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  • 1.
    Anand, K J S
    et al.
    Department of Pediatrics, University of Arkansas for Medical Sciences, Little Rock, AR, USA; Department of Anestheslogy, Neurobiology, and Pharmacology, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
    Hall, R Whit
    Department of Pediatrics, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
    Desai, Nirmala
    Department of Pediatrics, University of Kentucky Medical Center, Lexington, KY.
    Shephard, Barbara
    Department of Pediatrics, Tufts University School of Medicine, Boston, MA.
    Bergqvist, Lena L
    Neonatal Research Unit, Karolinska Institute, Astrid Lindgren's Children's Hospital, Stockholm, Sweden.
    Young, Thomas E
    Department of Pediatrics, University of North Carolina at Chapel Hill and Wake Medical Center, Raleigh, NC, USA.
    Boyle, Elaine M
    Simpson Memorial Maternity Pavilion, University of Edinburgh, Edinburgh, UK.
    Carbajal, Ricardo
    Service de Pédiatrie et Médecine Néonatale, Centre Hospitaller Poissy Saint Germain, Poissy, France.
    Bhutani, Vinod K
    Department of Pediatrics, University of Pennsylvania and Pennsylvania Hospital, Philadelphia, PA, USA.
    Moore, Mary Beth
    Department of Radiology, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
    Kronsberg, Shari S
    Maryland Medical Research Institute, Baltimore, MD.
    Barton, Bruce A
    Maryland Medical Research Institute, Baltimore, MD.
    Effects of morphine analgesia in ventilated preterm neonates: primary outcomes from the NEOPAIN randomised trial2004Inngår i: The Lancet, ISSN 0140-6736, E-ISSN 1474-547X, Vol. 363, nr 9422, s. 1673-82Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Opioid analgesia is commonly used during neonatal intensive care. We undertook the Neurologic Outcomes and Pre-emptive Analgesia in Neonates (NEOPAIN) trial to investigate whether pre-emptive morphine analgesia decreases the rate of a composite primary outcome of neonatal death, severe intraventricular haemorrhage (IVH), and periventricular leucomalacia (PVL) in preterm neonates.

    METHODS: Ventilated preterm neonates (n=898) from 16 centres were randomly assigned masked placebo (n=449) or morphine (n=449) infusions. After a loading dose (100 microg/kg), morphine infusions (23-26 weeks of gestation 10 microg kg(-1) h(-1); 27-29 weeks 20 microg kg(-1) h(-1); 30-32 weeks 30 microg kg(-1) h(-1)) were continued as long as clinically justified (maximum 14 days). Open-label morphine could be given on clinical judgment (placebo group 242/443 [54.6%], morphine group 202/446 [45.3%]). Analyses were by intention to treat.

    FINDINGS: Baseline variables were similar in the randomised groups. The placebo and morphine groups had similar rates of the composite outcome (105/408 [26%] vs 115/419 [27%]), neonatal death (47/449 [11%] vs 58/449 [13%]), severe IVH (46/429 [11%] vs 55/411 [13%]), and PVL (34/367 [9%] vs 27/367 [7%]). For neonates who were not given open-label morphine, rates of the composite outcome (53/225 [24%] vs 27/179 [15%], p=0.0338) and severe IVH (19/219 [9%] vs 6/189 [3%], p=0.0209) were higher in the morphine group than the placebo group. Placebo-group neonates receiving open-label morphine had worse rates of the composite outcome than those not receiving open-label morphine (78/228 [34%] vs 27/179 [15%], p<0.0001). Morphine-group neonates receiving open-label morphine were more likely to develop severe IVH (36/190 [19%] vs 19/219 [9%], p=0.0024).

    INTERPRETATION: Pre-emptive morphine infusions did not reduce the frequency of severe IVH, PVL, or death in ventilated preterm neonates, but intermittent boluses of open-label morphine were associated with an increased rate of the composite outcome. The morphine doses used in this study decrease clinical signs of pain but can cause significant adverse effects in ventilated preterm neonates.

  • 2.
    Anderson, Ian
    et al.
    The University of Melbourne, Melbourne, Australia.
    Tano, Sofia
    School of Business and Economy, Umeå University, Umeå, Sweden.
    Yap, Leslie
    Native Hawaiian Center of Excellence, John A Burns School of Medicine, University of Hawaii, Honolulu HI, United States.
    Indigenous and tribal peoples' health (The Lancet-Lowitja Institute Global Collaboration): a population study2016Inngår i: The Lancet, ISSN 0140-6736, E-ISSN 1474-547X, Vol. 388, nr 10040, s. 131-157Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: International studies of the health of Indigenous and tribal peoples provide important public health insights. Reliable data are required for the development of policy and health services. Previous studies document poorer outcomes for Indigenous peoples compared with benchmark populations, but have been restricted in their coverage of countries or the range of health indicators. Our objective is to describe the health and social status of Indigenous and tribal peoples relative to benchmark populations from a sample of countries.

    Methods: Collaborators with expertise in Indigenous health data systems were identified for each country. Data were obtained for population, life expectancy at birth, infant mortality, low and high birthweight, maternal mortality, nutritional status, educational attainment, and economic status. Data sources consisted of governmental data, data from non-governmental organisations such as UNICEF, and other research. Absolute and relative differences were calculated.

    Findings: Our data (23 countries, 28 populations) provide evidence of poorer health and social outcomes for Indigenous peoples than for non-Indigenous populations. However, this is not uniformly the case, and the size of the rate difference varies. We document poorer outcomes for Indigenous populations for: life expectancy at birth for 16 of 18 populations with a difference greater than 1 year in 15 populations; infant mortality rate for 18 of 19 populations with a rate difference greater than one per 1000 livebirths in 16 populations; maternal mortality in ten populations; low birthweight with the rate difference greater than 2% in three populations; high birthweight with the rate difference greater than 2% in one population; child malnutrition for ten of 16 populations with a difference greater than 10% in five populations; child obesity for eight of 12 populations with a difference greater than 5% in four populations; adult obesity for seven of 13 populations with a difference greater than 10% in four populations; educational attainment for 26 of 27 populations with a difference greater than 1% in 24 populations; and economic status for 15 of 18 populations with a difference greater than 1% in 14 populations.

    Interpretation: We systematically collated data across a broader sample of countries and indicators than done in previous studies. Taking into account the UN Sustainable Development Goals, we recommend that national governments develop targeted policy responses to Indigenous health, improving access to health services, and Indigenous data within national surveillance systems.

  • 3.
    Appelros, Peter
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Department of Neurology, Örebro University Hospital, Örebro, Sweden.
    Terent, Andreas
    Department of Medical Sciences, Uppsala University Hospital, Uppsala, Sweden.
    Thrombolysis in acute stroke2015Inngår i: The Lancet, ISSN 0140-6736, E-ISSN 1474-547X, Vol. 385, nr 9976, s. 1394-1394Artikkel i tidsskrift (Fagfellevurdert)
  • 4.
    Blonde, Lawrence
    et al.
    Department of Endocrinology, Ochsner Medical Center, New Orleans LA, USA.
    Jendle, Johan
    Örebro universitet, Institutionen för medicinska vetenskaper. Endocrine and Diabetes Center, Karlstad Hospital, Karlstad, Sweden.
    Gross, Jorge
    Federal University of Rio Grande do Sul, Porto Alegre, Brazil.
    Woo, Vincent
    Section of Endocrinology and Metabolism, University of Manitoba, Winnipeg MB, Canada.
    Jiang, Honghua
    Lilly Diabetes, Eli Lilly and Company, Indianapolis IN, USA.
    Fahrbach, Jessie L.
    Diabetes, Eli Lilly and Company, Indianapolis IN, USA.
    Milicevic, Zvonko
    Lilly Research Laboratories, Vienna, Austria.
    Once-weekly dulaglutide versus bedtime insulin glargine, both in combination with prandial insulin lispro, in patients with type 2 diabetes (AWARD-4): a randomised, open-label, phase 3, non-inferiority study2015Inngår i: The Lancet, ISSN 0140-6736, E-ISSN 1474-547X, Vol. 385, nr 9982, s. 2057-2066Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: For patients with type 2 diabetes who do not achieve target glycaemic control with conventional insulin treatment, advancing to a basal-bolus insulin regimen is often recommended. We aimed to compare the efficacy and safety of long-acting glucagon-like peptide-1 receptor agonist dulaglutide with that of insulin glargine, both combined with prandial insulin lispro, in patients with type 2 diabetes.

    Methods: We did this 52 week, randomised, open-label, phase 3, non-inferiority trial at 105 study sites in 15 countries. Patients (aged ≥18 years) with type 2 diabetes inadequately controlled with conventional insulin treatment were randomly assigned (1:1:1), via a computer-generated randomisation sequence with an interactive voice-response system, to receive once-weekly dulaglutide 1·5 mg, dulaglutide 0·75 mg, or daily bedtime glargine. Randomisation was stratified by country and metformin use. Participants and study investigators were not masked to treatment allocation, but were unaware of dulaglutide dose assignment. The primary outcome was a change in glycated haemoglobin A1c (HbA1c) from baseline to week 26, with a 0·4% non-inferiority margin. Analysis was by intention to treat. This trial is registered with ClinicalTrials.gov, number NCT01191268.

    Findings: Between Dec 9, 2010, and Sept 21, 2012, we randomly assigned 884 patients to receive dulaglutide 1·5 mg (n=295), dulaglutide 0·75 mg (n=293), or glargine (n=296). At 26 weeks, the adjusted mean change in HbA1c was greater in patients receiving dulaglutide 1·5 mg (-1·64% [95% CI -1·78 to -1·50], -17·93 mmol/mol [-19·44 to -16·42]) and dulaglutide 0·75 mg (-1·59% [-1·73 to -1·45], -17·38 mmol/mol [-18·89 to -15·87]) than in those receiving glargine (-1·41% [-1·55 to -1·27], -15·41 mmol/mol [-16·92 to -13·90]). The adjusted mean difference versus glargine was -0·22% (95% CI -0·38 to -0·07, -2·40 mmol/mol [-4·15 to -0·77]; p=0·005) for dulaglutide 1·5 mg and -0·17% (-0·33 to -0·02, -1·86 mmol/mol [-3·61 to -0·22]; p=0·015) for dulaglutide 0·75 mg. Five (<1%) patients died after randomisation because of septicaemia (n=1 in the dulaglutide 1·5 mg group); pneumonia (n=1 in the dulaglutide 0·75 mg group); cardiogenic shock; ventricular fibrillation; and an unknown cause (n=3 in the glargine group). We recorded serious adverse events in 27 (9%) patients in the dulaglutide 1·5 mg group, 44 (15%) patients in the dulaglutide 0·75 mg group, and 54 (18%) patients in the glargine group. The most frequent adverse events, arising more often with dulaglutide than glargine, were nausea, diarrhoea, and vomiting.

    Iinterpretation: Dulaglutide in combination with lispro resulted in a significantly greater improvement in glycaemic control than did glargine and represents a new treatment option for patients unable to achieve glycaemic targets with conventional insulin treatment.

    FUNDING: Eli Lilly and Company.

  • 5.
    Cleynen, Isabelle
    et al.
    Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, UK; Department of Clinical and Experimental Medicine TARGID, KU Leuven, Leuven, Belgium.
    Boucher, Gabrielle
    Montreal Heart Institute Research Center, Université de Montréal, Montréal, Canada.
    Jostins, Luke
    Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, UK; Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK; Christ Church, University of Oxford, St Aldates, UK.
    Schumm, L. Philip
    Department of Public Health Sciences, University of Chicago, Chicago IL, USA.
    Zeissig, Sebastian
    Department for General Internal Medicine, Christian-Albrechts-University, Kiel, Germany.
    Ahmad, Tariq
    Peninsula College of Medicine and Dentistry, Exeter, UK.
    Andersen, Vibeke
    Medical Department, Viborg Regional Hospital, Viborg, Denmark; Hospital of Southern Jutland Aabenraa, Aabenraa, Denmark.
    Andrews, Jane M.
    Inflammatory Bowel Disease Service, Department of Gastroenterology and Hepatology, Royal Adelaide Hospital, Adelaide, Australia; School of Medicine, University of Adelaide, Adelaide, Australia.
    Annese, Vito
    Unit of Gastroenterology, Istituto di Ricovero e Cura a Carattere Scientifico-Casa Sollievo della Sofferenza (IRCCS-CSS) Hospital, San Giovanni Rotondo, Italy; Unit of Gastroenterology SOD2, Azienda Ospedaliero Universitaria (AOU) Careggi, Florence, Italy.
    Brand, Stephan
    Department of Medicine II, University Hospital Munich-Grosshadern, Ludwig-Maximilians-University, Munich, Germany.
    Brant, Steven R.
    Meyerhoff Inflammatory Bowel Disease Center, Department of Medicine, School of Medicine, Johns Hopkins University, Baltimore MD, USA; Department of Epidemiology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore MD, USA.
    Cho, Judy H.
    Department of Genetics, Yale School of Medicine, New Haven CT, USA.
    Daly, Mark J.
    Broad Institute of MIT and Harvard, Cambridge MA, USA.
    Dubinsky, Marla
    Department of Pediatrics, Cedars Sinai Medical Center, Los Angeles CA, USA.
    Duerr, Richard H.
    Division of Gastroenterology, Hepatology and Nutrition, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh PA, USA; Department of Human Genetics, University of Pittsburgh Graduate School of Public Health, Pittsburgh PA, USA.
    Ferguson, Lynnette R.
    School of Medical Sciences, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand.
    Franke, Andre
    Institute of Clinical Molecular Biology, Christian-Albrechts-University, Kiel, Germany.
    Gearry, Richard B.
    Department of Medicine, University of Otago, Christchurch, New Zealand; Department of Gastroenterology, Christchurch Hospital, Christchurch, New Zealand.
    Goyette, Philippe
    Montreal Heart Institute, Research Center, Université de Montréal, Montréal, Canada.
    Hakonarson, Hakon
    Center for Applied Genomics, Children's Hospital of Philadelphia, Philadelphia PA, USA.
    Halfvarson, Jonas
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Gastroenterology, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Hov, Johannes R.
    Norwegian PSC Research Center, Research Insitute of Internal Medicine and Department of Transplantation Medicine, Oslo University Hospital, University of Oslo, Oslo, Norway.
    Huang, Hailang
    Broad Institute of MIT and Harvard, Cambridge MA, USA.
    Kennedy, Nicholas A.
    Gastrointestinal Unit, Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, UK.
    Kupcinskas, Limas
    Department of Gastroenterology, Lithuanian University of Health Sciences, Kaunas, Lithuania.
    Lawrance, Ian C.
    Centre for Inflammatory Bowel Diseases, Saint John of God Hospital, Perth WA, Australia; Harry Perkins Institute for Medical Research, School of Medicine and Pharmacology, University of Western Australia, Murdoch WA, Australia.
    Lee, James C.
    Inflammatory Bowel Disease Research Group, Addenbrooke's Hospital, University of Cambridge, Cambridge, UK.
    Satsangi, Jack
    Gastrointestinal Unit, Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, UK.
    Schreiber, Stephan
    Institute of Clinical Molecular Biology, Christian-Albrechts-University, Kiel, Germany; Hospital of Southern Jutland Aabenraa, Aabenraa, Denmark.
    Théâtre, Emilie
    Unit of Animal Genomics, Groupe Interdisciplinaire de Genoproteomique Appliquee (GIGA-R) and Faculty of Veterinary Medicine, University of Liege, Liege, Belgium; Division of Gastroenterology, Centre Hospitalier Universitaire, Universite de Liege, Liege, Belgium.
    van der Meulen-de Jong, Andrea E.
    Department of Gastroenterology and Hepatology, Leiden University Medical Center, Leiden, Netherlands.
    Weersma, Rinse K.
    Department of Gastroenterology and Hepatology, University Medical Center Groningen, University of Groningen, Groningen, Netherlands.
    Wilson, David C.
    Child Life and Health, University of Edinburgh, Edinburgh, UK; Paediatric Gastroenterology and Nutrition, Royal Hospital for Sick Children, Glasgow, UK.
    Parkes, Miles
    Inflammatory Bowel Disease Research Group, Addenbrooke's Hospital, University of Cambridge, Cambridge, UK.
    Vermeire, Severine
    Department of Clinical and Experimental Medicine TARGID, KU Leuven, Leuven, Belgium; Division of Gastroenterology, University Hospital Gasthuisberg, Leuven, Belgium.
    Rioux, John D.
    Research Center, Université de Montréal, the Montreal Heart Institute, Montréal, Canada.
    Mansfield, John
    Institute of Human Genetics, Newcastle University, Newcastle upon Tyne, UK.
    Silverberg, Mark S.
    Mount Sinai Hospital Inflammatory Bowel Disease Centre, University of Toronto, Toronto ON, Canada.
    Radford-Smith, Graham
    Inflammatory Bowel Diseases, Genetics and Computational Biology, Queensland Institute of Medical Research, Brisbane, Australia; Department of Gastroenterology, Royal Brisbane and Women's Hospital, Brisbane, Australia; School of Medicine, University of Queensland, Brisbane, Australia.
    McGovern, Dermot P. B.
    F Widjaja Foundation Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles CA, USA.
    Barrett, Jeffrey C.
    Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, UK.
    Lees, Charlie W.
    Gastrointestinal Unit, Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, UK.
    Inherited determinants of Crohn's disease and ulcerative colitis phenotypes: a genetic association study2016Inngår i: The Lancet, ISSN 0140-6736, E-ISSN 1474-547X, Vol. 387, nr 10014, s. 156-167Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Crohn's disease and ulcerative colitis are the two major forms of inflammatory bowel disease; treatment strategies have historically been determined by this binary categorisation. Genetic studies have identified 163 susceptibility loci for inflammatory bowel disease, mostly shared between Crohn's disease and ulcerative colitis. We undertook the largest genotype association study, to date, in widely used clinical subphenotypes of inflammatory bowel disease with the goal of further understanding the biological relations between diseases.

    Methods This study included patients from 49 centres in 16 countries in Europe, North America, and Australasia. We applied the Montreal classification system of inflammatory bowel disease subphenotypes to 34,819 patients (19,713 with Crohn's disease, 14,683 with ulcerative colitis) genotyped on the Immunochip array. We tested for genotype-phenotype associations across 156,154 genetic variants. We generated genetic risk scores by combining information from all known inflammatory bowel disease associations to summarise the total load of genetic risk for a particular phenotype. We used these risk scores to test the hypothesis that colonic Crohn's disease, ileal Crohn's disease, and ulcerative colitis are all genetically distinct from each other, and to attempt to identify patients with a mismatch between clinical diagnosis and genetic risk profile.

    Findings: After quality control, the primary analysis included 29,838 patients (16,902 with Crohn's disease, 12,597 with ulcerative colitis). Three loci (NOD2, MHC, and MST1 3p21) were associated with subphenotypes of inflammatory bowel disease, mainly disease location (essentially fixed over time; median follow-up of 10·5 years). Little or no genetic association with disease behaviour (which changed dramatically over time) remained after conditioning on disease location and age at onset. The genetic risk score representing all known risk alleles for inflammatory bowel disease showed strong association with disease subphenotype (p=1·65 × 10(-78)), even after exclusion of NOD2, MHC, and 3p21 (p=9·23 × 10(-18)). Predictive models based on the genetic risk score strongly distinguished colonic from ileal Crohn's disease. Our genetic risk score could also identify a small number of patients with discrepant genetic risk profiles who were significantly more likely to have a revised diagnosis after follow-up (p=6·8 × 10(-4)).

    Interpretation: Our data support a continuum of disorders within inflammatory bowel disease, much better explained by three groups (ileal Crohn's disease, colonic Crohn's disease, and ulcerative colitis) than by Crohn's disease and ulcerative colitis as currently defined. Disease location is an intrinsic aspect of a patient's disease, in part genetically determined, and the major driver to changes in disease behaviour over time.

    Funding: International Inflammatory Bowel Disease Genetics Consortium members funding sources (see Acknowledgments for full list).

  • 6.
    Dalal, Koustuv
    Örebro universitet, Institutionen för hälsovetenskaper.
    Healthcare Access and Quality Index based on mortality from causes amenable to personal health care in 195 countries and territories, 1990-2015: a novel analysis from the Global Burden of Disease Study 20152017Inngår i: The Lancet, ISSN 0140-6736, E-ISSN 1474-547X, Vol. 390, nr 10091, s. 231-266Artikkel i tidsskrift (Fagfellevurdert)
  • 7.
    Dieleman, Joseph
    et al.
    Institute for Health Metrics and Evaluation, University of Washington, Seattle WA, USA.
    Dalal, Koustuv
    Örebro universitet, Institutionen för hälsovetenskaper. Centre for Injury Prevention and Safety Promotion.
    Murray, Christopher, J. L.
    Institute for Health Metrics and Evaluation, University of Washington, Seattle WA, USA.
    Evolution and patterns of global health financing 1995-2014: development assistance for health, and government, prepaid private, and out-of-pocket health spending in 184 countries2017Inngår i: The Lancet, ISSN 0140-6736, E-ISSN 1474-547X, Vol. 389, nr 10083, s. 1981-2004Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: An adequate amount of prepaid resources for health is important to ensure access to health services and for the pursuit of universal health coverage. Previous studies on global health financing have described the relationship between economic development and health financing. In this study, we further explore global health financing trends and examine how the sources of funds used, types of services purchased, and development assistance for health disbursed change with economic development. We also identify countries that deviate from the trends.

    Methods: We estimated national health spending by type of care and by source, including development assistance for health, based on a diverse set of data including programme reports, budget data, national estimates, and 964 National Health Accounts. These data represent health spending for 184 countries from 1995 through 2014. We converted these data into a common inflation-adjusted and purchasing power-adjusted currency, and used non-linear regression methods to model the relationship between health financing, time, and economic development.

    Findings: Between 1995 and 2014, economic development was positively associated with total health spending and a shift away from a reliance on development assistance and out-of-pocket (OOP) towards government spending. The largest absolute increase in spending was in high-income countries, which increased to purchasing power-adjusted $5221 per capita based on an annual growth rate of 3.0%. The largest health spending growth rates were in upper-middle-income (5.9) and lower-middle-income groups (5.0), which both increased spending at more than 5% per year, and spent $914 and $267 per capita in 2014, respectively. Spending in low-income countries grew nearly as fast, at 4.6%, and health spending increased from $51 to $120 per capita. In 2014, 59.2% of all health spending was financed by the government, although in low-income and lower-middle-income countries, 29.1% and 58.0% of spending was OOP spending and 35.7% and 3.0% of spending was development assistance. Recent growth in development assistance for health has been tepid; between 2010 and 2016, it grew annually at 1.8%, and reached US$37.6 billion in 2016. Nonetheless, there is a great deal of variation revolving around these averages. 29 countries spend at least 50% more than expected per capita, based on their level of economic development alone, whereas 11 countries spend less than 50% their expected amount.

    Interpretation: Health spending remains disparate, with low-income and lower-middle-income countries increasing spending in absolute terms the least, and relying heavily on OOP spending and development assistance. Moreover, tremendous variation shows that neither time nor economic development guarantee adequate prepaid health resources, which are vital for the pursuit of universal health coverage.

  • 8.
    Dieleman, Joseph L.
    et al.
    Institute for Health Metrics and Evaluation, University of Washington, Seattle WA, USA .
    Dalal, Koustuv
    Örebro universitet, Institutionen för hälsovetenskaper. Centre for Injury Prevention and Safety Promotion.
    Murray, Christopher J. L.
    Institute for Health Metrics and Evaluation, University of Washington, Seattle WA, USA .
    Future and potential spending on health 2015-40: development assistance for health, and government, prepaid private, and out-of-pocket health spending in 184 countries2017Inngår i: The Lancet, ISSN 0140-6736, E-ISSN 1474-547X, Vol. 389, nr 10083, s. 2005-2030Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: The amount of resources, particularly prepaid resources, available for health can affect access to health care and health outcomes. Although health spending tends to increase with economic development, tremendous variation exists among health financing systems. Estimates of future spending can be beneficial for policy makers and planners, and can identify financing gaps. In this study, we estimate future gross domestic product (GDP), all-sector government spending, and health spending disaggregated by source, and we compare expected future spending to potential future spending.

    Methods: We extracted GDP, government spending in 184 countries from 1980-2015, and health spend data from 1995-2014. We used a series of ensemble models to estimate future GDP, all-sector government spending, development assistance for health, and government, out-of-pocket, and prepaid private health spending through 2040. We used frontier analyses to identify patterns exhibited by the countries that dedicate the most funding to health, and used these frontiers to estimate potential health spending for each low-income or middle-income country. All estimates are inflation and purchasing power adjusted.

    Findings: We estimated that global spending on health will increase from US$9.21 trillion in 2014 to $24.24 trillion (uncertainty interval [UI] 20.47-29.72) in 2040. We expect per capita health spending to increase fastest in upper-middle-income countries, at 5.3% (UI 4.1-6.8) per year. This growth is driven by continued growth in GDP, government spending, and government health spending. Lower-middle income countries are expected to grow at 4.2% (3.8-4.9). High-income countries are expected to grow at 2.1% (UI 1.8-2.4) and low-income countries are expected to grow at 1.8% (1.0-2.8). Despite this growth, health spending per capita in low-income countries is expected to remain low, at $154 (UI 133-181) per capita in 2030 and $195 (157-258) per capita in 2040. Increases in national health spending to reach the level of the countries who spend the most on health, relative to their level of economic development, would mean $321 (157-258) per capita was available for health in 2040 in low-income countries.

    Interpretation: Health spending is associated with economic development but past trends and relationships suggest that spending will remain variable, and low in some low-resource settings. Policy change could lead to increased health spending, although for the poorest countries external support might remain essential.

  • 9.
    Fazel, Seena
    et al.
    Department of Psychiatry, University of Oxford, Warneford Hospital, Oxford, UK.
    Zetterqvist, Johan
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Larsson, Henrik
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Långström, Niklas
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Lichtenstein, Paul
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Antipsychotics, mood stabilisers, and risk of violent crime2014Inngår i: The Lancet, ISSN 0140-6736, E-ISSN 1474-547X, Vol. 384, nr 9949, s. 1206-1214Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Antipsychotics and mood stabilisers are prescribed widely to patients with psychiatric disorders worldwide. Despite clear evidence for their efficacy in relapse prevention and symptom relief, their effect on some adverse outcomes, including the perpetration of violent crime, is unclear. We aimed to establish the effect of antipsychotics and mood stabilisers on the rate of violent crime committed by patients with psychiatric disorders in Sweden.

    Methods: We used linked Swedish national registers to study 82,647 patients who were prescribed antipsychotics or mood stabilisers, their psychiatric diagnoses, and subsequent criminal convictions in 2006-09. We did within-individual analyses to compare the rate of violent criminality during the time that patients were prescribed these medications versus the rate for the same patients while they were not receiving the drugs to adjust for all confounders that remained constant within each participant during follow-up. The primary outcome was the occurrence of violent crime, according to Sweden's national crime register.

    Findings: In 2006-09, 40,937 men in Sweden were prescribed antipsychotics or mood stabilisers, of whom 2657 (6·5%) were convicted of a violent crime during the study period. In the same period, 41,710 women were prescribed these drugs, of whom 604 (1·4 %) had convictions for violent crime. Compared with periods when participants were not on medication, violent crime fell by 45% in patients receiving antipsychotics (hazard ratio [HR] 0·55, 95% CI 0·47-0·64) and by 24% in patients prescribed mood stabilisers (0·76, 0·62-0·93). However, we identified potentially important differences by diagnosis-mood stabilisers were associated with a reduced rate of violent crime only in patients with bipolar disorder. The rate of violence reduction for antipsychotics remained between 22% and 29% in sensitivity analyses that used different outcomes (any crime, drug-related crime, less severe crime, and violent arrest), and was stronger in patients who were prescribed higher drug doses than in those prescribed low doses. Notable reductions in violent crime were also recorded for depot medication (HR adjusted for concomitant oral medications 0·60, 95% CI 0·39-0·92).

    Interpretation: In addition to relapse prevention and psychiatric symptom relief, the benefits of antipsychotics and mood stabilisers might also include reductions in the rates of violent crime. The potential effects of these drugs on violence and crime should be taken into account when treatment options for patients with psychiatric disorders are being considered.

    Funding: The Wellcome Trust, the Swedish Prison and Probation Service, the Swedish Research Council, and the Swedish Research Council for Health, Working Life and Welfare.

  • 10.
    Fazel, Seena
    et al.
    Department of Psychiatry, University of Oxford, Warneford Hospital, Oxford, United Kingdom.
    Zetterqvist, Johan
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Larsson, Henrik
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Långström, Niklas
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Lichtenstein, Paul
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Psychotropics and risk of violent crime: Authors' reply2014Inngår i: The Lancet, ISSN 0140-6736, E-ISSN 1474-547X, Vol. 384, nr 9959, s. 2025-2026Artikkel i tidsskrift (Fagfellevurdert)
  • 11.
    Fröbert, Ole
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    James, Stefan K.
    Uppsala Clin Res Ctr, Dept Med Sci, Uppsala Univ, Uppsala, Sweden; Uppsala Clin Res Ctr, Dept Cardiol, Uppsala Univ, Uppsala, Sweden.
    Coronary thrombus aspiration: a lesson for clinical medicine2016Inngår i: The Lancet, ISSN 0140-6736, E-ISSN 1474-547X, Vol. 387, nr 10014, s. 97-98Artikkel i tidsskrift (Fagfellevurdert)
  • 12.
    Gilbert, R. E.
    et al.
    UCL Institute of Child Health, London, UK.
    Fluke, J.
    Child Protection Research Center, American Humane Association, Englewood, USA .
    O'Donnell, M.
    Centre for Child Health Research, University of Western Australia, Perth, Australia .
    Gonzalez-Izquierdo, A.
    UCL Institute of Child Health, London, UK.
    Brownell, M.
    Department of Community Health Sciences, University of Manitoba, Winnipeg, Canada .
    Gulliver, P.
    Injury Prevention Research Unit, University of Otago, Dunedin, New Zealand .
    Janson, Staffan
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Department of Public Health, Karlstad University, Karlstad, Sweden.
    Sidebotham, P.
    Warwick Medical School, University of Warwick, Coventry, UK.
    Trends in child maltreatment reply2012Inngår i: The Lancet, ISSN 0140-6736, E-ISSN 1474-547X, Vol. 379, nr 9831, s. 2049-2049Artikkel i tidsskrift (Fagfellevurdert)
  • 13.
    Gilbert, Ruth
    et al.
    MRC Centre of Epidemiology for Child Health, UCL Institute of Child Health, London, United Kingdom.
    Fluke, John
    Child Protection Research Center, American Humane Association, Englewood, United States.
    O'Donnell, Melissa
    Centre for Child Health Research, University of Western Australia, Perth, Australia .
    Gonzalez-Izquierdo, Arturo
    MRC Centre of Epidemiology for Child Health, UCL Institute of Child Health, London, United Kingdom.
    Brownell, Marni
    Department of Community Health Sciences, University of Manitoba, Winnipeg, Canada .
    Gulliver, Pauline
    Injury Prevention Research Unit, University of Otago, Dunedin, New Zealand.
    Janson, Staffan
    Örebro universitet, Institutionen för juridik, psykologi och socialt arbete. Department of Paediatrics, Örebro University, Örebro, Sweden; Department of Public Health, Karlstad University, Karlstad, Sweden.
    Sidebotham, Peter
    Warwick Medical School, University of Warwick, Coventry, United Kingdom.
    Child maltreatment: variation in trends and policies in six developed countries2012Inngår i: The Lancet, ISSN 0140-6736, E-ISSN 1474-547X, Vol. 379, nr 9817, s. 758-772Artikkel, forskningsoversikt (Fagfellevurdert)
    Abstract [en]

    We explored trends in six developed countries in three types of indicators of child maltreatment for children younger than 11 years, since the inception of modern child protection systems in the 1970s. Despite several policy initiatives for child protection, we recorded no consistent evidence for a decrease in all types of indicators of child maltreatment. We noted falling rates of violent death in a few age and country groups, but these decreases coincided with reductions in admissions to hospital for maltreatment-related injury only in Sweden and Manitoba (Canada). One or more child protection agency indicators increased in five of six countries, particularly in infants, possibly as a result of early intervention policies. Comparisons of mean rates between countries showed five-fold to ten-fold differences in rates of agency indicators, but less than two-fold variation in violent deaths or maltreatment-related injury, apart from high rates of violent child death in the USA. These analyses draw attention to the need for robust research to establish whether the high and rising rates of agency contacts and out-of-home care in some settings are effectively reducing child maltreatment.

  • 14.
    Hay, Simon I.
    et al.
    Inst Hlth Metr & Evaluat, Univ Washington, Seattle WA, USA; Oxford Big Data Inst, Li Ka Shing Ctr Hlth Informat & Discovery, Oxford University, Oxford, England.
    Dalal, Koustuv
    Örebro universitet, Institutionen för hälsovetenskaper.
    Murray, Christopher J. L.
    Inst Hlth Metr & Evaluat, Univ Washington, Seattle WA, USA.
    GBD 2016 DALYs, Group author
    HALE Collaborators, Group author
    Global, regional, and national disability-adjusted life-years (DALYs) for 333 diseases and injuries and healthy life expectancy (HALE) for 195 countries and territories, 1990-2016: a systematic analysis for the Global Burden of Disease Study 20162017Inngår i: The Lancet, ISSN 0140-6736, E-ISSN 1474-547X, Vol. 390, nr 10100, s. 1260-1344Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Measurement of changes in health across locations is useful to compare and contrast changing epidemiological patterns against health system performance and identify specific needs for resource allocation in research, policy development, and programme decision making. Using the Global Burden of Diseases, Injuries, and Risk Factors Study 2016, we drew from two widely used summary measures to monitor such changes in population health: disability-adjusted life-years (DALYs) and healthy life expectancy (HALE). We used these measures to track trends and benchmark progress compared with expected trends on the basis of the Socio-demographic Index (SDI).

    Methods: We used results from the Global Burden of Diseases, Injuries, and Risk Factors Study 2016 for all-cause mortality, cause-specific mortality, and non-fatal disease burden to derive HALE and DALYs by sex for 195 countries and territories from 1990 to 2016. We calculated DALYs by summing years of life lost and years of life lived with disability for each location, age group, sex, and year. We estimated HALE using age-specific death rates and years of life lived with disability per capita. We explored how DALYs and HALE differed from expected trends when compared with the SDI: the geometric mean of income per person, educational attainment in the population older than age 15 years, and total fertility rate.

    Findings: The highest globally observed HALE at birth for both women and men was in Singapore, at 75.2 years (95% uncertainty interval 71.9-78.6) for females and 72.0 years (68.8-75.1) for males. The lowest for females was in the Central African Republic (45.6 years [42.0-49.5]) and for males was in Lesotho (41.5 years [39.0-44.0]). From 1990 to 2016, global HALE increased by an average of 6.24 years (5.97-6.48) for both sexes combined. Global HALE increased by 6.04 years (5.74-6.27) for males and 6.49 years (6.08-6.77) for females, whereas HALE at age 65 years increased by 1.78 years (1.61-1.93) for males and 1.96 years (1.69-2.13) for females. Total global DALYs remained largely unchanged from 1990 to 2016 (-2.3% [-5.9 to 0.9]), with decreases in communicable, maternal, neonatal, and nutritional (CMNN) disease DALYs offset by increased DALYs due to non-communicable diseases (NCDs). The exemplars, calculated as the five lowest ratios of observed to expected age-standardised DALY rates in 2016, were Nicaragua, Costa Rica, the Maldives, Peru, and Israel. The leading three causes of DALYs globally were ischaemic heart disease, cerebrovascular disease, and lower respiratory infections, comprising 16.1% of all DALYs. Total DALYs and age-standardised DALY rates due to most CMNN causes decreased from 1990 to 2016. Conversely, the total DALY burden rose for most NCDs; however, age-standardised DALY rates due to NCDs declined globally.

    Interpretation: At a global level, DALYs and HALE continue to show improvements. At the same time, we observe that many populations are facing growing functional health loss. Rising SDI was associated with increases in cumulative years of life lived with disability and decreases in CMNN DALYs offset by increased NCD DALYs. Relative compression of morbidity highlights the importance of continued health interventions, which has changed in most locations in pace with the gross domestic product per person, education, and family planning. The analysis of DALYs and HALE and their relationship to SDI represents a robust framework with which to benchmark location-specific health performance. Country-specific drivers of disease burden, particularly for causes with higher-than-expected DALYs, should inform health policies, health system improvement initiatives, targeted prevention efforts, and development assistance for health, including financial and research investments for all countries, regardless of their level of sociodemographic development. The presence of countries that substantially outperform others suggests the need for increased scrutiny for proven examples of best practices, which can help to extend gains, whereas the presence of underperforming countries suggests the need for devotion of extra attention to health systems that need more robust support.

  • 15.
    Imel, Erik A.
    et al.
    Department of Medicine and Department of Pediatrics, Indiana University School of Medicine, Indianapolis IN, USA.
    Glorieux, Francis H.
    Shriners Hospital for Children — Canada, McGill University, Montreal QC, Canada.
    Whyte, Michael P.
    Shriners Hospitals for Children — St Louis, St Louis MO, USA.
    Munns, Craig F.
    The University of Sydney Children's Hospital Westmead Clinical School, The Children's Hospital at Westmead, Westmead, NSW, Australia; Department of Endocrinology, The Children's Hospital at Westmead, Westmead NSW, Australia.
    Ward, Leanne M.
    Department of Pediatrics, Faculty of Medicine, University of Ottawa, Ottawa ON, Canada.
    Nilsson, Ola
    Örebro universitet, Institutionen för medicinska vetenskaper. Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
    Simmons, Jill H.
    Department of Pediatrics, Division of Endocrinology and Diabetes, Vanderbilt University School of Medicine, Vanderbilt University, Nashville TN, USA.
    Padidela, Raja
    Department of Paediatric Endocrinology, Royal Manchester Children's Hospital, Manchester, UK.
    Namba, Noriyuki
    Department of Pediatrics, Osaka Hospital, Japan Community Healthcare Organization, Osaka, Japan; Department of Pediatrics, Osaka University Graduate School of Medicine, Osaka, Japan.
    Cheong, Hae Il
    Seoul National University Children's Hospital, Seoul, Korea.
    Pitukcheewanont, Pisit
    Center of Endocrinology, Diabetes and Metabolism, Children's Hospital of Los Angeles, Los Angeles CA, USA.
    Sochett, Etienne
    Department of Pediatrics, Hospital for Sick Children, Toronto ON, Canada.
    Högler, Wolfgang
    Department of Paediatrics and Adolescent Medicine, Johannes Kepler University Linz, Linz, Austria; Institute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK.
    Muroya, Koji
    Kanagawa Children's Medical Center, Yokohama, Japan.
    Tanaka, Hiroyuki
    Okayama Saiseikai General Hospital Outpatient Center, Okayama, Japan.
    Gottesman, Gary S.
    Shriners Hospitals for Children — St Louis, St Louis MO, USA.
    Biggin, Andrew
    The University of Sydney Children's Hospital Westmead Clinical School, The Children's Hospital at Westmead, Westmead NSW, Australia.
    Perwad, Farzana
    Department of Pediatrics, University of California, San Francisco, San Francisco CA, USA.
    Mao, Meng
    Ultragenyx Pharmaceutical, Novato CA, USA.
    Chen, Chao-Yin
    Ultragenyx Pharmaceutical, Novato CA, USA.
    Skrinar, Alison
    Ultragenyx Pharmaceutical, Novato CA, USA.
    San Martin, Javier
    Ultragenyx Pharmaceutical, Novato CA, USA.
    Portale, Anthony A.
    Department of Pediatrics, University of California, San Francisco, San Francisco CA, USA.
    Burosumab versus conventional therapy in children with X-linked hypophosphataemia: a randomised, active-controlled, open-label, phase 3 trial2019Inngår i: The Lancet, ISSN 0140-6736, E-ISSN 1474-547X, Vol. 393, nr 10189, s. 2416-2427Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: X-linked hypophosphataemia in children is characterised by elevated serum concentrations of fibroblast growth factor 23 (FGF23), hypophosphataemia, rickets, lower extremity bowing, and growth impairment. We compared the efficacy and safety of continuing conventional therapy, consisting of oral phosphate and active vitamin D, versus switching to burosumab, a fully human monoclonal antibody against FGF23, in paediatric X-linked hypophosphataemia.

    Methods: In this randomised, active-controlled, open-label, phase 3 trial at 16 clinical sites, we enrolled children with X-linked hypophosphataemia aged 1-12 years. Key eligibility criteria were a total Thacher rickets severity score of at least 2.0, fasting serum phosphorus lower than 0.97 mmol/L (3.0 mg/dL), confirmed PHEX (phosphate-regulating endopep-tidase homolog, X-linked) mutation or variant of unknown significance in the patient or a family member with appropriate X-linked dominant inheritance, and receipt of conventional therapy for at least 6 consecutive months for children younger than 3 years or at least 12 consecutive months for children older than 3 years. Eligible patients were randomly assigned (1: 1) to receive either subcutaneous burosumab starting at 0.8 mg/kg every 2 weeks (burosumab group) or conventional therapy prescribed by investigators (conventional therapy group). Both interventions lasted 64 weeks. The primary endpoint was change in rickets severity at week 40, assessed by the Radiographic Global Impression of Change global score. All patients who received at least one dose of treatment were included in the primary and safety analyses. The trial is registered with ClinicalTrials.gov, number NCT02915705.

    Findings: Recruitment took place between Aug 3, 2016, and May 8, 2017. Of 122 patients assessed, 61 were enrolled. Of these, 32 (18 girls, 14 boys) were randomly assigned to continue receiving conventional therapy and 29 (16 girls, 13 boys) to receive burosumab. For the primary endpoint at week 40, patients in the burosumab group had significantly greater improvement in Radiographic Global Impression of Change global score than did patients in the conventional therapy group (least squares mean +1.9 [SE 0.1] with burosumab vs +0.8 [0.1] with conventional therapy; difference 1.1, 95% CI 0.8-1.5; p<0.0001). Treatment-emergent adverse events considered possibly, probably, or definitely related to treatment by the investigator occurred more frequently with burosumab (17 [59%] of 29 patients in the burosumab group vs seven [22%] of 32 patients in the conventional therapy group). Three serious adverse events occurred in each group, all considered unrelated to treatment and resolved.

    Interpretation: Significantly greater clinical improvements were shown in rickets severity, growth, and biochemistries among children with X-linked hypophosphataemia treated with burosumab compared with those continuing conventional therapy. Copyright (C) 2019 Elsevier Ltd. All rights reserved.

  • 16.
    Kalla, Rahul
    et al.
    Univ Edinburgh, Inst Genet & Mol Med, Edinburgh, UK.
    Adams, Alex
    Univ Edinburgh, Inst Genet & Mol Med, Edinburgh, UK.
    Nimmo, Elaine
    Univ Edinburgh, Inst Genet & Mol Med, Edinburgh, UK.
    Kennedy, Nicholas
    Univ Edinburgh, Inst Genet & Mol Med, Edinburgh, UK.
    Ventham, Nicholas
    Univ Edinburgh, Inst Genet & Mol Med, Edinburgh,UK.
    Vatn, Morten
    Inst Clin Med, EpiGen, Univ Oslo, Oslo, Norway.
    Jahnsen, Jorgen
    Akershus Univ Hosp, Lørenskog, Norway.
    Ricanek, Petr
    Akershus Univ Hosp, Lørenskog, Norway.
    Halfvarson, Jonas
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län. Department of Gastroenterology, Örebro University Hospital, Örebro, Sweden.
    Pierik, Marieke
    Med Ctr, Maastricht Univ, Maastricht, Netherlands.
    Gomollon, Fernando
    Hosp Clin, IIS Aragon, Univ Lozano Blesa, Zaragoza, Spain.
    Gut, Ivo
    Barcelona Inst Sci & Technol, Centro Nacional de Análisis Genómico, Centre for Genomic Regulation (CNAG-CRG), Barcelona Institute of Science and Technology (BIST), Barcelona, Spain.
    D'Amato, Mauro
    BioCruces Hlth Res Inst, Bilbao, Spain.
    Satsangi, Jack
    Univ Edinburgh, Inst Genet & Mol Med, Edinburgh, UK.
    Epigenetic alterations in inflammatory bowel disease: the complex interplay between genome-wide methylation alterations, germline variation, and gene expression2017Inngår i: The Lancet, ISSN 0140-6736, E-ISSN 1474-547X, Vol. 389, nr Suppl. 1, s. 52-52Artikkel i tidsskrift (Fagfellevurdert)
  • 17.
    Mosleh, Marwan
    et al.
    Ministry of Health, Gaza City, Gaza Strip (occupied Palestinian territory).
    Dalal, Koustuv
    Örebro universitet, Institutionen för hälsovetenskaper.
    Aljeesh, Yousef
    Faculty of Medicine & Nursing, Islamic University, Gaza City, Gaza Strip (occupied Palestinian territory).
    Burden of chronic diseases in the Palestinian health-care sector using disability-adjusted life-years2018Inngår i: The Lancet, ISSN 0140-6736, E-ISSN 1474-547X, Vol. 391, nr Suppl. 1, s. 21-21Artikkel i tidsskrift (Annet vitenskapelig)
    Abstract [en]

    Background: Chronic diseases are the greatest public health concern worldwide, contribute to a large burden of disease in the developed world, and are increasing rapidly in prevalence in developing countries. The aim of this study was to quantify the burden of reported chronic diseases in the occupied Palestinian territory.

    Methods: We used the global burden of disease (GBD) approach and its templates to quantify disability-adjusted life years (DALYs). To estimate years of life lost, we used mortality data from Ministry of Health materials, and we used local morbidity data from the Palestinian Central Bureau of Statistics (heath survey 2010) to estimate years lived with disability. The study was approved by the Palestinian Health Research Council.

    Findings: In 2010, DALYS lost due to selected chronic diseases were estimated as 60 per 1000 DALYs in the West Bank and 57 per 1000 DALYs in Gaza Strip, with each DALY defined as 1 year of optimum healthy life lost. Ischaemic heart disease and hypertension contributed the highest proportion of DALYs in men and women in 2010, followed by lung cancer in men and breast cancer in women. Respiratory disease also contributed a high proportion of DALYs, with a small difference in rank between the Gaza Strip and West Bank. Cancer was ranked the third largest contributor and respiratory disease the fourth largest contributor to DALYs in the Gaza Strip, whereas respiratory disease was the third and cancer the fourth largest contributors to DALYs in the West Bank. We also found differences by sex and region. Heart disease and cancer continued to rank highly as causes of years of life lost in the West Bank and Gaza Strip for both sexes in 2010, indicating the major causes of chronic disease burden in the occupied Palestinian territory in 2010.

    Interpretation: The burden of chronic disease is increasing substantially in the occupied Palestinian territory, and interventions are needed to tackle these burdens. Further studies using recent data and increasing attention to chronic non-communicable diseases are needed in the occupied Palestinian territories.

  • 18.
    Möller, Claes
    Örebro universitet, Hälsoakademin.
    Deafblindness: living with sensory deprivation2003Inngår i: The Lancet, ISSN 0140-6736, E-ISSN 1474-547X, Vol. 362, nr Dec, suppl., s. 46-47Artikkel i tidsskrift (Fagfellevurdert)
  • 19.
    Ortiz-Catalan, Max
    et al.
    Department of Signals and Systems, Chalmers University of Technology, Gothenburg, Sweden; Centre for Advanced Reconstruction of Extremities, Sahlgrenska University Hospital, Mölndal, Sweden; Integrum AB, Mölndal, Sweden.
    Gudmundsdottir, Rannveig A.
    Department of Signals and Systems, Chalmers University of Technology, Gothenburg, Sweden; Integrum AB, Mölndal, Sweden.
    Kristoffersen, Morten B.
    Department of Signals and Systems, Chalmers University of Technology, Gothenburg, Sweden; Integrum AB, Mölndal, Sweden.
    Zepeda-Echavarria, Alejandra
    Department of Signals and Systems, Chalmers University of Technology, Gothenburg, Sweden; Integrum AB, Mölndal, Sweden.
    Caine-Winterberger, Kerstin
    Centre for Advanced Reconstruction of Extremities, Sahlgrenska University Hospital, Mölndal, Sweden.
    Kulbacka-Ortiz, Katarzyna
    Centre for Advanced Reconstruction of Extremities, Sahlgrenska University Hospital, Mölndal, Sweden.
    Widehammar, Cathrine
    Örebro universitet, Institutionen för hälsovetenskaper. University Health Care Research Centre, Region Örebro County, Örebro, Sweden; Department of Pediatrics, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Eriksson, Karin
    Department of Pediatrics, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
    Stockselius, Anita
    Bräcke Diakoni Rehabcenter Sfären, Solna, Sweden.
    Ragnö, Christina
    Bräcke Diakoni Rehabcenter Sfären, Solna, Sweden.
    Pihlar, Zdenka
    University Rehabilitation Institute, Ljubljana, Slovenia.
    Burger, Helena
    University Rehabilitation Institute, Ljubljana, Slovenia.
    Hermansson, Liselotte
    Örebro universitet, Institutionen för hälsovetenskaper. University Health Care Research Centre, Region Örebro County, Örebro, Sweden; Department of Prosthetics and Orthotics, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Phantom motor execution facilitated by machine learning and augmented reality as treatment for phantom limb pain: a single group, clinical trial in patients with chronic intractable phantom limb pain2016Inngår i: The Lancet, ISSN 0140-6736, E-ISSN 1474-547X, Vol. 388, nr 10062, s. 2885-2894Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Phantom limb pain is a debilitating condition for which no eff ective treatment has been found. We hypothesised that re-engagement of central and peripheral circuitry involved in motor execution could reduce phantom limb pain via competitive plasticity and reversal of cortical reorganisation.

    Methods: Patients with upper limb amputation and known chronic intractable phantom limb pain were recruited at three clinics in Sweden and one in Slovenia. Patients received 12 sessions of phantom motor execution using machine learning, augmented and virtual reality, and serious gaming. Changes in intensity, frequency, duration, quality, and intrusion of phantom limb pain were assessed by the use of the numeric rating scale, the pain rating index, the weighted pain distribution scale, and a study-specifi c frequency scale before each session and at follow-up interviews 1, 3, and 6 months after the last session. Changes in medication and prostheses were also monitored. Results are reported using descriptive statistics and analysed by non-parametric tests. The trial is registered at ClinicalTrials. gov, number NCT02281539.

    Findings: Between Sept 15, 2014, and April 10, 2015, 14 patients with intractable chronic phantom limb pain, for whom conventional treatments failed, were enrolled. After 12 sessions, patients showed statistically and clinically signifi cant improvements in all metrics of phantom limb pain. Phantom limb pain decreased from pre-treatment to the last treatment session by 47% (SD 39; absolute mean change 1 . 0 [0 . 8]; p= 0 . 001) for weighted pain distribution, 32% (38; absolute mean change 1 . 6 [1 . 8]; p= 0 . 007) for the numeric rating scale, and 51% (33; absolute mean change 9 . 6 [8 . 1]; p= 0 . 0001) for the pain rating index. The numeric rating scale score for intrusion of phantom limb pain in activities of daily living and sleep was reduced by 43% (SD 37; absolute mean change 2 . 4 [2 . 3]; p= 0 . 004) and 61% (39; absolute mean change 2 . 3 [1 . 8]; p= 0 . 001), respectively. Two of four patients who were on medication reduced their intake by 81% (absolute reduction 1300 mg, gabapentin) and 33% (absolute reduction 75 mg, pregabalin). Improvements remained 6 months after the last treatment.

    Interpretation: Our fi ndings suggest potential value in motor execution of the phantom limb as a treatment for phantom limb pain. Promotion of phantom motor execution aided by machine learning, augmented and virtual reality, and gaming is a non-invasive, non-pharmacological, and engaging treatment with no identifi ed side-eff ects at present.

  • 20.
    Stenberg, Erik
    et al.
    Department of Surgery, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
    Szabo, Eva
    Department of Surgery, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
    Ågren, Göran
    Department of Surgery, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
    Ottosson, Johan
    Department of Surgery, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
    Marsk, Richard
    Division of Surgery, Department of Clinical Sciences, Danderyd Hospital, Karolinska Institutet, Stockholm, Sweden.
    Lönroth, Hans
    Institute of Surgery, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Boman, Lars
    Department of Surgery, Lycksele Hospital, Lycksele, Sweden.
    Magnuson, Anders
    Thorell, Anders
    Division of Surgery, Department of Clinical Sciences, Danderyd Hospital, Karolinska Institutet, Stockholm, Sweden; Department of Surgery, Ersta Hospital, Stockholm, Sweden.
    Näslund, Ingmar
    Department of Surgery, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
    Closure of mesenteric defects in laparoscopic gastric bypass: a multicentre, randomised, parallel, open-label trial2016Inngår i: The Lancet, ISSN 0140-6736, E-ISSN 1474-547X, Vol. 387, nr 10026, s. 1397-1404Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Small bowel obstruction due to internal hernia is a common and potentially serious complication after laparoscopic gastric bypass surgery. Whether closure of surgically created mesenteric defects might reduce the incidence is unknown, so we did a large randomised trial to investigate.

    Method: This study was a multicentre, randomised trial with a two-arm, parallel design done at 12 centres for bariatric surgery in Sweden. Patients planned for laparoscopic gastric bypass surgery at any of the participating centres were off ered inclusion. During the operation, a concealed envelope was opened and the patient was randomly assigned to either closure of mesenteric defects beneath the jejunojejunostomy and at Petersen's space or non-closure. After surgery, assignment was open label. The main outcomes were reoperation for small bowel obstruction and severe postoperative complications. Outcome data and safety were analysed in the intention-to-treat population. This trial is registered with ClinicalTrials. gov, number NCT01137201.

    Findings: Between May 1, 2010, and Nov 14, 2011, 2507 patients were recruited to the study and randomly assigned to closure of the mesenteric defects (n= 1259) or non-closure (n= 1248). 2503 (99.8%) patients had follow-up for severe postoperative complications at day 30 and 2482 (99.0%) patients had follow-up for reoperation due to small bowel obstruction at 25 months. At 3 years after surgery, the cumulative incidence of reoperation because of small bowel obstruction was signifi cantly reduced in the closure group (cumulative probability 0.055 for closure vs 0.102 for non-closure, hazard ratio 0.56, 95% CI 0.41-0.76, p= 0.0002). Closure of mesenteric defects increased the risk for severe postoperative complications (54 [4.3%] for closure vs 35 [2.8%] for non-closure, odds ratio 1.55, 95% CI 1.01-2.39, p= 0.044), mainly because of kinking of the jejunojejunostomy.

    Interpretation: The results of our study support the routine closure of the mesenteric defects in laparoscopic gastric bypass surgery. However, closure of the mesenteric defects might be associated with increased risk of early small bowel obstruction caused by kinking of the jejunojejunostomy.

  • 21.
    Vos, Theo
    et al.
    Inst Hlth Metr & Evaluat, Univ Washington, Seattle WA, USA.
    Dalal, Koustuv
    Örebro universitet, Institutionen för hälsovetenskaper.
    Murray, Christopher J. L.
    Inst Hlth Metr & Evaluat, Univ Washington, Seattle WA, USA.
    Global, regional, and national incidence, prevalence, and years lived with disability for 328 diseases and injuries for 195 countries, 1990-2016: a systematic analysis for the Global Burden of Disease Study 20162017Inngår i: The Lancet, ISSN 0140-6736, E-ISSN 1474-547X, Vol. 390, nr 10100, s. 1211-1259Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: As mortality rates decline, life expectancy increases, and populations age, non-fatal outcomes of diseases and injuries are becoming a larger component of the global burden of disease. The Global Burden of Diseases, Injuries, and Risk Factors Study 2016 (GBD 2016) provides a comprehensive assessment of prevalence, incidence, and years lived with disability (YLDs) for 328 causes in 195 countries and territories from 1990 to 2016.

    Methods: We estimated prevalence and incidence for 328 diseases and injuries and 2982 sequelae, their non-fatal consequences. We used DisMod-MR 2.1, a Bayesian meta-regression tool, as the main method of estimation, ensuring consistency between incidence, prevalence, remission, and cause of death rates for each condition. For some causes, we used alternative modelling strategies if incidence or prevalence needed to be derived from other data. YLDs were estimated as the product of prevalence and a disability weight for all mutually exclusive sequelae, corrected for comorbidity and aggregated to cause level. We updated the Socio-demographic Index (SDI), a summary indicator of income per capita, years of schooling, and total fertility rate. GBD 2016 complies with the Guidelines for Accurate and Transparent Health Estimates Reporting (GATHER).

    Findings: Globally, low back pain, migraine, age-related and other hearing loss, iron-deficiency anaemia, and major depressive disorder were the five leading causes of YLDs in 2016, contributing 57.6 million (95% uncertainty interval [UI] 40.8-75.9 million [7.2%, 6.0-8.3]), 45.1 million (29.0-62.8 million [5.6%, 4.0-7.2]), 36.3 million (25.3-50.9 million [4.5%, 3.8-5.3]), 34.7 million (23.0-49.6 million [4.3%, 3.5-5.2]), and 34.1 million (23.5-46.0 million [4.2%, 3.2-5.3]) of total YLDs, respectively. Age-standardised rates of YLDs for all causes combined decreased between 1990 and 2016 by 2.7% (95% UI 2.3-3.1). Despite mostly stagnant age-standardised rates, the absolute number of YLDs from non-communicable diseases has been growing rapidly across all SDI quintiles, partly because of population growth, but also the ageing of populations. The largest absolute increases in total numbers of YLDs globally were between the ages of 40 and 69 years. Age-standardised YLD rates for all conditions combined were 10.4% (95% UI 9.0-11.8) higher in women than in men. Iron-deficiency anaemia, migraine, Alzheimer's disease and other dementias, major depressive disorder, anxiety, and all musculoskeletal disorders apart from gout were the main conditions contributing to higher YLD rates in women. Men had higher age-standardised rates of substance use disorders, diabetes, cardiovascular diseases, cancers, and all injuries apart from sexual violence. Globally, we noted much less geographical variation in disability than has been documented for premature mortality. In 2016, there was a less than two times difference in age-standardised YLD rates for all causes between the location with the lowest rate (China, 9201 YLDs per 100 000, 95% UI 6862-11943) and highest rate (Yemen, 14 774 YLDs per 100 000, 11 018-19 228).

    Interpretation: The decrease in death rates since 1990 for most causes has not been matched by a similar decline in age-standardised YLD rates. For many large causes, YLD rates have either been stagnant or have increased for some causes, such as diabetes. As populations are ageing, and the prevalence of disabling disease generally increases steeply with age, health systems will face increasing demand for services that are generally costlier than the interventions that have led to declines in mortality in childhood or for the major causes of mortality in adults. Up-todate information about the trends of disease and how this varies between countries is essential to plan for an adequate health-system response.

  • 22.
    Widmark, Anders
    et al.
    Department of Radiation Sciences, Oncology, Umeå University, Umeå, Sweden.
    Gunnlaugsson, Adalsteinn
    Department of Hematology, Oncology and Radiation Physics, Skåne University Hospital, Lund University, Lund, Sweden.
    Beckman, Lars
    Department of Oncology, Sundsvall Hospital, Sundsvall, Sweden.
    Thellenberg-Karlsson, Camilla
    Department of Radiation Sciences, Oncology, Umeå University, Umeå, Sweden.
    Hoyer, Morten
    Department of Oncology and Danish Centre for Particle Therapy, Aarhus University Hospital, Aarhus, Denmark.
    Lagerlund, Magnus
    Department of Oncology, Kalmar Hospital, Kalmar, Sweden.
    Kindblom, Jon
    Department of Oncology, Institute of Clinical Sciences, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Ginman, Claes
    Department of Oncology, Karlstad Central Hospital, Karlstad, Sweden.
    Johansson, Bengt
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län. Department of Oncology.
    Björnlinger, Kirsten
    Department of Oncology, Ryhov Hospital, Jönköping, Sweden.
    Seke, Mihajl
    Department of Oncology, Centrallasarettet, Växjö, Sweden.
    Agrup, Mans
    Department of Oncology, Linköping University Hospital, Linköping, Sweden.
    Fransson, Per
    Department of Nursing, Umeå University, Umeå, Sweden.
    Tavelin, Björn
    Department of Radiation Sciences, Oncology, Umeå University, Umeå, Sweden.
    Norman, David
    Department of Radiation Sciences, Oncology, Umeå University, Umeå, Sweden.
    Zackrisson, Björn
    Department of Radiation Sciences, Oncology, Umeå University, Umeå, Sweden.
    Anderson, Harald
    Department of Clinical Sciences Lund, Cancer Epidemiology, Lund University, Lund, Sweden.
    Kjellén, Elisabeth
    Department of Hematology, Oncology and Radiation Physics, Skåne University Hospital, Lund University, Lund, Sweden.
    Franzén, Lars
    Department of Radiation Sciences, Oncology, Umeå University, Umeå, Sweden.
    Nilsson, Per
    Department of Hematology, Oncology and Radiation Physics, Skåne University Hospital, Lund University, Lund, Sweden.
    Ultra-hypofractionated versus conventionally fractionated radiotherapy for prostate cancer: 5-year outcomes of the HYPO-RT-PC randomised, non-inferiority, phase 3 trial2019Inngår i: The Lancet, ISSN 0140-6736, E-ISSN 1474-547X, Vol. 394, nr 10196, s. 385-395Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Hypofractionated radiotherapy for prostate cancer has gained increased attention due to its proposed high radiation-fraction sensitivity. Recent reports from studies comparing moderately hypofractionated and conventionally fractionated radiotherapy support the clinical use of moderate hypofractionation. To date, there are no published randomised studies on ultra-hypofractionated radiotherapy. Here, we report the outcomes of the Scandinavian HYPO-RTPC phase 3 trial with the aim to show non-inferiority of ultra-hypofractionation compared with conventional fractionation.

    Methods: In this open-label, randomised, phase 3 non-inferiority trial done in 12 centres in Sweden and Denmark, we recruited men up to 75 years of age with intermediate-to-high-risk prostate cancer and a WHO performance status between 0 and 2. Patients were randomly assigned to ultra-hypofractionation (42.7 Gy in seven fractions, 3 days per week for 2.5 weeks) or conventional fractionated radiotherapy (78.0 Gy in 39 fractions, 5 days per week for 8 weeks). No androgen deprivation therapy was allowed. The primary endpoint was time to biochemical or clinical failure, analysed in the per-protocol population. The prespecified non-inferiority margin was 4% at 5 years, corresponding to a critical hazard ratio (HR) limit of 1.338. Physician-recorded toxicity was measured according to the Radiation Therapy Oncology Group (RTOG) morbidity scale and patient-reported outcome measurements with the Prostate Cancer Symptom Scale (PCSS) questionnaire. This trial is registered with the ISRCTN registry, number ISRCTN45905321.

    Findings: Between July 1, 2005, and Nov 4, 2015, 1200 patients were randomly assigned to conventional fractionation (n=602) or ultra-hypofractionation (n=598), of whom 1180 (591 conventional fractionation and 589 ultra-hypofractionation) constituted the per-protocol population. 1054 (89%) participants were intermediate risk and 126 (11%) were high risk. Median follow-up time was 5.0 years (IQR 3.1-7.0). The estimated failure-free survival at 5 years was 84% (95% CI 80-87) in both treatment groups, with an adjusted HR of 1.002 (95% CI 0.758-1.325; log-rank p=0.99). There was weak evidence of an increased frequency of acute physician-reported RTOG grade 2 or worse urinary toxicity in the ultra-hypofractionation group at end of radiotherapy (158 [28%] of 569 patients vs 132 [23%] of 578 patients; p=0.057). There were no significant differences in grade 2 or worse urinary or bowel late toxicity between the two treatment groups at any point after radiotherapy, except for an increase in urinary toxicity in the ultra-hypofractionation group compared to the conventional fractionation group at 1-year follow-up (32 [6%] of 528 patients vs 13 [2%] of 529 patients; (p=0.0037). We observed no differences between groups in frequencies at 5 years of RTOG grade 2 or worse urinary toxicity (11 [5%] of 243 patients for the ultra-hypofractionation group vs 12 [5%] of 249 for the conventional fractionation group; p=1.00) and bowel toxicity (three [1%] of 244 patients vs nine [4%] of 249 patients; p=0.14). Patient-reported outcomes revealed significantly higher levels of acute urinary and bowel symptoms in the ultra-hypofractionation group compared with the conventional fractionation group but no significant increases in late symptoms were found, except for increased urinary symptoms at 1-year follow-up, consistent with the physician-evaluated toxicity.

    Interpretation: Ultra-hypofractionated radiotherapy is non-inferior to conventionally fractionated radiotherapy for intermediate-to-high risk prostate cancer regarding failure-free survival. Early side-effects are more pronounced with ultra-hypofractionation compared with conventional fractionation whereas late toxicity is similar in both treatment groups. The results support the use of ultra-hypofractionation for radiotherapy of prostate cancer. Copyright (C) 2019 Elsevier Ltd. All rights reserved.

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