTING:  Records from England based Clinical Practice Research Datalink (CPRD) linked to Hospital Episode Statistics (HES) and data from Sweden based registry.

    PARTICIPANTS:  All pregnant women registered with CPRD-HES linked data between 1997 and 2014 and Swedish medical birth registry between 2005 and 2011 with postpartum follow-up.

    MAIN OUTCOME MEASURE:  Multivariable logistic regression analysis was used to develop a risk prediction model for postpartum venous thromboembolism based on the English data, which was externally validated in the Swedish data.

    RESULTS:  433 353 deliveries were identified in the English cohort and 662 387 in the Swedish cohort. The absolute rate of venous thromboembolism was 7.2 per 10 000 deliveries in the English cohort and 7.9 per 10 000 in the Swedish cohort. Emergency caesarean delivery, stillbirth, varicose veins, pre-eclampsia/eclampsia, postpartum infection, and comorbidities were the strongest predictors of venous thromboembolism in the final multivariable model. Discrimination of the model was similar in both cohorts, with a C statistic above 0.70, with excellent calibration of observed and predicted risks. The model identified more venous thromboembolism events than the existing national English (sensitivity 68% v 63%) and Swedish guidelines (30% v 21%) at similar thresholds.

    CONCLUSION:  A new prediction model that quantifies absolute risk of postpartum venous thromboembolism has been developed and externally validated. It is based on clinical variables that are available in many developed countries at the point of delivery and could serve as the basis for real time decisions on obstetric thromboprophylaxis.

1 - 10 of 10
CiteExportLink to result list
Permanent link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf