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  • 1. Adami, Johanna
    et al.
    Nyrén, Olof
    Bergström, Reinhold
    Ekbom, Anders
    McLaughlin, Joseph
    Hogman, Claes
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för onkologi, radiologi och klinisk immunologi.
    Fraumeni, Joseph F.
    Glimelius, Bengt
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för onkologi, radiologi och klinisk immunologi.
    Blood transfusion and non-Hodgkins lymphoma: Lack of association1997Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 127, nr 5, s. 365-371Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Non-Hodgkin lymphoma is the seventh most commonly diagnosed malignant condition worldwide, and its incidence has increased markedly in recent decades. Blood transfusions have been implicated as a possible risk factor for non-Hodgkin lymphoma. OBJECTIVE: To determine whether blood transfusions are associated with an elevated risk for non-Hodgkin lymphoma. DESIGN: Population-based, nested case-control study. SETTING: Nationwide cohort in Sweden. PATIENTS: 361 patients with non-Hodgkin lymphoma and 705 matched controls, nested within a population-based cohort of 96795 patients at risk for blood transfusion between 1970 and 1983. Prospectively collected information on exposure was retrieved from computerized transfusion registries. MEASUREMENTS: Odds ratios obtained from conditional logistic regression models were used as measures of relative risks. RESULTS: No association was found between blood transfusions and the risk for non-Hodgkin lymphoma when patients who had received transfusions were compared with patients who had not received transfusions (odds ratio, 0.93 [95% CI, 0.71 to 1.23]). A reduction in risk was seen among persons who received transfusion of blood without leukocyte depletion (odds ratio, 0.72 [CI, 0.53 to 0.97]). Risk was not related to number of transfusions, and no interaction was seen with latency after transfusion. CONCLUSION: The findings in this study do not support previous observations of an association between blood transfusions and the risk for non-Hodgkin lymphoma.

  • 2. Axelsen, M
    et al.
    Smith, U
    Eriksson, Jan W
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Endokrin diabetes och metabolism.
    Taskinen, M R
    Jansson, P A
    Postprandial hypertriglyceridemia and insulin resistance in normoglycemic first-degree relatives of patients with type 2 diabetes.1999Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 131, nr 1, s. 27-31Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Impaired ability to eliminate lipids in the postprandial state is an atherogenic trait associated with insulin resistance.

    OBJECTIVE: To assess insulin sensitivity and postprandial triglyceride metabolism in prediabetic persons.

    DESIGN: Cross-sectional study.

    SETTING: Sahlgrenska University Hospital, Göteborg, Sweden.

    PARTICIPANTS: 13 healthy, normotriglyceridemic men with two first-degree relatives with type 2 diabetes and 13 carefully matched controls without known diabetes heredity.

    MEASUREMENTS: Oral glucose tolerance test, insulin sensitivity (euglycemic clamp technique), and fasting and postprandial triglyceride levels after a mixed meal.

    RESULTS: Relatives of persons with type 2 diabetes were insulin resistant but had normal glucose tolerance. They exhibited postprandial hypertriglyceridemia; the 6-hour triglyceride incremental area under the curve was 50% higher than that of the control group (P = 0.037).

    CONCLUSIONS: These healthy male first-degree relatives of patients with type 2 diabetes are insulin resistant and exhibit postprandial lipid intolerance despite having normal fasting triglyceride levels. These characteristics, which occur in the absence of glucose intolerance, are associated with an increased risk for macroangiopathy.

  • 3.
    Chaturvedi, N
    Univ London Imperial Coll Sci Technol & Med, Dept Epidemiol & Publ Hlth, London W2 1PG, England Univ Birmingham, Birmingham B15 2TT, W Midlands, England S Cleveland Hosp, Middlesbrough, Cleveland, England Univ Warwick, Coventry CV4 7AL, W Midlands, England Univ London Kings Coll, London WC2R 2LS, England Linkoping Univ Hosp, S-58185 Linkoping, Sweden Univ Padua & Sassari, Padua, Italy Natl Res Ctr Study Aging, Padua, Italy Hop Broussais, F-75674 Paris, France Steno Diabet Ctr, Copenhagen, Denmark Aarhus Univ Hosp, DK-8000 Aarhus, Denmark Joslin Diabet Ctr, Boston, MA 02215 USA.
    Should all patients with type 1 diabetes mellitus and microalbuminuria receive angiotensin-converting enzyme inhibitors? A meta-analysis of individual patient data2001Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 134, nr 5, s. 370-379Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Purpose: To determine whether response of albumin excretion rate, to angiotensin-converting enzyme (ACE) inhibitors has a threshold in patients with type 1 diabetes mellitus and microalbuminuria and to examine treatment effect according to covariates. Data Sources: Studies were identified by searching MEDLINE and related bibliographies. Study Selection: selected studies included at least 10 normotensive patients with type 1 diabetes mellitus and microalbuminuria, had a placebo or nonintervention group, and included at least 1 year of follow-up. Data Extraction: Raw data were obtained for 698 patients from the 12 identified trials. Analysis of treatment effect at 2 years was restricted to trials with at least 2 years of follow-up (646 patients from 10 trials). Data Synthesis: In patients receiving ACE inhibitors, progression to macroalbuminuria was reduced (odds ratio, 0.38 [95% Cl, 0.25 to 0.57]) and the odds ratio for regression to normoalbuminuria was 3.07 (Cl, 2.15 to 4.44). At 2 years, albumin excretion rate was 50.5% (Cl, 29.2% to 65.5%) lower in treated patients than in those receiving placebo (P < 0.001). Estimated treatment effect varied by baseline albumin excretion rate (74.1% and 17.8% in patients with a rate of 200 g/min and 20 mug/min, respectively [P = 0.04]) but not by patient subgroup. Adjustment for change in blood pressure attenuated the treatment difference in albumin excretion rate at 2 years to 45.1% (Cl, 18.6% to 63.1%, P < 0.001). Conclusions: In normotensive patients with type 1 diabetes mellitus and microalbuminuria, ACE inhibitors significantly reduced progression to macroalbuminuria and increased chances of regression. Beneficial effects were weaker at the lowest levels of microalbuminuria but did not differ according to other baseline risk factors. Changes in blood pressure cannot entirely explain the antiproteinuric effect of ACE inhibitors.

  • 4. Cho, Eunyoung
    et al.
    Smith-Warner, Stephanie A.
    Ritz, John
    van der Brandt, Piet A.
    Colditz, Graham A.
    Folsom, Aaron R.
    Feudenheim, Jo L.
    Giovannucci, Edward
    Goldbohm, R. Alexandra
    Graham, Saxon
    Holmberg, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper.
    Kim, Dong-Hyun
    Malila, Nea
    Miller, Anthony B.
    Pietinen, Pirjo
    Rohan, Thomas E.
    Sellers, Thomas A.
    Speizer, Frank E.
    Willett, Walter C.
    Wolk, Alicja
    Hunter, David J.
    Alcohol intake and colorectal cancer: a pooled analysis of 8 cohort studies2004Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 140, nr 8, s. 603-613Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Epidemiologic studies have generally reported positive associations between alcohol consumption and risk for colorectal cancer. However, findings related to specific alcoholic beverages or different anatomic sites in the large bowel have been inconsistent. OBJECTIVE: To examine the relationship of total alcohol intake and intake from specific beverages to the incidence of colorectal cancer and to evaluate whether other potential risk factors modify the association. DESIGN: Pooled analysis of primary data from 8 cohort studies in 5 countries. SETTING: North America and Europe. PARTICIPANTS: 489,979 women and men with no history of cancer other than nonmelanoma skin cancer at baseline. MEASUREMENTS: Alcohol intake was assessed in each study at baseline by using a validated food-frequency questionnaire. RESULTS: During a maximum of 6 to 16 years of follow-up across the studies, 4687 cases of colorectal cancer were documented. In categorical analyses, increased risk for colorectal cancer was limited to persons with an alcohol intake of 30 g/d or greater (approximately > or =2 drinks/d), a consumption level reported by 4% of women and 13% of men. Compared with nondrinkers, the pooled multivariate relative risks were 1.16 (95% CI, 0.99 to 1.36) for persons who consumed 30 to less than 45 g/d and 1.41 (CI, 1.16 to 1.72) for those who consumed 45 g/d or greater. No significant heterogeneity by study or sex was observed. The association was evident for cancer of the proximal colon, distal colon, and rectum. No clear difference in relative risks was found among specific alcoholic beverages. LIMITATIONS: The study included only one measure of alcohol consumption at baseline and could not investigate lifetime alcohol consumption, alcohol consumption at younger ages, or changes in alcohol consumption during follow-up. It also could not examine drinking patterns or duration of alcohol use. CONCLUSIONS: A single determination of alcohol intake correlated with a modest relative elevation in colorectal cancer rate, mainly at the highest levels of alcohol intake.

  • 5. Cullhed, I
    et al.
    Smedby, B
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Hälso- och sjukvårdsforskning.
    Waern, U
    Letter: Coronary care1975Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 83, nr 4, s. 575-Artikel i tidskrift (Refereegranskat)
  • 6. Dahlen, Torsten
    et al.
    Edgren, Gustaf
    Lambe, Mats
    Hoglund, Martin
    Bjorkholm, Magnus
    Sandin, Fredrik
    Själander, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Richter, Johan
    Olsson-Stromberg, Ulla
    Ohm, Lotta
    Back, Magnus
    Stenke, Leif
    Cardiovascular Events Associated With Use of Tyrosine Kinase Inhibitors in Chronic Myeloid Leukemia: A Population-Based Cohort Study2016Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 165, nr 3, s. 161-166Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Tyrosine kinase inhibitors (TKIs) have increased survival dramatically for patients with chronic myeloid leukemia (CML), but continuous administration of these drugs may elicit long-term toxicity. Objective: To investigate the incidence of vascular events in patients with CML treated with first-and second-generation TKIs. Design: Retrospective cohort study using nationwide population-based registries. Setting: Sweden. Patients: All patients diagnosed with chronic-phase CML in Sweden from 2002 to 2012 and treated with a TKI, and 5 age- and sex-matched control individuals per patient. Measurements: Relative risks, expressed as incidence rate ratios comparing patients with control individuals, were calculated. Events per 1000 person-years were assessed in interdrug comparisons. Results: 896 patients, 94.4% with documented TKI treatment, were followed for a median of 4.2 years. There were 54 arterial and 20 venous events in the CML cohort, corresponding to relative risks of 1.5 (95% CI, 1.1 to 2.1) and 2.0 (CI, 1.2 to 3.3), respectively. The event rate for myocardial infarction was higher in patients treated with nilotinib or dasatinib (29 and 19 per 1000 person-years, respectively) than in those receiving imatinib (8 per 1000 person-years), although data are limited and the CIs were wide and overlapped. Among 31 patients treated with a TKI who had myocardial infarction, 26 (84%) had at least 1 major cardiac risk factor diagnosed before the event occurred. Limitations: Patients may have been exposed to multiple TKIs. Data on second-and third-generation TKIs were limited. Conclusion: An increased risk for arterial and venous vascular events was seen in patients with CML treated with a TKI. Further study is needed to determine whether the risk for myocardial infarction increases with second-generation drugs.

  • 7.
    Dahlen, Torsten
    et al.
    Department of Medicine, Division of Hematology, Karolinska University Hospital Solna, SE-17176 Stockholm, Sweden..
    Edgren, Gustaf
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, SE-17177 Stockholm, Sweden..
    Lambe, Mats
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, SE-17177 Stockholm, Sweden..
    Höglund, Martin
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Hematologi.
    Björkholm, Magnus
    Department of Medicine, Division of Hematology, Karolinska University Hospital Solna, SE-17176 Stockholm, Sweden..
    Sandin, Fredrik
    Regional Cancer Centre, Uppsala University Hospital, SE-75185 Uppsala, Sweden..
    Själander, Anders
    Department Public Health and Clinical Medicine, Umeå University, SE-90185 Umeå, Sweden..
    Richter, Johan
    Department of Hematology and Vascular Disorders, Skåne University Hospital, Getingevägen 4, SE-22241 Lund, Sweden..
    Olsson-Strömberg, Ulla
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Hematologi.
    Ohm, Lotta
    Department of Medicine, Division of Hematology, Karolinska University Hospital Solna, SE-17176 Stockholm, Sweden..
    Bäck, Magnus
    Department of Cardiology, Karolinska University Hospital, Stockholm, SE-17176 Stockholm, Sweden..
    Stenke, Leif
    Department of Medicine, Division of Hematology, Karolinska University Hospital Solna, SE-17176 Stockholm, Sweden..
    Cardiovascular Events Associated With Use of Tyrosine Kinase Inhibitors in Chronic Myeloid Leukemia: A Population-Based Cohort Study2016Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 165, nr 3, s. 161-166Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Tyrosine kinase inhibitors (TKIs) have increased survival dramatically for patients with chronic myeloid leukemia (CML), but continuous administration of these drugs may elicit long-term toxicity.

    Objective: To investigate the incidence of vascular events in patients with CML treated with first-and second-generation TKIs.

    Design: Retrospective cohort study using nationwide population-based registries.

    Setting: Sweden.

    Patients: All patients diagnosed with chronic-phase CML in Sweden from 2002 to 2012 and treated with a TKI, and 5 age- and sex-matched control individuals per patient.

    Measurements: Relative risks, expressed as incidence rate ratios comparing patients with control individuals, were calculated. Events per 1000 person-years were assessed in interdrug comparisons.

    Results: 896 patients, 94.4% with documented TKI treatment, were followed for a median of 4.2 years. There were 54 arterial and 20 venous events in the CML cohort, corresponding to relative risks of 1.5 (95% CI, 1.1 to 2.1) and 2.0 (CI, 1.2 to 3.3), respectively. The event rate for myocardial infarction was higher in patients treated with nilotinib or dasatinib (29 and 19 per 1000 person-years, respectively) than in those receiving imatinib (8 per 1000 person-years), although data are limited and the CIs were wide and overlapped. Among 31 patients treated with a TKI who had myocardial infarction, 26 (84%) had at least 1 major cardiac risk factor diagnosed before the event occurred.

    Limitations: Patients may have been exposed to multiple TKIs. Data on second-and third-generation TKIs were limited.

    Conclusion: An increased risk for arterial and venous vascular events was seen in patients with CML treated with a TKI. Further study is needed to determine whether the risk for myocardial infarction increases with second-generation drugs.

  • 8.
    Edgren, Gustaf
    et al.
    Karolinska Inst, Dept Med Epidemiol & Biostat, Box 281, SE-17177 Stockholm, Sweden..
    Hjalgrim, Henrik
    Statens Serum Inst, Dept Epidemiol Res, 5 Artillerivej, DK-2300 Copenhagen S, Denmark..
    Rostgaard, Klaus
    Statens Serum Inst, Dept Epidemiol Res, 5 Artillerivej, DK-2300 Copenhagen S, Denmark..
    Lambert, Paul
    Univ Leicester, Dept Hlth Sci, Adrian Bldg,Univ Rd, Leicester LE1 7RH, Leics, England. Uppsala Univ, Dept Immunol Genet & Pathol, Akad Sjukhuset, SE-75185 Uppsala, Sweden..
    Wikman, Agneta
    Karolinska Univ Hosp, Dept Clin Immunol & Transfus Med, C2 66 Huddinge, SE-17777 Stockholm, Sweden..
    Norda, Rut
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Titlestad, Kjell-Einar
    Odense Univ Hosp, Dept Clin Immunol, Sondre Blvd 29, DK-5000 Odense, Denmark..
    Erikstrup, Christian
    Aarhus Univ Hosp, Dept Clin Immunol, Palle Juul Jensens Blvd 99, DK-8000 Aarhus, Denmark. Stanford Univ, Sch Med, Stanford, CA 94305 USA..
    Ullum, Henrik
    Copenhagen Univ Hosp, Dept Clin Immunol, Blegdamsvej 9, DK-2100 Copenhagen, Denmark..
    Melbye, Mads
    Statens Serum Inst, Dept Epidemiol Res, 5 Artillerivej, DK-2300 Copenhagen S, Denmark..
    Busch, Michael P.
    Blood Syst Res Inst, 270 Masonic Ave, San Francisco, CA 94118 USA. Univ Calif San Francisco, San Francisco, CA USA..
    Nyren, Olof
    Karolinska Inst, Dept Med Epidemiol & Biostat, Box 281, SE-17177 Stockholm, Sweden..
    Transmission of Neurodegenerative Disorders Through Blood Transfusion A Cohort Study2016Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 165, nr 5, s. 316-+Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: The aggregation of misfolded proteins in the brain occurs in several neurodegenerative disorders. Aberrant protein aggregation is inducible in rodents and primates by intracerebral inoculation. Possible transfusion transmission of neurodegenerative diseases has important public health implications. Objective: To investigate possible transfusion transmission of neurodegenerative disorders. Design: Retrospective cohort study. Setting: Nationwide registers of transfusions in Sweden and Denmark. Participants: 1 465 845 patients who received transfusions between 1968 and 2012. Measurements: Multivariable Cox regression models were used to estimate hazard ratios for dementia of any type, Alzheimer disease, and Parkinson disease in patients receiving blood transfusions from donors who were later diagnosed with any of these diseases versus patients who received blood from healthy donors. Whether excess occurrence of neurodegenerative disease occurred among recipients of blood from a subset of donors was also investigated. As a positive control, transmission of chronic hepatitis before and after implementation of hepatitis C virus screening was assessed. Results: Among included patients, 2.9% received a transfusion from a donor diagnosed with one of the studied neurodegenerative diseases. No evidence of transmission of any of these diseases was found, regardless of approach. The hazard ratio for dementia in recipients of blood from donors with dementia versus recipients of blood from healthy donors was 1.04 (95% CI, 0.99 to 1.09). Corresponding estimates for Alzheimer disease and Parkinson disease were 0.99 (CI, 0.85 to 1.15) and 0.94 (CI, 0.78 to 1.14), respectively. Hepatitis transmission was detected before but not after implementation of hepatitis C virus screening. Limitation: Observational study design, underascertainment of the outcome, and possible insufficient statistical power. Conclusion: The data provide no evidence for the transmission of neurodegenerative diseases and suggest that if transmission does occur, it is rare.

  • 9. Fox, Keith A.
    et al.
    Bassand, Jean-Pierre
    Mehta, Shamir R.
    Wallentin, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Theroux, Pierre
    Piegas, Leopoldo Soares
    Valentin, Vicent
    Moccetti, Tiziano
    Chrolavicius, Susan
    Afzal, Rizwan
    Yusuf, Salim
    Influence of renal function on the efficacy and safety of fondaparinux relative to enoxaparin in non-ST-segment elevation acute coronary syndromes2007Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 147, nr 5, s. 304-310Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: A recent randomized, controlled trial, the Fifth Organization to Assess Strategies in Acute Ischemic Syndromes (OASIS 5) trial, reported that major bleeding was 2-fold less frequent with fondaparinux than with enoxaparin in acute coronary syndromes (ACS). Renal dysfunction increases the risk for major bleeding. OBJECTIVE: To compare the efficacy and safety of fondaparinux and enoxaparin over the spectrum of renal dysfunction observed in the OASIS 5 trial. DESIGN: Subgroup analysis of a randomized, controlled trial. SETTING: Patients presenting to the hospital with non-ST-segment elevation ACS. PATIENTS: 19,979 of the 20,078 patients in the OASIS 5 trial in whom creatinine was measured at baseline. MEASUREMENTS: Death, myocardial infarction, refractory ischemia, and major bleeding were evaluated separately and as a composite end point at 9, 30, and 180 days. Glomerular filtration rate (GFR) was calculated by using the Modification of Diet in Renal Disease formula. RESULTS: The absolute differences in favor of fondaparinux (efficacy and safety) were most marked in patients with a GFR less than 58 mL/min per 1.73 m2; the largest differences occurred in major bleeding events. At 9 days, death, myocardial infarction, or refractory ischemia occurred in 6.7% of patients receiving fondaparinux and 7.4% of those receiving enoxaparin (hazard ratio, 0.90 [95% CI, 0.73 to 1.11]); major bleeding occurred in 2.8% and 6.4%, respectively (hazard ratio, 0.42 [CI, 0.32 to 0.56]). Statistically significant differences in major bleeding persisted at 30 and 180 days. The rates of the composite end point were lower with fondaparinux than with enoxaparin in all quartiles of GFR, but the differences were statistically significant only among patients with a GFR less than 58 mL/min per 1.73 m2. Limitations: Subgroup analyses warrant caution; the study was powered to detect noninferiority at 9 days. Fondaparinux is not approved for use in patients with ACS in the United States. CONCLUSIONS: The benefits of fondaparinux over enoxaparin when administered for non-ST-segment elevation ACS are most marked among patients with renal dysfunction and are largely explained by lower rates of major bleeding with fondaparinux.

  • 10.
    Gartlehner, Gerald
    et al.
    Department for Evidence-based Medicine and Clinical Epidemiology, Danube University, Krems, Austria.
    Hansen, Richard A
    Department of Pharmacy Care Systems, Harrison School of Pharmacy, Auburn University, 207 Dunstan Hall, Auburn, AL 36849.
    Morgan, Laura C
    RTI International, Research Triangle Park, 3040 Cornwallis Road, PO Box 12194, NC 27709.
    Thaler, Kylie
    Department for Evidence-based Medicine and Clinical Epidemiology, Danube University, Krems, Austria.
    Lux, Linda
    RTI International, Research Triangle Park, 3040 Cornwallis Road, PO Box 12194, NC 27709.
    Van Noord, Megan
    Sheps Center for Health Services Research, The University of North Carolina at Chapel Hill, 725 Martin Luther King Jr. Boulevard, Chapel Hill, NC 27599.
    Mager, Ursula
    Ludwig Boltzmann Institute for Health Promotion Research, Vienna, Austria. .
    Thieda, Patricia
    226 Barclay Road, Chapel Hill, NC 27516.
    Gaynes, Bradley N
    Department of Psychiatry, University of North Carolina School of Medicine, Chapel Hill, NC.
    Wilkins, Tania
    Sheps Center for Health Services Research, The University of North Carolina at Chapel Hill, 725 Martin Luther King Jr. Boulevard, Chapel Hill, NC 27599.
    Strobelberger, Michaela
    Department for Evidence-based Medicine and Clinical Epidemiology, Danube University, Krems, Austria.
    Lloyd, Stacey
    RTI International, Research Triangle Park, 3040 Cornwallis Road, PO Box 12194, NC 27709.
    Reichenpfader, Ursula
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för samhällsmedicin. Linköpings universitet, Hälsouniversitetet.
    Lohr, Kathleen N
    RTI International, Research Triangle Park, 3040 Cornwallis Road, PO Box 12194, NC 27709.
    Comparative benefits and harms of second-generation antidepressants for treating major depressive disorder: an updated meta-analysis.2011Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 155, nr 11, s. 772-785Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Second-generation antidepressants dominate the management of major depressive disorder (MDD), but evidence on the comparative benefits and harms of these agents is contradictory.

    PURPOSE: To compare the benefits and harms of second-generation antidepressants for treating MDD in adults.

    DATA SOURCES: English-language studies from PubMed, Embase, the Cochrane Library, PsycINFO, and International Pharmaceutical Abstracts from 1980 to August 2011 and reference lists of pertinent review articles and gray literature.

    STUDY SELECTION: 2 independent reviewers identified randomized trials of at least 6 weeks' duration to evaluate efficacy and observational studies with at least 1000 participants to assess harm.

    DATA EXTRACTION: Reviewers abstracted data about study design and conduct, participants, and interventions and outcomes and rated study quality. A senior reviewer checked and confirmed extracted data and quality ratings.

    DATA SYNTHESIS: Meta-analyses and mixed-treatment comparisons of response to treatment and weighted mean differences were conducted on specific scales to rate depression. On the basis of 234 studies, no clinically relevant differences in efficacy or effectiveness were detected for the treatment of acute, continuation, and maintenance phases of MDD. No differences in efficacy were seen in patients with accompanying symptoms or in subgroups based on age, sex, ethnicity, or comorbid conditions. Individual drugs differed in onset of action, adverse events, and some measures of health-related quality of life.

    LIMITATIONS: Most trials were conducted in highly selected populations. Publication bias might affect the estimates of some comparisons. Mixed-treatment comparisons cannot conclusively exclude differences in efficacy. Evidence within subgroups was limited.

    CONCLUSION: Current evidence does not warrant recommending a particular second-generation antidepressant on the basis of differences in efficacy. Differences in onset of action and adverse events may be considered when choosing a medication.

    PRIMARY FUNDING SOURCE: Agency for Healthcare Research and Quality.

  • 11.
    Grosso, Giorgia
    et al.
    Karolinska Univ Hosp, Karolinska Inst, Stockholm, Sweden..
    Sippl, Natalie
    Karolinska Univ Hosp, Karolinska Inst, Stockholm, Sweden..
    Kjellström, Barbro
    Karolinska Univ Hosp, Karolinska Inst, Stockholm, Sweden..
    Amara, Khaled
    Karolinska Univ Hosp, Karolinska Inst, Stockholm, Sweden..
    de Faire, Ulf
    Karolinska Univ Hosp, Karolinska Inst, Stockholm, Sweden..
    Elvin, Kerstin
    Karolinska Univ Hosp, Karolinska Inst, Stockholm, Sweden..
    Lindahl, Bertil
    Uppsala Univ, Uppsala, Sweden..
    Näsman, Per
    KTH, Skolan för arkitektur och samhällsbyggnad (ABE), Fastigheter och byggande, Bygg- och fastighetsekonomi.
    Ryden, Lars
    Karolinska Univ Hosp, Karolinska Inst, Stockholm, Sweden..
    Norhammar, Anna
    Karolinska Univ Hosp, Karolinska Inst, Stockholm, Sweden.;Capio St Gorans Hosp, Stockholm, Sweden..
    Svenungsson, Elisabet
    Karolinska Univ Hosp, Karolinska Inst, Stockholm, Sweden..
    Antiphospholipid Antibodies in Patients With Myocardial Infarction2019Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 170, nr 4, s. 277-280Artikel i tidskrift (Refereegranskat)
  • 12. Grosso, Giorgia
    et al.
    Sippl, Natalie
    Kjellström, Barbro
    Amara, Khaled
    de Faire, Ulf
    Elvin, Kerstin
    Lindahl, Bertil
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Näsman, Per
    Rydén, Lars
    Norhammar, Anna
    Svenungsson, Elisabet
    Antiphospholipid Antibodies in Patients With Myocardial Infarction.2018Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 170, nr 4, s. 277-280Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Antiphospholipid syndrome (APS) is defined by arterial, venous, or microvascular thrombosis or obstetric morbidity together with confirmed positive test results, at least 12 weeks apart, for antiphospholipid antibodies (aPLs), including at least 1 of the following tests: anticardiolipin (anti-CL), anti–β2-glycoprotein I (anti-β2GPI), or the functional lupus anticoagulant test (1, 2). Long-term anticoagulation prevents new thrombotic events in most patients with APS. Information on prothrombotic aPLs in patients with myocardial infarction (MI) is conflicting, due to limited sample sizes, selected populations, and nonstandardized methods in previous studies (3). Objective: To assess the frequency of anti-β2GPI and anti-CL of IgG/IgA/IgM isotypes and antinuclear antibodies among patients with first-time MI and matched control participants in a large, multicenter, case–control study. Methods and Findings: The PAROKRANK (Periodontitis and Its Relation to Coronary Artery Disease) study included 805 consecutive patients younger than 75 years who were hospitalized for a first MI at 17 Swedish hospitals between 2010 and 2014 (4). Population control participants (n = 805) were individually matched for age, sex, and region to the patients. Persons who had prior MI or heart valve replacement or were unable to follow the protocol were excluded. Patients were recruited during hospitalization and scheduled for an inclusion visit 6 to 10 weeks later at their local cardiology clinic. The national quality registry SWEDEHEART (www.swedeheart.se) was used to collect medical information at the hospitalization and standardized follow-up data at the inclusion visit. More detailed clinical protocol and extensive questionnaires were also completed at the inclusion visit (5). The same information was collected for the matched control participants. All participants fasted and abstained from smoking for 12 hours before blood sampling at the inclusion visit. Autoantibodies targeting CL and β2GPI of IgG/IgM/IgA isotypes and specific nuclear antigens, as specified in the Table, were analyzed using multiplexed beads (BioPlex 2200 Multiplex Testing, Bio-Rad).

  • 13. Gunter, Marc J.
    et al.
    Murphy, Neil
    Cross, Amanda J..
    Dossus, Laure
    Dartois, Laureen
    Fagherazzi, Guy
    Kaaks, Rudolf
    Kühn, Tilman
    Boeing, Heiner
    Aleksandrova, Krasimira
    Tjønneland, Anne
    Olsen, Anja
    Overvad, Kim
    Larsen, Sofus Christian
    Redondo Cornejo, Maria Luisa
    Agudo, Antonio
    Sánchez Pérez, María José
    Altzibar, Jone M.
    Navarro, Carmen
    Ardanaz, Eva
    Khaw, Kay-Tee
    Butterworth, Adam
    Bradbury, Kathryn E.
    Trichopoulou, Antonia
    Lagiou, Pagona
    Trichopoulos, Dimitrios
    Palli, Domenico
    Grioni, Sara
    Vineis, Paolo
    Panico, Salvatore
    Tumino, Rosario
    Bueno-de-Mesquita, Bas
    Siersema, Peter
    Leenders, Max
    Beulens, Joline W. J.
    Uiterwaal, Cuno U.
    Wallström, Peter
    Nilsson, Lena Maria
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Näringsforskning.
    Landberg, Rikard
    Weiderpass, Elisabete
    Skeie, Guri
    Braaten, Tonje
    Brennan, Paul
    Licaj, Idlir
    Muller, David C.
    Sinha, Rashmi
    Wareham, Nick
    Riboli, Elio
    Coffee Drinking and Mortality in 10 European Countries: A Multinational Cohort Study2017Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 167, nr 4, s. 236-247Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: The relationship between coffee consumption and mortality in diverse European populations with variable coffee preparation methods is unclear.

    Objective: To examine whether coffee consumption is associated with all-cause and cause-specific mortality.

    Design: Prospective cohort study.

    Setting: 10 European countries.

    Participants: 521 330 persons enrolled in EPIC (European Prospective Investigation into Cancer and Nutrition).

    Measurements: Hazard ratios (HRs) and 95% CIs estimated using multivariable Cox proportional hazards models. The association of coffee consumption with serum biomarkers of liver function, inflammation, and metabolic health was evaluated in the EPIC Biomarkers subcohort (n = 14 800).

    Results: During a mean follow-up of 16.4 years, 41 693 deaths occurred. Compared with nonconsumers, participants in the highest quartile of coffee consumption had statistically significantly lower all-cause mortality (men: HR, 0.88 [95% CI, 0.82 to 0.95]; P for trend < 0.001; women: HR, 0.93 [CI, 0.87 to 0.98]; P for trend = 0.009). Inverse associations were also observed for digestive disease mortality for men (HR, 0.41 [CI, 0.32 to 0.54]; P for trend < 0.001) and women (HR, 0.60 [CI, 0.46 to 0.78]; P for trend < 0.001). Among women, there was a statistically significant inverse association of coffee drinking with circulatory disease mortality (HR, 0.78 [CI, 0.68 to 0.90]; P for trend < 0.001) and cerebrovascular disease mortality (HR, 0.70 [CI, 0.55 to 0.90]; P for trend = 0.002) and a positive association with ovarian cancer mortality (HR, 1.31 [CI, 1.07 to 1.61]; P for trend = 0.015). In the EPIC Biomarkers subcohort, higher coffee consumption was associated with lower serum alkaline phosphatase; alanine aminotransferase; aspartate aminotransferase; γ-glutamyltransferase; and, in women, C-reactive protein, lipoprotein(a), and glycated hemoglobin levels.

    Limitations: Reverse causality may have biased the findings; however, results did not differ after exclusion of participants who died within 8 years of baseline. Coffee-drinking habits were assessed only once.

    Conclusion: Coffee drinking was associated with reduced risk for death from various causes. This relationship did not vary by country.

    Primary Funding Source: European Commission Directorate-General for Health and Consumers and International Agency for Research on Cancer.

  • 14.
    Halmin, Märit
    et al.
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden. Karolinska Univ Hosp, Stockholm, Sweden. Uppsala Univ, Uppsala, Sweden. AnOpIVA, S-65185 Karlstad, Sweden..
    Rostgaard, Klaus
    Statens Serum Inst, Dept Epidemiol Res, Artillerivej 5, DK-2300 Copenhagen S, Denmark. Copenhagen Univ Hosp, Copenhagen, Denmark..
    Lee, Brian K.
    Drexel Univ, Sch Publ Hlth, Dept Epidemiol & Biostat, Philadelphia, PA 19104 USA..
    Wikman, Agneta
    Karolinska Univ Hosp, Clin Immunol & Transfus Med, C2 66, SE-14186 Huddinge, Sweden..
    Norda, Rut
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Nielsen, Kaspar Rene
    Aalborg Univ Hosp, Dept Clin Immunol, DK-9000 Aalborg, Denmark..
    Pedersen, Ole B.
    Naestved Hosp, Dept Clin Immunol, DK-4700 Naestved, Denmark..
    Holmqvist, Jacob
    Centralsjukhuset, AnOpIVA, S-65185 Karlstad, Sweden..
    Hjalgrim, Henrik
    Afdeling Epidemiol Forskning, Sektor Epidemiol & Smitteberedskab, Artillerivej 5, DK-2300 Copenhagen S, Denmark..
    Edgren, Gustaf
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
    Length of Storage of Red Blood Cells and Patient Survival After Blood Transfusion: A Binational Cohort Study2017Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 166, nr 4, s. 248-256Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Possible negative effects, including increased mortality, among persons who receive stored red blood cells (RBCs) have recently garnered considerable attention. Despite many studies, including 4 randomized trials, no consensus exists.

    Objective: To study the association between the length of RBC storage and mortality in a large population-based cohort of patients who received transfusions, allowing detection of small yet clinically significant effects.

    Design: Binational cohort study.

    Setting: All transfusion recipients in Sweden and Denmark. Patients: 854 862 adult patients who received transfusions from 2003 to 2012.

    Measurements: Patients were followed from first blood transfusion. Relative and absolute risks for death in 30 days or 1 year in relation to length of RBC storage were assessed by using 3 independent analytic approaches. All analyses were conducted by using Cox proportional hazards regression.

    Results: Regardless of the analytic approach, no association was found between the length of RBC storage and mortality. The difference in 30-day cumulative mortality between patients receiving blood stored for 30 to 42 days and those receiving blood stored for 10 to 19 days was -0.2% (95% CI, -0.5% to 0.1%). Even among patients who received more than 6 units of RBCs stored for 30 days or longer, the hazard ratio of death was 1.00 (CI, 0.96 to 1.05) compared with those who received no such units.

    Limitation: Observational study; risk of confounding by indication.

    Conclusion: Consistent with previous randomized trials, this study found no association between the length of storage of transfused RBCs and patient mortality. Results were homogeneous, with differences in absolute mortality consistently less than 1% among the most extreme exposure categories. These findings suggest that the current practice of storing RBCs for up to 42 days does not need to be changed.

  • 15. Hamer, Davidson H.
    et al.
    Barbre, Kira A.
    Chen, Lin H.
    Grobusch, Martin P.
    Schlagenhauf, Patricia
    Goorhuis, Abraham
    van Genderen, Perry J. J.
    Molina, Israel
    Asgeirsson, Hilmir
    Kozarsky, Phyllis E.
    Caumes, Eric
    Hagmann, Stefan H.
    Mockenhaupt, Frank P.
    Eperon, Gilles
    Barnett, Elizabeth D.
    Bottieau, Emmanuel
    Boggild, Andrea K.
    Gautret, Philippe
    Hynes, Noreen A.
    Kuhn, Susan
    Lash, Ryan
    Leder, Karin
    Libman, Michael
    Malvy, Denis J. M.
    Perret, Cecilia
    Rothe, Camilla
    Schwartz, Eli
    Wilder-Smith, Annelies
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Epidemiologi och global hälsa.
    Cetron, Martin S.
    Esposito, Douglas H.
    Travel-Associated Zika Virus Disease Acquired in the Americas Through February 2016 A GeoSentinel Analysis2017Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 166, nr 2, s. 99-108Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Zika virus has spread rapidly in the Americas and has been imported into many nonendemic countries by travelers. Objective: To describe clinical manifestations and epidemiology of Zika virus disease in travelers exposed in the Americas. Design: Descriptive, using GeoSentinel records. Setting: 63 travel and tropical medicine clinics in 30 countries. Patients: Ill returned travelers with a confirmed, probable, or clinically suspected diagnosis of Zika virus disease seen between January 2013 and 29 February 2016. Measurements: Frequencies of demographic, trip, and clinical characteristics and complications. Results: Starting in May 2015, 93 cases of Zika virus disease were reported. Common symptoms included exanthema (88%), fever (76%), and arthralgia (72%). Fifty-nine percent of patients were exposed in South America; 71% were diagnosed in Europe. Case status was established most commonly by polymerase chain reaction (PCR) testing of blood and less often by PCR testing of other body fluids or serology and plaque-reduction neutralization testing. Two patients developed Guillain-Barre syndrome, and 3 of 4 pregnancies had adverse outcomes (microcephaly, major fetal neurologic abnormalities, and intrauterine fetal death). Limitation: Surveillance data collected by specialized clinics may not be representative of all ill returned travelers, and denominator data are unavailable. Conclusion: These surveillance data help characterize the clinical manifestations and adverse outcomes of Zika virus disease among travelers infected in the Americas and show a need for global standardization of diagnostic testing. The serious fetal complications observed in this study highlight the importance of travel advisories and prevention measures for pregnant women and their partners. Travelers are sentinels for global Zika virus circulation and may facilitate further transmission.

  • 16.
    Henriksson, Pontus
    et al.
    Karolinska Inst, Sweden; Univ Granada, Spain; Karolinska Inst, Sweden.
    Henriksson, Hanna
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för samhällsmedicin. Linköpings universitet, Medicinska fakulteten. Univ Granada, Spain.
    Tynelius, Per
    Karolinska Inst, Sweden; Stockholm Cty Council, Sweden; Karolinska Inst, Sweden.
    Berglind, Daniel
    Karolinska Inst, Sweden.
    Löf, Marie
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för samhällsmedicin. Linköpings universitet, Medicinska fakulteten. Karolinska Inst, Sweden; Karolinska Inst, Sweden.
    Lee, I-Min
    Harvard Med Sch, MA 02115 USA; Harvard TH Chan Sch Publ Hlth, MA USA.
    Shiroma, Eric J.
    NIA, MD 20892 USA.
    Ortega, Francisco B.
    Karolinska Inst, Sweden; Univ Granada, Spain.
    Fitness and Body Mass Index During Adolescence and Disability Later in Life A Cohort Study2019Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 170, nr 4, s. 230-+Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Low physical fitness, obesity, and the combination of the two in adolescence may be related to risk for disability in adulthood, but this has rarely been studied. Objective: To examine individual and combined associations of cardiorespiratory fitness and obesity in male adolescents with later receipt of a disability pension due to all and specific causes. Design: Population-based cohort study. Setting: Sweden. Participants: 1 079 128 Swedish adolescents aged 16 to 19 years who were conscripted into the military between 1972 and 1994. Measurements: Cardiorespiratory fitness and body mass index (BMI) were measured at conscription and were related to information on later receipt of a disability pension obtained from the Social Insurance Agency. Results: Over a median follow-up of 28.3 years, 54 304 men were granted a disability pension. Low cardiorespiratory fitness was strongly associated with later receipt of a disability pension due to all causes (hazard ratio, 3.74 [95% CI, 3.55 to 3.95] for lowest vs. highest fitness decile) and specific causes (psychiatric, musculoskeletal, injuries, nervous system, circulatory, and tumors). Obesity was associated with greater risk for receipt of a disability pension due to all and specific causes, with the greatest risks observed for class II and III obesity. Compared with being unfit, being moderately or highly fit was associated with attenuated risk for receipt of a disability pension across BMI categories. Limitation: The cohort did not include women, had data on smoking and alcohol intake only in a subsample, and lacked repeated measures of exposures and covariates. Conclusion: Low cardiorespiratory fitness, obesity, and the combination of the two were strongly associated with later chronic disability due to a wide range of diseases and causes. Although additional well-designed studies are required, these findings support the importance of high cardiorespiratory fitness and healthy body weight during adolescence to prevent later chronic disease.

  • 17. Holme, Oyvind
    et al.
    Loberg, Magnus
    Kalager, Mette
    Bretthauer, Michael
    Hernan, Miguel A.
    Aas, Eline
    Eide, Tor J.
    Skovlund, Eva
    Lekven, Jon
    Schneede, Jørn
    Umeå universitet, Medicinska fakulteten, Institutionen för farmakologi och klinisk neurovetenskap, Farmakologi.
    Tveit, Kjell Magne
    Vatn, Morten
    Ursin, Giske
    Hoff, Geir
    Long-Term Effectiveness of Sigmoidoscopy Screening on Colorectal Cancer Incidence and Mortality in Women and Men A Randomized Trial2018Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 168, nr 11, s. 775-782Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: The long-term effects of sigmoidoscopy screening on colorectal cancer (CRC) incidence and mortality in women and men are unclear.

    Objective: To determine the effectiveness of flexible sigmoidoscopy screening after 15 years of follow-up in women and men.

    Design: Randomized controlled trial. (ClinicalTrials.gov: NCT00119912)

    Setting: Oslo and Telemark County, Norway. Participants: Adults aged 50 to 64 years at baseline without prior CRC.

    Intervention: Screening (between 1999 and 2001) with flexible sigmoidoscopy with and without additional fecal blood testing versus no screening. Participants with positive screening results were offered colonoscopy.

    Measurements: Age-adjusted CRC incidence and mortality stratified by sex.

    Results: Of 98 678 persons, 20 552 were randomly assigned to screening and 78 126 to no screening. Adherence rates were 64.7% in women and 61.4% in men. Median follow-up was 14.8 years. The absolute risks for CRC in women were 1.86% in the screening group and 2.05% in the control group (risk difference, -0.19 percentage point [95% CI, -0.49 to 0.11 percentage point]; HR, 0.92 [CI, 0.79 to 1.07]). In men, the corresponding risks were 1.72% and 2.50%, respectively (risk difference, -0.78 percentage point [CI, -1.08 to -0.48 percentage points]; hazard ratio [HR], 0.66 [CI, 0.57 to 0.78]) (P for heterogeneity = 0.004). The absolute risks for death from CRC in women were 0.60% in the screening group and 0.59% in the control group (risk difference, 0.01 percentage point [CI, -0.16 to 0.18 percentage point]; HR, 1.01 [CI, 0.77 to 1.33]). The corresponding risks for death from CRC in men were 0.49% and 0.81%, respectively (risk difference, -0.33 percentage point [CI, -0.49 to -0.16 percentage point]; HR, 0.63 [CI, 0.47 to 0.83]) (P for heterogeneity = 0.014).

    Limitation: Follow-up through national registries.

    Conclusion: Offering sigmoidoscopy screening in Norway reduced CRC incidence and mortality in men but had little or no effect in women.

  • 18.
    Jensen, Jane
    et al.
    Umeå universitet, Institutionen för Samhällsmedicin, Avdelningen för Sjukgymnastik.
    Lundin-Olsson, Lillemor
    Umeå universitet, Institutionen för Samhällsmedicin, Avdelningen för Sjukgymnastik.
    Nyberg, Lars
    Gustafson, Yngve
    Umeå universitet, Institutionen för Samhällsmedicin och Rehabilitering, Geriatrik.
    Fall and injury prevention in older people living in residential care facilities: A cluster randomized trial2002Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 136, nr 10, s. 733-41Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Falls and resulting injuries are particularly common in older people living in residential care facilities, but knowledge about the prevention of falls is limited. OBJECTIVE: To investigate whether a multifactorial intervention program would reduce falls and fall-related injuries. DESIGN: A cluster randomized, controlled, nonblinded trial. SETTING: 9 residential care facilities located in a northern Swedish city. PATIENTS: 439 residents 65 years of age or older. INTERVENTION: An 11-week multidisciplinary program that included both general and resident-specific, tailored strategies. The strategies comprised educating staff, modifying the environment, implementing exercise programs, supplying and repairing aids, reviewing drug regimens, providing free hip protectors, having post-fall problem-solving conferences, and guiding staff. MEASUREMENTS: The primary outcomes were the number of residents sustaining a fall, the number of falls, and the time to occurrence of the first fall. A secondary outcome was the number of injuries resulting from falls. RESULTS: During the 34-week follow-up period, 82 residents (44%) in the intervention program sustained a fall compared with 109 residents (56%) in the control group (risk ratio, 0.78 [95% CI, 0.64 to 0.96]). The adjusted odds ratio was 0.49 (CI, 0.37 to 0.65), and the adjusted incidence rate ratio of falls was 0.60 (CI, 0.50 to 0.73). Each of 3 residents in the intervention group and 12 in the control group had 1 femoral fracture (adjusted odds ratio, 0.23 [CI, 0.06 to 0.94]). Clustering was considered in all regression models. CONCLUSION: An interdisciplinary and multifactorial prevention program targeting residents, staff, and the environment may reduce falls and femoral fractures.

  • 19.
    Johnston, Nina
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Christersson, Christina
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR). Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Koagulation och inflammationsvetenskap.
    Sex-Specific Research: A Key Component in Improving Prognosis After Transcatheter Aortic Valve Replacement2016Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 164, nr 6, s. 442-443Artikel i tidskrift (Övrigt vetenskapligt)
  • 20. Kechagias, S
    et al.
    Jönsson, K-Å
    Jones, A Wayne
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för biomedicin och kirurgi, Klinisk kemi.
    Breath tests for alcohol in gastroesophageal reflux disease (letter).1999Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 130, s. 328-329Artikel i tidskrift (Refereegranskat)
  • 21. Lebwohl, Benjamin
    et al.
    Granath, Fredrik
    Ekbom, Anders
    Smedby, Karin E.
    Murray, Joseph A.
    Neugut, Alfred I.
    Green, Peter H. R.
    Ludvigsson, Jonas F.
    Region Örebro län.
    Mucosal Healing and Risk for Lymphoproliferative Malignancy in Celiac Disease A Population-Based Cohort Study2013Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 159, nr 3, s. 169-+Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Celiac disease (CD) is associated with an increased risk for lymphoproliferative malignancy (LPM). Whether this risk is affected by the results of follow-up intestinal biopsy, performed to document mucosal healing, is unknown. Objective: To examine the association between mucosal healing in CD and subsequent LPM. Design: Population-based cohort study. Setting: 28 pathology departments in Sweden. Patients: 7625 patients with CD who had follow-up biopsy after initial diagnosis. Measurements: The risk for LPM was compared with that of the general population by using expected rates. The rate of LPM in patients with persistent villous atrophy was compared with that of those with mucosal healing by using Cox regression. Results: Among 7625 patients with CD and follow-up biopsy, 3308 (43%) had persistent villous atrophy. The overall risk for LPM was higher than that in the general population (standardized incidence ratio [SIR], 2.81 [95% CI, 2.10 to 3.67]) and was greater among patients with persistent villous atrophy (SIR, 3.78 [CI, 2.71 to 5.12]) than among those with mucosal healing (SIR, 1.50 [CI, 0.77 to 2.62]). Persistent villous atrophy compared with mucosal healing was associated with an increased risk for LPM (hazard ratio [HR], 2.26 [CI, 1.18 to 4.34]). The risk for T-cell lymphoma was increased (HR, 3.51 [CI, 0.75 to 16.34]) but not for B-cell lymphoma (HR, 0.97 [CI, 0.21 to 4.49]). Limitation: No data on dietary adherence. Conclusion: Increased risk for LPM in CD is associated with the follow-up biopsy results, with a higher risk among patients with persistent villous atrophy. Follow-up biopsy may effectively stratify patients with CD by risk for subsequent LPM.

  • 22.
    Ludvigsson, Jonas F.
    et al.
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län. Karolinska Institutet, Stockholm, Sweden: University of Nottingham, Nottingham, United Kingdom; Columbia University College of Physicians and Surgeons NY, New York, USA.
    Neovius, Martin
    Karolinska Institutet, Stockholm, Sweden.
    Söderling, Jonas
    Karolinska Institutet, Stockholm, Sweden.
    Gudbjörnsdottir, Soffia
    Karolinska Institutet, Stockholm, Sweden; Centre of Registers Västra Götaland and University of Gothenburg, Gothenburg, Sweden.
    Svensson, Ann-Marie
    Centre of Registers Västra Götaland, Gothenburg, Sweden.
    Franzen, Stefan
    Karolinska Institutet, Stockholm, Sweden; Centre of Registers Västra Götaland and University of Gothenburg, Gothenburg, Sweden.
    Stephansson, Olof
    Karolinska Institutet, Stockholm, Sweden.
    Pasternak, Björn
    Karolinska Institutet, Stockholm, Sweden; Statens Serum Institut, Copenhagen, Denmark.
    Maternal Glycemic Control in Type 1 Diabetes and the Risk for Preterm Birth: A Population-Based Cohort Study2019Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 170, nr 10, s. 691-701Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Maternal type 1 diabetes (T1D) has been linked to preterm birth and other adverse pregnancy outcomes. How these risks vary with glycated hemoglobin (or hemoglobin A(1c) [HbA(1c)]) levels is unclear.

    Objective: To examine preterm birth risk according to periconceptional HbA(1c) levels in women with T1D.

    Design: Population-based cohort study.

    Setting: Sweden, 2003 to 2014.

    Patients: 2474 singletons born to women with T1D and 1 165 216 reference infants born to women without diabetes.

    Measurements: Risk for preterm birth (< 37 gestational weeks). Secondary outcomes were neonatal death, large for gestational age, macrosomia, infant birth injury, hypoglycemia, respiratory distress, 5-minute Apgar score less than 7, and stillbirth. Results: Preterm birth occurred in 552 (22.3%) of 2474 infants born to mothers with T1D versus 54 287 (4.7%) in 1 165 216 infants born to mothers without diabetes. The incidence of preterm birth was 13.2% in women with a periconceptional HbA(1c) level below 6.5% (adjusted risk ratio [aRR] vs. women without T1D, 2.83 [95% CI, 2.28 to 3.52]), 20.6% in those with a level from 6.5% to less than 7.8% (aRR, 4.22 [CI, 3.74 to 4.75]), 28.3% in those with a level from 7.8% to less than 9.1% (aRR, 5.56 [CI, 4.84 to 6.38]), and 37.5% in those with a level of 9.1% or higher (aRR, 6.91 [CI, 5.85 to 8.17]). The corresponding aRRs for medically indicated preterm birth (n = 320) were 5.26 (CI, 3.83 to 7.22), 7.42 (CI, 6.21 to 8.86), 11.75 (CI, 9.72 to 14.20), and 17.51 (CI, 14.14 to 21.69), respectively. The corresponding aRRs for spontaneous preterm birth (n = 223) were 1.81 (CI, 1.31 to 2.52), 2.86 (CI, 2.38 to 3.44), 2.88 (CI, 2.23 to 3.71), and 2.80 (CI, 1.94 to 4.03), respectively. Increasing HbA(1c) levels were associated with the study's secondary outcomes: large for gestational age, hypoglycemia, respiratory distress, low Apgar score, neonatal death, and stillbirth.

    Limitation: Because HbA(1c) levels were registered annually at routine visits, they were not available for all pregnant women with T1D.

    Conclusion: The risk for preterm birth was strongly linked to periconceptional HbA(1c) levels. Women with HbA(1c) levels consistent with recommended target levels also were at increased risk. Primary Funding Source: Swedish Diabetes Foundation.

  • 23.
    Ludvigsson, Jonas F.
    et al.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden .
    Ström, Peter
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden .
    Lundholm, Cecilia
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden .
    Cnattingius, Sven
    Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Ekbom, Anders
    Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Örtqvist, Åke
    Department of Communicable Disease Control and Prevention, Stockholm County Council, Stockholm, Sweden.
    Feltelius, Nils
    Medical Products Agency, Uppsala, Sweden.
    Granath, Fredrik
    Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Stephansson, Olof
    Department of Women's and Children's Health, Karolinska Institutet and Hospital, Stockholm, Sweden .
    Risk for Congenital Malformation With H1N1 Influenza Vaccine: A Cohort Study With Sibling Analysis2016Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 165, nr 12, s. 848-855Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Earlier studies reporting varying risk estimates for congenital malformation in offspring of mothers undergoing vaccination against H1N1 influenza during pregnancy did not consider the potential role of confounding by familial (genetic and shared environmental) factors.

    Objective: To evaluate an association between maternal H1N1 vaccination during pregnancy and offspring malformation, with familial factors taken into account.

    Design: Population-based prospective study.

    Setting: Sweden.

    Participants: Liveborn offspring born between 1 October 2009 and 1 October 2011 to mothers receiving monovalent AS03-adjuvanted H1N1 influenza vaccine (Pandemrix [GlaxoSmithKline]) during pregnancy. A total of 40 983 offspring were prenatally exposed to the vaccine, 14 385 were exposed within the first trimester (14 weeks), and 7502 were exposed during the first 8 weeks of pregnancy. Exposed offspring were compared with 197 588 unexposed offspring. Corresponding risks in exposed versus unexposed siblings were also estimated.

    Measurements: Congenital malformation, with subanalyses for congenital heart disease, oral cleft, and limb deficiency.

    Results: Congenital malformation was observed in 2037 (4.97%) exposed offspring and 9443 (4.78%) unexposed offspring. Adjusted risk for congenital malformation was 4.98% in exposed offspring versus 4.96% in unexposed offspring (risk difference, 0.02% [95% CI, -0.26% to 0.30%]). The corresponding risk differences were 0.16% (CI, -0.23% to 0.56%) for vaccination during the first trimester and 0.10% (CI, -0.41% to 0.62%) for vaccination in the first 8 weeks. Using siblings as comparators yielded no statistically significant risk differences.

    Limitations: The study was based on live births, and the possibility that data on miscarriage or induced abortion could have influenced the findings cannot be ruled out. Study power was limited in analyses of specific malformations.

    Conclusion: When intrafamilial factors were taken into consideration, H1N1 vaccination during pregnancy did not seem to be linked to overall congenital malformation in offspring, although risk increases for specific malformations could not be ruled out completely.

  • 24.
    Mascalzoni, Deborah
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Centrum för forsknings- och bioetik. Eurac Res, Inst Biomed, Via Galvani 31, I-39100 Bolzano, Italy;Eurac Res, Inst Biomed, Balzano, Italy.
    Bentzen, Heidi Beate
    Univ Oslo, Norwegian Res Ctr Comp & Law, Dept Private Law, Fac Law, POB 6706, N-0130 Oslo, Norway;Univ Oslo, Ctr Med Eth, Oslo, Norway.
    Budin-Ljosne, Isabelle
    Norwegian Inst Publ Hlth, POB 222, N-0213 Oslo, Norway.
    Bygrave, Lee Andrew
    Univ Oslo, Norwegian Res Ctr Comp & Law, Dept Private Law, Fac Law, POB 6706, N-0130 Oslo, Norway.
    Bell, Jessica
    Univ Oslo, Norwegian Res Ctr Comp & Law, Dept Private Law, Fac Law, POB 6706, N-0130 Oslo, Norway;Univ Oxford, Oxford, England;Univ Melbourne, Melbourne, Vic, Australia;Univ Melbourne, Melbourne Law Sch, 185 Pelham St, Melbourne, Vic 3010, Australia.
    Dove, Edward S.
    Univ Edinburgh, Sch Law, LG 12,Old Coll,South Bridge, Edinburgh EH8 9YL, Midlothian, Scotland.
    Fuchsberger, Christian
    Eurac Res, Inst Biomed, Via Galvani 31, I-39100 Bolzano, Italy.
    Hveem, Kristian
    Norwegian Univ Sci & Technol, HUNT Res Ctr, Levanger, Norway;Norwegian Univ Sci & Technol, KG Jebsen Ctr Genet Epidemiol, Levanger, Norway;HUNT Res Ctr, Forskningsvegen 2, N-7600 Levanger, Norway.
    Mayrhofer, Michaela Th.
    BBMRI ERIC, Neue Stiftingtalstr 2-B-6, A-8010 Graz, Austria.
    Meraviglia, Viviana
    Eurac Res, Inst Biomed, Via Galvani 31, I-39100 Bolzano, Italy.
    O'Brien, David R.
    Harvard Univ, Boston, MA 02115 USA;Harvard Univ, Berkman Klein Ctr Internet & Soc, 23 Everett St,2nd Floor, Cambridge, MA 02138 USA.
    Pattaro, Cristian
    Eurac Res, Inst Biomed, Via Galvani 31, I-39100 Bolzano, Italy.
    Pramstaller, Peter P.
    Eurac Res, Inst Biomed, Via Galvani 31, I-39100 Bolzano, Italy.
    Rakic, Vojin
    Univ Belgrade, Ctr Study Bioeth, Inst Social Sci, Kraljice Natalije 45,POB 605, Belgrade 11000, Serbia.
    Rossini, Alessandra
    Eurac Res, Inst Biomed, Via Galvani 31, I-39100 Bolzano, Italy.
    Shabani, Mahsa
    Katholieke Univ Leuven, Leuven, Belgium;Leuven Inst Human Genom & Soc, Leuven, Belgium;Univ Leuven, Ctr Biomed Eth & Law, Kapucijnenvoer 35, B-3000 Leuven, Belgium.
    Svantesson, Dan Jerker B.
    Bond Univ, Fac Law, Gold Coast, Qld 4229, Australia.
    Tomasi, Marta
    Univ Trento, Fac Law, Via Verdi 53, I-38100 Trento, Italy;Free Univ Bozen Bolzano, Bolzano, Italy.
    Ursin, Lars
    Norwegian Univ Sci & Technol, Trondheim, Norway;Norwegian Univ Sci & Technol, Dept Publ Hlth & Nursing, KG Jebsen Ctr Genet Epidemiol, Hakon Jarls Gate 11, N-7030 Trondheim, Norway.
    Wjst, Matthias
    Helmholtz Zentrum Munchen, Natl Res Ctr Environm Hlth, Inst Lung Biol & Dis, D-85764 Munich, Germany;Tech Univ Munich, Munich, Germany.
    Kaye, Jane
    Univ Oslo, Norwegian Res Ctr Comp & Law, Dept Private Law, Fac Law, POB 6706, N-0130 Oslo, Norway;Univ Oxford, Oxford, England;Univ Melbourne, Melbourne, Vic, Australia;Univ Oxford, Nuffield Dept Populat Hlth, HeLEX Ctr Hlth Law & Emerging Technol, Ewert House,Ewert Pl, Oxford OX2 7DD, England.
    Are Requirements to Deposit Data in Research Repositories Compatible With the European Union's General Data Protection Regulation?2019Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 170, nr 5, s. 332-334Artikel i tidskrift (Övrigt vetenskapligt)
  • 25.
    Melhus, Håkan
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Michaëlsson, Karl
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper.
    Kindmark, Andreas
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Dietary vitamin A intake and risk for hip fracture: Response1999Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 131, nr 5, s. 392-392Artikel i tidskrift (Refereegranskat)
  • 26.
    Melhus, Håkan
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Michaëlsson, Karl
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Kindmark, Andreas
    Bergström, Reinhold
    Holmberg, Lars
    Mallmin, Hans
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Wolk, Alicja
    Ljunghall, Sverker
    Excessive dietary intake of vitamin A is associated with reduced bone mineral density and increased risk for hip fracture1998Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 129, nr 10, s. 770-8Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: The highest incidence of osteoporotic fractures is found in northern Europe, where dietary intake of vitamin A (retinol) is unusually high. In animals, the most common adverse effect of toxic doses of retinol is spontaneous fracture. OBJECTIVE: To investigate whether excessive dietary intake of vitamin A is associated with decreased bone mineral density and increased risk for hip fracture. DESIGN: A cross-sectional study and a nested case-control study. SETTING: Two counties in central Sweden. PARTICIPANTS: For the cross-sectional study, 175 women 28 to 74 years of age were randomly selected. For the nested case-control study, 247 women who had a first hip fracture within 2 to 64 months after enrollment and 873 age-matched controls were selected from a mammography study cohort of 66,651 women 40 to 76 years of age. MEASUREMENTS: Retinol intake was estimated from dietary records and a food-frequency questionnaire. Bone mineral density was measured with dual-energy x-ray absorptiometry. Hip fracture was identified by using hospital discharge records and was confirmed by record review. RESULTS: In multivariate analysis, retinol intake was negatively associated with bone mineral density. For every 1-mg increase in daily intake of retinol, risk for hip fracture increased by 68% (95% CI, 18% to 140%; P for trend, 0.006). For intake greater than 1.5 mg/d compared with intake less than 0.5 mg/d, bone mineral density was reduced by 10% at the femoral neck (P = 0.05), 14% at the lumbar spine (P = 0.001), and 6% for the total body (P = 0.009) and risk for hip fracture was doubled (odds ratio, 2.1 [CI, 1.1 to 4.0]). CONCLUSION: High dietary intake of retinol seems to be associated with osteoporosis.

  • 27. Nichols, Hazel B.
    et al.
    Schoemaker, Minouk J.
    Cai, Jianwen
    Xu, Jiawei
    Wright, Lauren B.
    Brook, Mark N.
    Jones, Michael E.
    Adami, Hans-Olov
    Baglietto, Laura
    Bertrand, Kimberly A.
    Blot, William J.
    Boutron-Ruault, Marie-Christine
    Dorronsoro, Miren
    Dossus, Laure
    Eliassen, A. Heather
    Giles, Graham G.
    Gram, Inger T.
    Hankinson, Susan E.
    Hoffman-Bolton, Judy
    Kaaks, Rudolf
    Key, Timothy J.
    Kitahara, Cari M.
    Larsson, Susanna C.
    Linet, Martha
    Merritt, Melissa A.
    Milne, Roger L.
    Pala, Valeria
    Palmer, Julie R.
    Peeters, Petra H.
    Riboli, Elio
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap.
    Tamimi, Rulla M.
    Tjønneland, Anne
    Trichopoulou, Antonia
    Ursin, Giske
    Vatten, Lars
    Visvanathan, Kala
    Weiderpass, Elisabete
    Wolk, Alicja
    Zheng, Wei
    Weinberg, Clarice R.
    Swerdlow, Anthony J.
    Sandler, Dale P.
    Breast Cancer Risk After Recent Childbirth: A Pooled Analysis of 15 Prospective Studies2019Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 170, nr 1, s. 22-30Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Parity is widely recognized as protective for breast cancer, but breast cancer risk may be increased shortly after childbirth. Whether this risk varies with breastfeeding, family history of breast cancer, or specific tumor subtype has rarely been evaluated.

    Objective: To characterize breast cancer risk in relation to recent childbirth.

    Design: Pooled analysis of individual-level data from 15 prospective cohort studies.

    Setting: The international Premenopausal Breast Cancer Collaborative Group.

    Participants: Women younger than 55 years.

    Measurements: During 9.6 million person-years of follow-up, 18 826 incident cases of breast cancer were diagnosed. Hazard ratios (HRs) and 95% CIs for breast cancer were calculated using Cox proportional hazards regression.

    Results: Compared with nulliparous women, parous women had an HR for breast cancer that peaked about 5 years after birth (HR, 1.80 [95% CI, 1.63 to 1.99]) before decreasing to 0.77 (CI, 0.67 to 0.88) after 34 years. The association crossed over from positive to negative about 24 years after birth. The overall pattern was driven by estrogen receptor (ER)-positive breast cancer; no crossover was seen for ER-negative cancer. Increases in breast cancer risk after childbirth were pronounced when combined with a family history of breast cancer and were greater for women who were older at first birth or who had more births. Breastfeeding did not modify overall risk patterns.

    Limitations: Breast cancer diagnoses during pregnancy were not uniformly distinguishable from early postpartum diagnoses. Data on human epidermal growth factor receptor 2 (HER2) oncogene overexpression were limited.

    Conclusion: Compared with nulliparous women, parous women have an increased risk for breast cancer for more than 20 years after childbirth. Health care providers should consider recent childbirth a risk factor for breast cancer in young women.

    Primary Funding Source: The Avon Foundation, the National Institute of Environmental Health Sciences, Breast Cancer Now and the UK National Health Service, and the Institute of Cancer Research.

  • 28. Nichols, Hazel B
    et al.
    Schoemaker, Minouk J
    Cai, Jianwen
    Xu, Jiawei
    Wright, Lauren B
    Brook, Mark N
    Jones, Michael E
    Adami, Hans-Olov
    Baglietto, Laura
    Bertrand, Kimberly A
    Blot, William J
    Boutron-Ruault, Marie-Christine
    Dorronsoro, Miren
    Dossus, Laure
    Eliassen, A Heather
    Giles, Graham G
    Gram, Inger T
    Hankinson, Susan E
    Hoffman-Bolton, Judy
    Kaaks, Rudolf
    Key, Timothy J
    Kitahara, Cari M
    Larsson, Susanna C
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Linet, Martha
    Merritt, Melissa A
    Milne, Roger L
    Pala, Valeria
    Palmer, Julie R
    Peeters, Petra H
    Riboli, Elio
    Sund, Malin
    Tamimi, Rulla M
    Tjønneland, Anne
    Trichopoulou, Antonia
    Ursin, Giske
    Vatten, Lars
    Visvanathan, Kala
    Weiderpass, Elisabete
    Wolk, Alicja
    Zheng, Wei
    Weinberg, Clarice R
    Swerdlow, Anthony J
    Sandler, Dale P
    Breast Cancer Risk After Recent Childbirth: A Pooled Analysis of 15 Prospective Studies.2019Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 170, nr 1, s. 22-30Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Parity is widely recognized as protective for breast cancer, but breast cancer risk may be increased shortly after childbirth. Whether this risk varies with breastfeeding, family history of breast cancer, or specific tumor subtype has rarely been evaluated.

    Objective: To characterize breast cancer risk in relation to recent childbirth.

    Design: Pooled analysis of individual-level data from 15 prospective cohort studies.

    Setting: The international Premenopausal Breast Cancer Collaborative Group.

    Participants: Women younger than 55 years.

    Measurements: During 9.6 million person-years of follow-up, 18 826 incident cases of breast cancer were diagnosed. Hazard ratios (HRs) and 95% CIs for breast cancer were calculated using Cox proportional hazards regression.

    Results: Compared with nulliparous women, parous women had an HR for breast cancer that peaked about 5 years after birth (HR, 1.80 [95% CI, 1.63 to 1.99]) before decreasing to 0.77 (CI, 0.67 to 0.88) after 34 years. The association crossed over from positive to negative about 24 years after birth. The overall pattern was driven by estrogen receptor (ER)-positive breast cancer; no crossover was seen for ER-negative cancer. Increases in breast cancer risk after childbirth were pronounced when combined with a family history of breast cancer and were greater for women who were older at first birth or who had more births. Breastfeeding did not modify overall risk patterns.

    Limitations: Breast cancer diagnoses during pregnancy were not uniformly distinguishable from early postpartum diagnoses. Data on human epidermal growth factor receptor 2 (HER2) oncogene overexpression were limited.

    Conclusion: Compared with nulliparous women, parous women have an increased risk for breast cancer for more than 20 years after childbirth. Health care providers should consider recent childbirth a risk factor for breast cancer in young women.

    Primary Funding Source: The Avon Foundation, the National Institute of Environmental Health Sciences, Breast Cancer Now and the UK National Health Service, and the Institute of Cancer Research.

  • 29.
    Oldgren, Jonas
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Alings, Marco
    Darius, Harald
    Diener, Hans-Christoph
    Eikelboom, John
    Ezekowitz, Michael D.
    Kamensky, Gabriel
    Reilly, Paul A.
    Yang, Sean
    Yusuf, Salim
    Wallentin, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Connolly, Stuart J.
    Risks for Stroke, Bleeding, and Death in Patients With Atrial Fibrillation Receiving Dabigatran or Warfarin in Relation to the CHADS(2) Score: A Subgroup Analysis of the RE-LY Trial2011Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 155, nr 10, s. 660-667Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: CHADS(2) is a simple, validated risk score for predicting the risk for stroke in patients with atrial fibrillation not treated with anticoagulants. There are sparse data on the risk for thrombotic and bleeding complications according to the CHADS(2) score in patients receiving anticoagulant therapy.

    Objective: To evaluate the prognostic importance of CHADS(2) risk score in patients with atrial fibrillation receiving oral anticoagulants, including the vitamin K antagonist warfarin and the direct thrombin inhibitor dabigatran.

    Design: Subgroup analysis of a randomized, controlled trial. (ClinicalTrials.gov registration number: NCT00262600)

    Setting: Multinational study setting.

    Patients: 18 112 patients with atrial fibrillation who were receiving oral anticoagulants.

    Measurements: Baseline CHADS(2) score, which assigns 1 point each for congestive heart failure, hypertension, age 75 years or older, and diabetes mellitus and 2 points for stroke.

    Results: Distribution of CHADS(2) scores were as follows: 0 to 1-5775 patients; 2-6455 patients; and 3 to 6-5882 patients. Annual rates of the primary outcome of stroke or systemic embolism among all participants were 0.93% in patients with a CHADS(2) score of 0 to 1, 1.22% in those with a score of 2, and 2.24% in those with a score of 3 to 6. Annual rates of other outcomes among all participants with CHADS(2) scores of 0 to 1, 2, and 3 to 6, respectively, were the following: major bleeding, 2.26%, 3.11%, and 4.42%; intracranial bleeding, 0.31%, 0.40%, and 0.61%; and vascular mortality, 1.35%, 2.39%, and 3.68% (P < 0.001 for all comparisons). Rates of stroke or systemic embolism, major and intracranial bleeding, and vascular and total mortality each increased in the warfarin and dabigatran groups as CHADS(2) score increased. The rates of stroke or systemic embolism with dabigatran, 150 mg twice daily, and of intracranial bleeding with dabigatran, 150 mg or 110 mg twice daily, were lower than those with warfarin; there was no significant heterogeneity in subgroups defined by CHADS(2) scores.

    Limitation: These analyses were not prespecified and should be deemed exploratory.

    Conclusion: Higher CHADS(2) scores were associated with increased risks for stroke or systemic embolism, bleeding, and death in patients with atrial fibrillation receiving oral anticoagulants.

  • 30.
    Pickering, John W.
    et al.
    Christchurch Heart Inst, Christchurch, New Zealand.;Hop Lapeyronie, Montpellier, France..
    Than, Martin P.
    Univ Manchester, Cent Manchester Univ Hosp NHS Fdn Trust, Manchester, Lancs, England..
    Cullen, Louise
    Royal Brisbane & Womens Hosp, Herston, Qld, Australia.;Univ Manchester, Cent Manchester Univ Hosp NHS Fdn Trust, Manchester, Lancs, England.;North Bristol NHS Trust, Southmead Hosp, Bristol, Avon, England.;Hop Lapeyronie, Montpellier, France..
    Aldous, Sally
    Univ Otago Christchurch, Christchurch Hosp, Christchurch, New Zealand.;Royal Brisbane & Womens Hosp, Herston, Qld, Australia.;North Bristol NHS Trust, Southmead Hosp, Bristol, Avon, England.;Hop Lapeyronie, Montpellier, France..
    ter Avest, Ewoud
    Christchurch Heart Inst, Christchurch, New Zealand.;Hop Lapeyronie, Montpellier, France..
    Body, Richard
    Royal Brisbane & Womens Hosp, Herston, Qld, Australia.;Univ Manchester, Cent Manchester Univ Hosp NHS Fdn Trust, Manchester, Lancs, England.;North Bristol NHS Trust, Southmead Hosp, Bristol, Avon, England..
    Carlton, Edward W.
    Royal Brisbane & Womens Hosp, Herston, Qld, Australia.;Med Ctr Leeuwarden, Leeuwarden, Netherlands.;St Georges Univ, Hosp NHS Fdn Trust, London, England..
    Collinson, Paul
    North Bristol NHS Trust, Southmead Hosp, Bristol, Avon, England.;St Georges Univ, Hosp NHS Fdn Trust, London, England..
    Dupuy, Anne Marie
    Christchurch Heart Inst, Christchurch, New Zealand.;Univ Manchester, Cent Manchester Univ Hosp NHS Fdn Trust, Manchester, Lancs, England.;St Georges Univ London, London, England..
    Ekelund, Ulf
    Queensland Univ Technol, Herston, Qld, Australia.;Med Ctr Leeuwarden, Leeuwarden, Netherlands.;Hop Lapeyronie, Montpellier, France.;Uppsala Univ, Lund, Sweden..
    Eggers, Kai M.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR). Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiologi. Hop Lapeyronie, Montpellier, France..
    Florkowski, Christopher M.
    Univ Otago Christchurch, Christchurch Hosp, Christchurch, New Zealand.;Royal Brisbane & Womens Hosp, Herston, Qld, Australia.;Med Ctr Leeuwarden, Leeuwarden, Netherlands.;Univ Manchester, Cent Manchester Univ Hosp NHS Fdn Trust, Manchester, Lancs, England.;St Georges Univ, Hosp NHS Fdn Trust, London, England.;St Georges Univ London, London, England.;Uppsala Univ, Lund, Sweden..
    Freund, Yonathan
    Queensland Univ Technol, Herston, Qld, Australia.;Royal Brisbane & Womens Hosp, Herston, Qld, Australia.;Uppsala Univ, Lund, Sweden..
    George, Peter
    Queensland Univ Technol, Herston, Qld, Australia..
    Goodacre, Steve
    St Georges Univ, Hosp NHS Fdn Trust, London, England..
    Greenslade, Jaimi H.
    Univ Otago Christchurch, Christchurch Hosp, Christchurch, New Zealand.;Christchurch Heart Inst, Christchurch, New Zealand.;Royal Brisbane & Womens Hosp, Herston, Qld, Australia.;Med Ctr Leeuwarden, Leeuwarden, Netherlands.;North Bristol NHS Trust, Southmead Hosp, Bristol, Avon, England.;Hop Lapeyronie, Montpellier, France.;Uppsala Univ, Lund, Sweden..
    Jaffe, Allan S.
    Med Ctr Leeuwarden, Leeuwarden, Netherlands.;St Georges Univ London, London, England..
    Lord, Sarah J.
    Univ Otago Christchurch, Christchurch Hosp, Christchurch, New Zealand.;North Bristol NHS Trust, Southmead Hosp, Bristol, Avon, England.;Hop Lapeyronie, Montpellier, France..
    Mokhtari, Arash
    Queensland Univ Technol, Herston, Qld, Australia.;Univ Manchester, Cent Manchester Univ Hosp NHS Fdn Trust, Manchester, Lancs, England.;St Georges Univ, Hosp NHS Fdn Trust, London, England..
    Mueller, Christian
    Munro, Andrew
    Christchurch Heart Inst, Christchurch, New Zealand.;St Georges Univ London, London, England..
    Mustapha, Sebbane
    Univ Otago Christchurch, Christchurch Hosp, Christchurch, New Zealand.;St Georges Univ, Hosp NHS Fdn Trust, London, England..
    Parsonage, William
    Univ Otago Christchurch, Christchurch Hosp, Christchurch, New Zealand.;Univ Manchester, Cent Manchester Univ Hosp NHS Fdn Trust, Manchester, Lancs, England.;Uppsala Univ, Lund, Sweden..
    Peacock, W. Frank
    North Bristol NHS Trust, Southmead Hosp, Bristol, Avon, England..
    Pemberton, Christopher
    Richards, A. Mark
    Sanchis, Juan
    Staub, Lukas P.
    Troughton, Richard
    Twerenbold, Raphael
    Wildi, Karin
    Young, Joanna
    Rapid Rule-out of Acute Myocardial Infarction With a Single High-Sensitivity Cardiac Troponin T Measurement Below the Limit of Detection A Collaborative Meta-analysis2017Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 166, nr 10, s. 715-724Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: High-sensitivity assays for cardiac troponin T (hs-cTnT) are sometimes used to rapidly rule out acute myocardial infarction (AMI). Purpose: To estimate the ability of a single hs-cTnT concentration below the limit of detection (<0.005 mu g/L) and a nonischemic electrocardiogram (ECG) to rule out AMI in adults presenting to the emergency department (ED) with chest pain. Data Sources: EMBASE and MEDLINE without language restrictions (1 January 2008 to 14 December 2016). Study Selection: Cohort studies involving adults presenting to the ED with possible acute coronary syndrome in whom an ECG and hs-cTnT measurements were obtained and AMI outcomes adjudicated during initial hospitalization. Data Extraction: Investigators of studies provided data on the number of low-risk patients (no new ischemia on ECG and hs-cTnT measurements <0.005 mu g/L) and the number who had AMI during hospitalization (primary outcome) or a major adverse cardiac event (MACE) or death within 30 days (secondary outcomes), by risk classification (low or not low risk). Two independent epidemiologists rated risk of bias of studies. Data Synthesis: Of 9241 patients in 11 cohort studies, 2825 (30.6%) were classified as low risk. Fourteen (0.5%) low-risk patients had AMI. Sensitivity of the risk classification for AMI ranged from 87.5% to 100% in individual studies. Pooled estimated sensitivity was 98.7% (95% CI, 96.6% to 99.5%). Sensitivity for 30-day MACEs ranged from 87.9% to 100%; pooled sensitivity was 98.0% (CI, 94.7% to 99.3%). No low-risk patients died. Limitation: Few studies, variation in timing and methods of reference standard troponin tests, and heterogeneity of risk and prevalence of AMI across studies. Conclusion: A single hs-cTnT concentration below the limit of detection in combination with a nonischemic ECG may successfully rule out AMI in patients presenting to EDs with possible emergency acute coronary syndrome.

  • 31.
    Qiu, Chengxuan
    et al.
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Centrum för forskning om äldre och åldrande (ARC), (tills m KI).
    Kivipelto, Miia
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Centrum för forskning om äldre och åldrande (ARC), (tills m KI).
    Fratiglioni, Laura
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Centrum för forskning om äldre och åldrande (ARC), (tills m KI).
    Preventing Alzheimer disease and cognitive decline2011Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 154, nr 3, s. 211-Artikel i tidskrift (Refereegranskat)
  • 32. Schunemann, Holger J.
    et al.
    Lerda, Donata
    Dimitrova, Nadya
    Alonso-Coello, Pablo
    Grawingholt, Axel
    Quinn, Cecily
    Follmann, Markus
    Mansel, Robert
    Sardanelli, Francesco
    Rossi, Paolo Giorgi
    Lebeau, Annette
    Nyström, Lennarth
    Umeå universitet, Medicinska fakulteten, Institutionen för epidemiologi och global hälsa.
    Broeders, Mireille
    Ioannidou-Mouzaka, Lydia
    Duffy, Stephen W.
    Borisch, Bettina
    Fitzpatrick, Patricia
    Hofvind, Solveig
    Castells, Xavier
    Giordano, Livia
    Warman, Sue
    Saz-Parkinson, Zuleika
    Autelitan, Mariangela
    Colzani, Edoardo
    Danes, Jan
    Knox, Susan
    Langendam, Miranda
    McGarrigle, Helen
    Perez Gomez, Elsa
    Torresin, Alberto
    van Engen, Ruben
    Young, Kenneth
    van Landsveld-Verhoeven, Cary
    Rigau, David
    Sola, Ivan
    Ballesteros, Monica
    Arevalo-Rodriguez, Ingrid
    Posso, Margarita
    Martinez Garcia, Laura
    Canelo-Aybar, Carlos
    Nino De Guzman, Ena
    Valli, Claudia
    Ricci-Cabello, Ignacio
    Superchi, Cecilia
    Piggott, Thomas
    Baldeh, Tejan
    Parmelli, Elena
    Methods for Development of the European Commission Initiative on Breast Cancer Guidelines Recommendations in the Era of Guideline Transparency2019Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 171, nr 4, s. 273-280Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Neither breast cancer prevention and early-detection programs, nor their outcomes, are uniform across Europe. This article describes the rationale, methods, and process for development of the European Commission ( EC) Initiative on Breast Cancer Screening and Diagnosis Guidelines. To be consistent with standards set by the Institute of Medicine and others, the EC followed 6 general principles. First, the EC selected, via an open call, a panel with broad representation of areas of expertise. Second, it ensured that all recommendations were supported by systematic reviews. Third, the EC separately considered important subgroups of women, included patient advocates in the guidelines development group, and focused on good communication to inform women's decisions. Fourth, EC rules on conflicts of interest were followed and the GRADE ( Grading of Recommendations Assessment, Development and Evaluation) Evidence to Decision frameworks were used to structure the process and minimize the influence of competing interests. Fifth, it focused its recommendations on outcomes that matter to women, and certainty of the evidence is rated for each. Sixth, the EC elicited stakeholder feedback to ensure that the recommendations remain up to date and relevant to practice. This article describes the approach and highlights ways of disseminating and adapting the recommendations both within and outside Europe, using innovative information technology tools.

  • 33.
    Simon, Tracey G.
    et al.
    Massachusetts General Hospital and Harvard Medical School, Boston Massachusetts, USA.
    Duberg, Ann-Sofi
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Aleman, Soo
    Karolinska University Hospital, Stockholm, Sweden.
    Hagström, Hannes
    Karolinska University Hospital and Karolinska Institutet, Stockholm, Sweden.
    Nguyen, Long H.
    Massachusetts General Hospital and Harvard Medical School, Boston Massachusetts, USA.
    Khalili, Hamed
    Massachusetts General Hospital and Harvard Medical School, Boston Massachusetts, USA; Karolinska Institutet, Stockholm, Sweden.
    Chung, Raymond T.
    Massachusetts General Hospital and Harvard Medical School, Boston Massachusetts, USA.
    Ludvigsson, Jonas F.
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län. Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden; Columbia University College of Physicians and Surgeons, New York, USA.
    Lipophilic Statins and Risk for Hepatocellular Carcinoma and Death in Patients With Chronic Viral Hepatitis: Results From a Nationwide Swedish Population2019Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 171, nr 5, s. 318-327Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Whether statin type influences hepatocellular carcinoma (HCC) incidence or mortality in chronic hepatitis B or C virus infection is unknown.

    Objective: To assess the relationship between lipophilic or hydrophilic statin use and HCC incidence and mortality in a nationwide population with viral hepatitis.

    Design: Prospective propensity score (PS)-matched cohort.

    Setting: Swedish registers, 2005 to 2013.

    Participants: A PS-matched cohort of 16 668 adults (8334 who initiated statin use [6554 lipophilic and 1780 hydrophilic] and 8334 nonusers) among 63 279 eligible adults.

    Measurements: Time to incident HCC, ascertained from validated registers. Statin use was defined from filled prescriptions as 30 or more cumulative defined daily doses (cDDDs).

    Results: Compared with matched nonusers, 10-year HCC risk was significantly lower among lipophilic statin users (8.1% vs. 3.3%; absolute risk difference [RD], -4.8 percentage points [95% CI, -6.2 to -3.3 percentage points]; adjusted subdistribution hazard ratio [aHR], 0.56 [CI, 0.41 to 0.79]) but not hydrophilic statin users (8.0% vs. 6.8%; RD, -1.2 percentage points [CI, -2.6 to 0.4 percentage points]; aHR, 0.95 [CI, 0.86 to 1.08]). The in- verse association between lipophilic statins and HCC risk seemed to be dose-dependent. Compared with nonusers, 10-year HCC risk was lowest with 600 or more lipophilic statin cDDDs (8.4% vs. 2.5%; RD, -5.9 percentage points [CI, -7.6 to -4.2 percentage points]; aHR, 0.41 [CI, 0.32 to 0.61]), and 10-year mortality was significantly lower among both lipophilic (15.2% vs. 7.3%; RD, -7.9 percentage points [CI, -9.6 to -62 percentage points]) and hydrophilic (16.0% vs. 11.5%; RD, -4.5 percentage points [CI, -6.0 to -3.0 percentage points]) statin users.

    Limitation: Lack of lipid, fibrosis, or HCC surveillance data.

    Conclusion: In a nationwide viral hepatitis cohort, lipophilic statins were associated with significantly reduced HCC incidence and mortality. An association between hydrophilic statins and reduced risk for HCC was not found. Further research is needed to determine whether lipophilic statin therapy is feasible for prevention of HCC.

  • 34.
    Sjölund, Maria
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Wreiber, Karin
    Andersson, Dan I
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap.
    Blaser, Martin J
    Engstrand, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Long-term persistence of resistant Enterococcus species after antibiotics to eradicate Helicobacter pylori2003Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 139, nr 6, s. 483-487Artikel i tidskrift (Övrigt vetenskapligt)
    Abstract [en]

    BACKGROUND:

    Antibiotic treatment selects for resistance not only in the pathogen to which it is directed but also in the indigenous microflora.

    OBJECTIVE:

    To determine whether a widely used regimen (clarithromycin, metronidazole, and omeprazole) for Helicobacter pylori eradication affects resistance development in enterococci.

    DESIGN:

    Cohort study.

    SETTING:

    Endoscopy units at 3 community hospitals in Sweden.

    PATIENTS:

    5 consecutive dyspeptic patients who were colonized with H. pylori, had endoscopy-confirmed duodenal ulcer, and received antibiotic treatment, and 5 consecutive controls with dyspepsia but no ulcer who did not receive treatment.

    MEASUREMENTS:

    Fecal samples were obtained from patients and controls before, immediately after, 1 year after, and 3 years after treatment. From each patient and sample, enterococci were isolated and analyzed for DNA fingerprint, clarithromycin susceptibility, and presence of the erm(B) gene.

    RESULTS:

    In treated patients, all enterococci isolated immediately after treatment showed high-level clarithromycin resistance due to erm(B). In 3 patients, resistant enterococci persisted for 1 to 3 years after treatment. No resistance developed among controls.

    CONCLUSION:

    A common H. pylori treatment selects for highly resistant enterococci that can persist for at least 3 years without further selection.

  • 35.
    Sundström, Johan
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiologi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Arima, Hisatomi
    Jackson, Rod
    Turnbull, Fiona
    Rahimi, Kazem
    Chalmers, John
    Woodward, Mark
    Neal, Bruce
    Effects of Blood Pressure Reduction in Mild Hypertension: A Systematic Review and Meta-analysis2015Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 162, nr 3, s. 184-191Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Effects of blood pressure reduction in persons with grade 1 hypertension are unclear. Purpose: To investigate whether pharmacologic blood pressure reduction prevents cardiovascular events and deaths in persons with grade 1 hypertension. Data Sources: Trials included in the BPLTTC (Blood Pressure Lowering Treatment Trialists' Collaboration) and trials identified from a previous review and electronic database searches. Study Selection: Patients without cardiovascular disease with blood pressures in the grade 1 hypertension range (140 to 159/90 to 99 mm Hg) who were randomly assigned to an active (antihypertensive drug or more intensive regimen) or control (placebo or less intensive regimen) blood pressure-lowering regimen. Data Extraction: Individual-patient data from BPLTTC trials and aggregate data from other trials were extracted. Risk of bias was assessed for all trials. Data Synthesis: Individual-patient data involved 10 comparisons from trials where most patients had diabetes, and aggregate data involved 3 comparisons from trials of patients without diabetes. The average blood pressure reduction was about 3.6/2.4 mm Hg. Over 5 years, odds ratios were 0.86 (95% CI, 0.74 to 1.01) for total cardiovascular events, 0.72 (CI, 0.55 to 0.94) for strokes, 0.91 (CI, 0.74 to 1.12) for coronary events, 0.80 (CI, 0.57 to 1.12) for heart failure, 0.75 (CI, 0.57 to 0.98) for cardiovascular deaths, and 0.78 (CI, 0.67 to 0.92) for total deaths. Results were similar in secondary analyses. Withdrawal from treatment due to adverse effects was more common in the active groups. Limitation: Blood pressure reductions and numbers of events were small. Conclusion: Blood pressure-lowering therapy is likely to prevent stroke and death in patients with uncomplicated grade 1 hypertension.

  • 36.
    Ärnlöv, Johan
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik.
    Pencina, Michael J.
    Amin, Shreyasee
    Nam, Byung-Ho
    Benjamin, Emelia J.
    Murabito, Joanne M.
    Wang, Thomas J.
    Knapp, Philip E.
    D'Agostino, Ralph B.
    Bhasin, Shalendar
    Vasan, Ramachandran S.
    Endogenous sex hormones and cardiovascular disease incidence in men2006Ingår i: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 145, nr 3, s. 176-184Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Data suggest that endogenous sex hormones (testosterone, dehydroepiandrosterone sulfate [DHEA-S], and estradiol) influence cardiovascular disease (CVD) risk factors and vascular function. Yet, prospective studies relating sex hormones to CVD incidence in men have yielded inconsistent results.

    Objective: To examine the association of circulating sex hormone levels and CVD risk in men.

    Design: Prospective cohort study.

    Setting: Community-based study in Framingham, Massachusetts.

    Participants: 2084 middle-aged white men without CVD at baseline.

    Measurements: The authors used multivariable Cox regression to relate baseline levels of testosterone, DHEA-S, and estradiol to the incidence of CVD (coronary, cerebrovascular, or peripheral vascular disease or heart failure) during 10 years of follow-up.

    Results: During follow-up, 386 men (18.5%) experienced a first CVD event. After adjustment for baseline standard CVD risk factors, higher estradiol level was associated with lower risk for CVD (hazard ratio per SD increment in log estradiol, 0.90 [95% Cl, 0.82 to 0.99]; P = 0.035). The authors observed effect modification by age: Higher estradiol levels were associated with lower CVD risk in older (median age > 56 years) men (hazard ratio per SD increment, 0.86 [Cl, 0.78 to 0.96]; P = 0.005) but not in younger (median age <= 56 years) men (hazard ratio per SD increment, 1.11 [Cl, 0.89 to 1.38]; P = 0.36). The association of higher estradiol level with lower CVD incidence remained robust in time-dependent Cox models (updating standard CVD risk factors during follow-up). Serum testosterone and DHEA-S levels were not statistically significantly associated with incident CVD.

    Limitations: Sex hormone levels were measured only at baseline, and the findings may not be generalizable to women and nonwhite people.

    Conclusions: In the community-based sample, a higher serum estradiol level was associated with lower risk for CVD events in older men. The findings are consistent with the hypothesis that endogenous estrogen has vasculoprotective influences in men.

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