liu.seSearch for publications in DiVA
Endre søk
Begrens søket
234567 201 - 250 of 338
RefereraExporteraLink til resultatlisten
Permanent link
Referera
Referensformat
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • oxford
  • Annet format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annet språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf
Treff pr side
  • 5
  • 10
  • 20
  • 50
  • 100
  • 250
Sortering
  • Standard (Relevans)
  • Forfatter A-Ø
  • Forfatter Ø-A
  • Tittel A-Ø
  • Tittel Ø-A
  • Type publikasjon A-Ø
  • Type publikasjon Ø-A
  • Eldste først
  • Nyeste først
  • Skapad (Eldste først)
  • Skapad (Nyeste først)
  • Senast uppdaterad (Eldste først)
  • Senast uppdaterad (Nyeste først)
  • Disputationsdatum (tidligste først)
  • Disputationsdatum (siste først)
  • Standard (Relevans)
  • Forfatter A-Ø
  • Forfatter Ø-A
  • Tittel A-Ø
  • Tittel Ø-A
  • Type publikasjon A-Ø
  • Type publikasjon Ø-A
  • Eldste først
  • Nyeste først
  • Skapad (Eldste først)
  • Skapad (Nyeste først)
  • Senast uppdaterad (Eldste først)
  • Senast uppdaterad (Nyeste først)
  • Disputationsdatum (tidligste først)
  • Disputationsdatum (siste først)
Merk
Maxantalet träffar du kan exportera från sökgränssnittet är 250. Vid större uttag använd dig av utsökningar.
  • 201.
    Olsson, Anders
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Det metabola syndromet och dess konsekvenser2005Inngår i: Incitament, ISSN 1103-503X, Vol. 1, s. 25-27Artikkel i tidsskrift (Fagfellevurdert)
  • 202.
    Olsson, Anders
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Faktum kvarstår att 80 mg simvastatin dagligen ger hög myopatirisk2009Inngår i: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 106, nr 43, s. 2783-Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    [No abstract available]

  • 203.
    Olsson, Anders
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Is high HDL cholesterol always good?2009Inngår i: ANNALS OF MEDICINE, ISSN 0785-3890, Vol. 41, nr 1, s. 11-18Artikkel, forskningsoversikt (Annet vitenskapelig)
    Abstract [en]

    Because of the obvious negative relation between high-density lipoprotein (HDL) cholesterol and cardiovascular disease and the substantial residual risk of this disease even during treatment with high-dose statin there has been an urgent need to investigate the possible therapeutic benefit of increasing HDL. Even if treatment with nicotinic acid with its marked HDL-increasing effect has been encouraging, there is no evidence so far that specific increase of HDL cholesterol results in less cardiovascular disease. Treatment with the cholesterol ester transfer protein (CETP) inhibitor and HDL-increasing drug torcetrapib resulted in increased risk of cardiovascular disease. These negative results were followed by a lively discussion regarding the possible benefit of HDL-increasing treatment in general and CETP inhibition in particular. Suggested possible causes for the negative outcome by torcetrapib treatment are off-target non-CETP-related effect of this particular inhibitor, inability of very high blood HDL cholesterol levels to protect, induction of dysfunctional HDL, and direct atherogenic effect of CETP inhibition. It is concluded that still today little is known about the effect of specific therapeutic elevation of HDL cholesterol, particularly so through CETP inhibition on cardiovascular risk. New interventional studies on this therapeutic principle are welcomed and under way.

  • 204.
    Olsson, Anders
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    JUPITER can yield paradigmatic shift in the prevention of cardiovascular disease. Focus on inflammation as a risk factor [JUPITER kan ge paradigmskifte i prevention av hjärt-kärlsjukdom. Fokus på inflammation som riskfaktor.]2009Inngår i: Läkartidningen, ISSN 0023-7205, Vol. 106, nr 21-22, s. 1471-1475Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    [No abstract available]

  • 205.
    Olsson, Anders
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Kontrollerade kliniska prövningar ger bästa svaret2005Inngår i: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 102, s. 2584-2587Artikkel i tidsskrift (Annet (populærvitenskap, debatt, mm))
  • 206.
    Olsson, Anders
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Laropiprant plus niacin for dyslipidemia and prevention of cardiovascular disease2010Inngår i: Expert Opinion on Pharmacotherapy, ISSN 1465-6566, E-ISSN 1744-7666, Vol. 11, nr 10, s. 1715-1726Artikkel, forskningsoversikt (Fagfellevurdert)
    Abstract [en]

    Importance of the field: Prevention of cardiovascular disease has been only partially successful with the use of cholesterol-lowering drugs like statins. There is a residual risk remaining, which may be addressed by increasing protective high-density lipoprotein (HDL) cholesterol and apolipoprotein A1. The best drug available for that purpose is niacin. In addition to increasing HDL cholesterol and apolipoprotein A1, niacin decreases triglycerides, low-density lipoprotein (LDL)-cholesterol and lipoprotein(a) and has been named the broad-spectrum lipid drug. Areas covered in this review: This review summarizes to what extent a new formulation of niacin may meet this request. The effects of niacin on lipoproteins, atherosclerosis and cardiovascular disease are described, from its first publication in 1955, and also its mechanism of action on lipoproteins and on flushing. The flushing inhibitor laropiprant is described as well as the antiflushing effect of this compound when added to extended-release niacin. What the reader will gain: The reader will gain knowledge of the development of niacin as an antiatherosclerosis treatment and of the added value that laropiprant may offer this treatment principle; and also the present place of niacin/laropiprant in the armamentarium of cardiovascular preventive drugs. Take home message: Niacin/laropiprant is a welcome means to address the residual risk in high-risk patients on statin therapy. However, the drug combination cannot completely eliminate niacin-induced side effects. Prescribing this treatment, therefore, will require careful provision of information and instruction to the patient.

  • 207.
    Olsson, Anders
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Lipoprotein Changes and Reduction in the Incidence of Major Coronary Heart Disease Events in teh Scandinavian Simvastatin Survival Study2004Inngår i: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 5, s. 99-106Artikkel i tidsskrift (Fagfellevurdert)
  • 208.
    Olsson, Anders
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Lägre LDL-kolesterol är bättre! Sikta på 2mmol/l i sekundärpreventiv behandling2006Inngår i: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 103, s. 22-23Artikkel i tidsskrift (Annet vitenskapelig)
  • 209.
    Olsson, Anders
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    PPAR agonists do not come up to expectations. Hope about the preventive effect in type 2 diabetes has comte to nought2006Inngår i: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 103, nr 35, s. 2454-2455Artikkel i tidsskrift (Fagfellevurdert)
  • 210.
    Olsson, Anders
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Prove-it2005Inngår i: Information från Läkemedelsverket, ISSN 1101-7104, Vol. 1, s. 14-15Artikkel i tidsskrift (Annet (populærvitenskap, debatt, mm))
  • 211.
    Olsson, Anders
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Psychosocial factors and coronary heart disease2004Inngår i: Current Atherosclerosis Reports, ISSN 1523-3804, E-ISSN 1534-6242, Vol. 6, nr 1Artikkel i tidsskrift (Annet vitenskapelig)
    Abstract [en]

    [No abstract available]

  • 212.
    Olsson, Anders
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Replik: Att följa Ravnskovs råd skulle innebära återgång i ökad dödlighet och sjuklighet. Slutreplik2004Inngår i: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 101, s. 1218-1222Artikkel i tidsskrift (Annet vitenskapelig)
  • 213.
    Olsson, Anders
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Risk factors for reaching renal endpoints in the assessment of lescol in renal transplantation (ALERT) trial2005Inngår i: Transplantation, ISSN 0041-1337, E-ISSN 1534-6080, Vol. 792, s. 205-212Artikkel i tidsskrift (Fagfellevurdert)
  • 214.
    Olsson, Anders
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Rosuvastatin: A Viewpoint by Anders C. Olsson2002Inngår i: Drugs, ISSN 0012-6667, E-ISSN 1179-1950, Vol. 62, nr 14, s. 2086-2086s. 2086-2086Artikkel i tidsskrift (Annet vitenskapelig)
    Abstract [en]

    n/a

  • 215.
    Olsson, Anders
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Rosuvastatin in dyslipidaemia and coronary heart disease2004Bok (Annet vitenskapelig)
  • 216.
    Olsson, Anders
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Rosuvastatin in Dyslipidaemia and Coronary Heart Disease2003Annet (Annet (populærvitenskap, debatt, mm))
  • 217.
    Olsson, Anders
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    The importance of the emergence of statins to a lipidologist-clinician: a personal perspective2004Inngår i: Atherosclerosis Supplements, ISSN 1567-5688, E-ISSN 1878-5050, Vol. 5, nr 3, s. 27-28Annet (Annet vitenskapelig)
  • 218.
    Olsson, Anders
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    The importance of the emergence of statins toa lipidologist - clinician: a personal perspective2004Inngår i: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 5, s. 27-28Artikkel i tidsskrift (Fagfellevurdert)
  • 219.
    Olsson, Anders
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    The lower the better? Experiences from cardiovascular disease and stroke prevention2006Inngår i: Acta Neurologica Scandinavica, ISSN 0001-6314, E-ISSN 1600-0404, Vol. 114, nr SUPPL. 185, s. 58-62Artikkel, forskningsoversikt (Fagfellevurdert)
    Abstract [en]

    [No abstract available]

  • 220.
    Olsson, Anders
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    TNT-studien ger skjuts i debatten om högdos statiner2005Inngår i: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 102, s. 18-19Artikkel i tidsskrift (Annet vitenskapelig)
  • 221.
    Olsson, Anders
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Varning för simvastatin 80 mg!2009Inngår i: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 106, nr 40, s. 2549-2550Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    [No abstract available]

  • 222.
    Olsson, Anders
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Bengtsson, Finn
    Linköpings universitet, Institutionen för medicin och hälsa, Klinisk farmakologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Laboratoriemedicinskt centrum, Klinisk farmakologi.
    Rosengren, A.
    Avdelningen för akut och kardiovaskulär medicin, Sahlgrenska akademin, Göteborg, Sweden.
    Tornvall, P.
    Svenska cardiologföreningen, hjärtkliniken, Karolinska Universitetssjukhuset, Stockholm, Sweden.
    Kolesterolhypotesen står sig2010Inngår i: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 107, nr 12, s. 831-836Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [sv]

    Då kolesterolhypotesen nyligen ifrågasatts har en uppdatering gjorts av kolesterolets roll i aterogenesen hos människa.

    Genetiska, epidemiologiska, cellbiologiska, molekylärbiologiska och kliniska skäl som anförs visar entydigt på en viktig roll för low-density lipoprotein (LDL) i aterosklerosutvecklingen.

    Behandlingsstudier med olika typer av LDL-sänkande behandling styrker ytterligare att kolesterol har stor betydelseför uppkomsten av atero­skleros.

    Fortfarande kvarstår en stor risk för hjärt–kärlsjukdom i Sverige. Nya hypoteser kring orsaken till ateroskleros är därför välkomna.

    Nya tankar kan vara att optimal LDL-nivå ännu inte uppnåtts och/eller att andra lipoproteiner, såsom high-density lipoprotein (HDL) eller triglycerider också måste tas med som viktiga aterogena faktorer.

  • 223.
    Olsson, Anders
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Bengtsson, Finn
    Linköpings universitet, Institutionen för medicin och hälsa, Klinisk farmakologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Laboratoriemedicinskt centrum, Klinisk farmakologi.
    Rosengren, A.
    Sahlgrenska akademin, Göteborg.
    Tornvall, P.
    Karolinska universitetssjukhuset.
    Patienten framför allt!2010Inngår i: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 107, nr 24, s. 1639-Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    [No abstract available]

  • 224.
    Olsson, Anders
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Casciano, Roman
    USA.
    Stern, Lee
    USA.
    Svengren, Per
    Pfizer, Sverige.
    A pharmacoeconomic evaluation of aggressive cholesterol lowering in Sweden2004Inngår i: International Journal of Cardiology, ISSN 0167-5273, E-ISSN 1874-1754, Vol. 96, nr 1, s. 51-57Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objective: To estimate the short-term healthcare costs and incremental cost per event avoided, associated with aggressive atorvastatin treatment in patients with acute coronary syndrome in Sweden. Methods: The total expected 16-week healthcare costs per patient on atorvastatin 80 mg per day and placebo were compared using clinical outcomes data from The Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL) study and Swedish cost data sources. The incremental cost per event avoided was also assessed for. The clinical outcomes measured in this pharmacoeconomic analysis included: death, cardiac arrest, non-fatal myocardial infarction, fatal myocardial infarction, angina pectoris, non-fatal stroke, congestive heart failure, and surgical or percutaneous coronary revascularizations. All direct medical costs were taken into account. Results: The probability of the occurrence of an event was 40.4% per patient in the placebo cohort and 36.6% per patient in the atorvastatin cohort. The total expected cost per patient was SEK 17,887 (1950. 21€11 EUR=9.17231 SEK.) in the placebo group and SEK 18,465 (2013.06€) in the atorvastatin group, resulting in an incremental cost of SEK 578 (63.0137€) per patient. The cost per event avoided was SEK 15,076 (1643.64€). Sixty six percent of the cost of atorvastatin treatment was offset by the cost savings obtained through the reduction in the number of events in the atorvastatin group compared to the placebo group. Conclusions: In Sweden, the clinical benefits of aggressive short-term atorvastatin treatment administered within a few days after acute coronary syndrome is associated with a substantial hospitalization cost offset secondary to the clinical benefits of atorvastatin. © 2003 Elsevier Ireland Ltd. All rights reserved.

  • 225.
    Olsson, Anders
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Cherfan, P
    Blomqvist, Henrik
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin.
    Jonasson, Lena
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Kardiologi. Östergötlands Läns Landsting, Hjärtcentrum, Kardiologiska kliniken.
    Serum adiponectin - its association with inflammation and statin treatment2005Inngår i: EAS Congress,2005, 2005Konferansepaper (Annet vitenskapelig)
  • 226.
    Olsson, Anders G.
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Expanding options with a wider range of rosuvastatin doses2006Inngår i: Clinical Therapeutics, ISSN 0149-2918, E-ISSN 1879-114X, Vol. 28, nr 11, s. 1747-1763Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: The dose range for rosuvastatin in Europe has recently been expanded to 5 to 40 mg and is now in line with the dose range currently available in the United States. Objective: The goal of this article was to review the efficacy and safety data available for the rosuvastatin 5-mg dose and discuss these data in the context of the full 5- to 40-mg dose range. Methods: Articles referring to clinical efficacy or safety data for the 5-mg dose of rosuvastatin were identified and reviewed after a search of the MEDLINE database (2000-August 2006, English language only) using the search term rosuvastatin. Proceedings from major cardiology congresses (2000-2006) were also searched for additional information. Results: Rosuvastatin 5 mg is significantly (P < 0.001) more effective at reducing low-density lipoprotein cholesterol (LDL-C) and total cholesterol (42% and 30%) levels compared with atorvastatin 10 mg (36% and 27%), simvastatin 20 mg (36% and 25%), and pravastatin 20 mg (27% and 19%). Rosuvastatin 5 mg allows significantly more patients to reach their LDL-C goals as recommended by the 2003 European guidelines and the Third Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) (49%-52% and 67%-71%) than atorvastatin 10 mg (36%, P < 0.001, 53%, P < 0.01), simvastatin 20 mg (37%, P < 0.001, 64%, P < 0.05), and pravastatin 20 mg (12%, P < 0.001, 49%, P < 0.001). Rosuvastatin is well tolerated across the 5- to 40-mg dose range, with a type and incidence of adverse events similar to the other commonly available, but less effective, statins. The introduction of a 5-mg dose offers greater flexibility to prescribing physicians in that it provides an additional dosing option for those patients who are at a lower cardiovascular risk or who have an increased potential for developing myopathy with statin therapy. Conclusions: Rosuvastatin 5 mg is well tolerated and has beneficial effects across the atherogenic lipid profile by reducing LDL-C and total cholesterol, raising high-density lipoprotein cholesterol, and helping a greater proportion of patients reach their LDL-C goals. © 2006 Excerpta Medica, Inc.

  • 227.
    Olsson, Anders G
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    HDL and LDL as therapeutic targets for cardiovascular disease prevention: The possible role of niacin2010Inngår i: NUTRITION METABOLISM AND CARDIOVASCULAR DISEASES, ISSN 0939-4753, Vol. 20, nr 8, s. 553-557Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Recently two studies on the effect of addition of extended-release niacin to statin treatment on measures of carotid atherosclerosis were estimated in the ARBITER 6-HALTS study (Arterial Biology for the Investigation of the Treatment Effects of Reducing Cholesterol 6-HDL and LDL Treatment Strategies) study and the Oxford Niacin Study were published. Adding niacin to statin treatment significantly diminished carotid atherosclerosis as measured by ultrasound carotid intima-media thickness or magnetic resonance imaging. An inhibitor of niacin induced flushing, laropiprant has been developed and demonstrated to considerably improve the tolerability of niacin therapy without impeding on its effect on lipoproteins. Still however clear evidence for the clinical benefit of long-term niacin treatment on cardiovascular morbidity and mortality is lacking. The development situation for ezetimibe is similar to that of niacin. Long-term interventional studies with hard endpoints of both therapies are ongoing. Also both drugs, when proven efficient and safe, are eagerly needed in the prevention of cardiovascular disease.

  • 228.
    Olsson, Anders G
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    JUPITER-studien lyfter fram primärprevention2009Inngår i: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 106, nr 23, s. 1577-Artikkel i tidsskrift (Fagfellevurdert)
  • 229.
    Olsson, Anders G
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Livsstilsförändring och läkemedel kompletterar varandra2009Inngår i: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 106, nr 34, s. 2069-Artikkel i tidsskrift (Fagfellevurdert)
  • 230.
    Olsson, Anders G
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Slutrunda om statiner: Faktum kvarstår att 80 mg simvastatin dagligen ger hög myopatirisk2009Inngår i: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 106, nr 43, s. 2783-4; author reply 2784Artikkel i tidsskrift (Fagfellevurdert)
  • 231.
    Olsson, Anders
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Jardine, A
    Holdaas, H
    Fellström, B
    Cole, E
    Nyberg, G
    Grönhagen-Riska, C
    Madsen, S
    Neumayer, H-H
    Maes, B
    Fluvastatin prevents cardiac death and myocardial infarction in renal transplant recipients: Post-hoc subgroup analyses of the ALERT study2004Inngår i: American Journal of Transplantation, ISSN 1600-6135, E-ISSN 1600-6143, Vol. 4, nr 6, s. 988-995Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Renal transplant recipients have a greatly increased risk of premature cardiovascular disease. The ALERT study was a multicenter, randomized, double-blind, placebo-controlled trial of fluvastatin (40-80 mg/day) in 2102 renal transplant recipients followed for 5-6 years. The main study used a composite cardiac end-point including myocardial infarction, cardiac death and cardiac interventions. Although reduced by fluvastatin, this primary end-point failed to achieve statistical significance thus precluding analysis of predefined subgroups. Therefore, in the present survival analysis, we used an alternative primary end-point of cardiac death or definite nonfatal myocardial infarction (as used in other cardiac outcome trials) which was significantly reduced by Fluvastatin therapy and permits subgroup analysis. Fluvastatin reduced LDL-cholesterol by 1 mmol/L compared with placebo, and the incidence of cardiac death or definite myocardial infarction was reduced from 104 to 70 events (RR 0.65, 95% CI 0.48, 0.88, p = 0.005). Fluvastatin use was associated with reduction in cardiac death or nonfatal myocardial infarction, which achieved statistical significance in many subgroups. The subgroups included patients at lower cardiovascular risk, who were younger, nondiabetic, nonsmokers and without pre-existing CVD. These data support the early introduction of statins following renal transplantation.

  • 232.
    Olsson, Anders
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Lindahl, C
    Stockholm County Council, Stockholm, Sweden .
    Fayyad, R
    Pfizer Inc, New York, USA.
    Bhatia, S
    Pfizer Inc, New York, USA.
    Holme, I
    Oslo University Hospital, Oslo.
    CAN LIPID/APOLIPOPROTEIN FACTORS ACCOUNT FOR RESIDUAL RISK IN PATIENTS ATTAINING CURRENT LDL-C TARGETS?2009Inngår i: ATHEROSCLEROSIS SUPPLEMENTS, Elsevier, 2009, Vol. 10, nr 2, s. e1214-e1214Konferansepaper (Annet vitenskapelig)
  • 233.
    Olsson, Anders
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Lindahl, C
    Pfizer Sweden.
    Holme, I
    Oslo University Hospital.
    Fayyad, R
    Pfizer Inc.
    Faergeman, O
    Aarhus University Hospital,.
    Kastelein, J
    Academic Hospital, Amsterdam.
    Tikkanen, M
    Helsinki University Hospital.
    Lytken Larsen, M
    Aarhus University Hospital.
    Pedersen, T
    Oslo University Hospital.
    CORONARY PATIENTS REACHING LDL-CHOLESTEROL andlt; 2.0 mmol/L HAVE THE LOWEST RISK OF CARDIOVASCULAR EVENTS DURING STATIN TREATMENT: THE IDEAL STUDY in ATHEROSCLEROSIS SUPPLEMENTS, vol 11, issue 2, pp 53-532010Inngår i: ATHEROSCLEROSIS SUPPLEMENTS, Elsevier Science B.V., Amsterdam. , 2010, Vol. 11, nr 2, s. 53-53Konferansepaper (Fagfellevurdert)
    Abstract [en]

    n/a

  • 234.
    Olsson, Anders
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    McTaggart, F
    Raza, AG
    Rosuvastatin: A highly effective new HMG-CoA reductase inhibitor2002Inngår i: Cardiovascular Drug Reviews, ISSN 0897-5957, E-ISSN 1527-3466, Vol. 20, nr 4, s. 303-328Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Rosuvastatin, a new statin, has been shown to possess a number of advantageous pharmacological properties, including enhanced HMG-CoA reductase binding characteristics, relative hydrophilicity, and selective uptake into/activity in hepatic cells. Cytochrome P450 (CYP) metabolism of rosuvastatin appears to be minimal and is principally mediated by the 2C9 enzyme, with little involvement of 3A4, this finding is consistent with the absence of clinically significant pharmacokinetic drug-drug interactions between rosuvastatin and other drugs known to inhibit CYP enzymes. Dose-ranging studies in hypercholesterolemic patients demonstrated dose-dependent effects in reducing low-density lipoprotein cholesterol (LDL-C) (up to 63%), total cholesterol, and apolipoprotein (apo) B across a 1- to 40-mg dose range and a significant 8.4% additional reduction in LDL-C, compared with atorvastatin, across the dose ranges of the two agents. Rosuvastatin has also been shown to be highly effective in reducing LDL-C, increasing high-density lipoprotein cholesterol (HDL-C), and producing favorable modifications of other elements of the atherogenic lipid profile in a wide range of dyslipidemic patients. In patients with mild to moderate hypercholesterolemia, rosuvastatin has been shown to produce large decreases in LDL-C at starting doses, thus reducing the need for subsequent dose titration, and to allow greater percentages of patients to attain lipid goals, compared with available statins. The substantial LDL-C reductions and improvements in other lipid measures with rosuvastatin treatment should facilitate achievement of lipid goals and reduce the requirement for combination therapy in patients with severe hypercholesterolemia. In addition, rosuvastatin's effects in reducing triglycerides, tfiglyceride-containing lipoproteins, non-HDL-C, and LDL-C and increasing HDL-C in patients with mixed dyslipidemia or elevated triglycerides should be of considerable value in enabling achievement of LDL-C and non-HDL-C goals in the numerous patients with combined dyslipidemias or metabolic syndrome who require lipid-lowering therapy. Rosuvastatin is well tolerated alone, and in combination with fenofibrate, extended-release niacin, and cholestyramine, and has a safety profile similar to that of currently marketed statins. A large, long-term clinical trials program is under way to investigate the effects of rosuvastatin on atherosclerosis and cardiovascular morbidity and mortality.

  • 235.
    Olsson, Anders
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Nilsson, Peter M.
    institutionen för kliniska vetenskaper, Lunds universitet, Universitetssjukhuset MAS, Malmö.
    "The lower LDL cholesterol levels, the better" still valid. Negative/neutral conclusions of three studies on statins do not change the clinical practice ["Ju lägre LDL-kolesterol, desto bättre" gäller fortsatt Negativa/neutrala slutsatser av tre statinstudier ändrar inte klinisk praxis.]2009Inngår i: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 106, nr 12, s. 854-857Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    [No abstract available]

  • 236.
    Olsson, Anders
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Pears, J.
    AstraZeneca, Alderley Park, Cheshire, United Kingdom.
    McKellar, J.
    AstraZeneca, Alderley Park, Cheshire, United Kingdom.
    Mizan, J.
    AstraZeneca, Alderley Park, Cheshire, United Kingdom.
    Raza, A.
    AstraZeneca, Alderley Park, Cheshire, United Kingdom.
    Effect of rosuvastatin on low-density lipoprotein cholesterol in patients with hypercholesterolemia2001Inngår i: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 88, nr 5, s. 504-508Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Rosuvastatin is a new, synthetic, orally active statin, with marked low-density lipoprotein (LDL) cholesterol-lowering activity. We conducted 2 dose-ranging studies. In the first study, after a 6-week dietary run-in, 142 moderately hypercholesterolemic patients were randomized equally to receive double-blind placebo or rosuvastatin 1, 2.5, 5, 10, 20, or 40 mg or open-label atorvastatin 10 or 80 mg once daily for 6 weeks, in the second study, conducted to extend the rosuvastatin dose range, 64 patients were randomized to double-blind, once-daily placebo or rosuvastatin 40 or 80 mg (1:1:2 ratio) for 6 weeks. Data from both studies were combined for analysis of lipid effects. No statistical comparison of atorvastatin arms with placebo or rosuvastatin was performed. Rosuvastatin was associated with highly significant dose-dependent reductions in LDL cholesterol compared with placebo (p <0.001), decreases ranged from 34% (1 mg) to 65% (80 mg). Linear regression analysis indicated an additional 4.5% LDL cholesterol reduction for each doubling of the rosuvastatin dose. Across the dose range, approximately 90% of LDL cholesterol reduction occurred within the first 2 weeks of treatment. Significant, dose-dependent reductions in total cholesterol and apolipoprotein B with rosuvastatin were also observed (p <0.001). High-density lipoprotein cholesterol increases and triglyceride reductions were consistently observed and statistically significant at some dose levels. All lipid ratios were significantly reduced at all rosuvastatin dose levels (p <0.001). Adverse events were similar across placebo and active treatments. No significant increases in alanine aminotransferase or creatine kinase were seen in any patient. Over 6 weeks, rosuvastatin produced large, rapid, dose-dependent LDL cholesterol reductions and was well tolerated in hypercholesterolemic patients. © 2001 by Excerpta Medica, Inc.

  • 237.
    Olsson, Anders
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Pears, JS
    Linkoping Univ Hosp, Dept Med & Care, S-58185 Linkoping, Sweden AstraZeneca, Alderly Pk, Cheshire, England AstraZeneca, Wilmington, DE USA.
    McKellar, J
    Linkoping Univ Hosp, Dept Med & Care, S-58185 Linkoping, Sweden AstraZeneca, Alderly Pk, Cheshire, England AstraZeneca, Wilmington, DE USA.
    Caplan, RJ
    Linkoping Univ Hosp, Dept Med & Care, S-58185 Linkoping, Sweden AstraZeneca, Alderly Pk, Cheshire, England AstraZeneca, Wilmington, DE USA.
    Raza, A
    Linkoping Univ Hosp, Dept Med & Care, S-58185 Linkoping, Sweden AstraZeneca, Alderly Pk, Cheshire, England AstraZeneca, Wilmington, DE USA.
    ZD4522 - a new HMG-CoA reductase inhibitor - causes rapid and profound reductions in plasma LDL-C levels in patients with primary hypercholesterolaemia2000Inngår i: European Heart Journal, ISSN 0195-668X, E-ISSN 1522-9645, Vol. 21, s. P975-Konferansepaper (Annet vitenskapelig)
  • 238.
    Olsson, Anders
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Schwartz, G
    Szarek, M
    Sasiela, W
    Ezekowitz, M
    Ganz, P
    Oliver, M
    Waters, D
    Zeiher, A
    High-density lipoprotein, but not low-density lipoprotein cholesterol levels influence short-term prognosis after acute coronary syndrome: Results from the MIRACL trial2005Inngår i: European Heart Journal, ISSN 0195-668X, E-ISSN 1522-9645, Vol. 26, nr 9, s. 890-896Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Aims: Patients with acute coronary syndrome (ACS) in the Myocardial lschaemia Reduction with Aggressive Cholesterol Lowering (MIRACL) study had diminished cardiovascular events after 16 weeks of treatment of atorvastatin 80 mg daily. We determined whether plasma lipoproteins at baseline and then at 6 weeks after randomization predicted clinical outcome. Methods and results: Cox proportional hazards models were constructed to determine relations between lipoproteins and clinical endpoint events. Baseline LDL cholesterol (LDL-C) did not predict outcome. In contrast, baseline HDL-C predicted outcome with a hazard ratio of 0.986 per mg/dL increment in HDL-C, P < 0.001, indicating 1.4% reduction in risk for each 1 mg/dL increase in HDL-C. Atorvastatin treatment profoundly lowered LDL-C, but had minimal effect on HDL-C. Neither Week 6 LDL-C nor absolute change of LDL-C from baseline by Week 6 had any significant impact on clinical endpoints occurring between Week 6 and Week 16 after randomization. Conclusion Plasma HDL-C, but not LDL-C, measured in the initial stage of ACS predicts the risk of recurrent cardiovascular events over the ensuing 16 weeks. LDL-C reduction does not account for the clinical risk reduction with atorvastatin treatment after ACS. This finding may suggest that the clinical benefit of atorvastatin after ACS is mediated by qualitative changes in the LDL particle and/or by non-lipid (pleiotropic) effects of the drug.

  • 239.
    Olsson, Andes G.
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Schwartz, G.G.
    VA Medical Center, University of Colorado Health Sciences, Denver, CO, United States.
    Szarek, M.
    Pfizer, Inc., New York, NY, United States.
    Luo, D.
    Pfizer, Inc., New York, NY, United States.
    Jamieson, M.J.
    Pfizer, Inc., New York, NY, United States.
    Effects of High-Dose Atorvastatin in Patients =65 Years of Age With Acute Coronary Syndrome (from the Myocardial Ischemia Reduction With Aggressive Cholesterol Lowering [MIRACL] Study)2007Inngår i: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 99, nr 5, s. 632-635Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    After acute coronary syndromes (ACSs), older patients are particularly susceptible to early complications, including death and recurrent ACS. Lipid management guidelines do not differentiate elderly from younger patients, and lack of evidence for statin benefits in older patients has led to underutilization of statins in the elderly. The MIRACL study randomized 3,086 patients to 16 weeks of 80 mg/day of atorvastatin or placebo 24 to 96 hours after ACS and demonstrated significant decreases in the combined primary end point (nonfatal acute myocardial infarction, resuscitated cardiac arrest, recurrent symptomatic myocardial ischemia). This post hoc analysis compared benefits of 80 mg of atorvastatin in older (=65 years) versus younger (<65 years) patients. Event rates were approximately two- to threefold higher in older than in younger patients. Treatment-by-age heterogeneity testing indicated no difference in treatment effect by age for any of the primary or secondary end points, and relative risk decreases in the primary end point with atorvastatin versus placebo were similar in younger and older patients (22% vs 14%, respectively). The safety profile of atorvastatin was similar between the 2 age groups. In conclusion, these results and a greater immediate cardiovascular risk in older patients argue for early, intensive atorvastatin therapy as routine practice after ACS. © 2007 Elsevier Inc. All rights reserved.

  • 240.
    Olsson, Rolf
    et al.
    Sahlgrens University Hospital.
    Glaumann, Hans
    Karolinska University Hospital.
    Almer, Sven
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Gastroenterologi och hepatologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Broome, Ulrika
    Karolinska University Hospital.
    Lebrun, Barbro
    Karolinska University Hospital.
    Bergquist, Annika
    Karolinska University Hospital.
    Bjornsson, Einar
    Sahlgrens University Hospital.
    Prytz, Hanne
    Lund University Hospital.
    Danielsson, Ake
    Umeå University Hospital.
    Lindgren, Stefan
    Malmö University.
    High prevalence of small duct primary sclerosing cholangitis among patients with overlapping autoimmune hepatitis and primary sclerosing cholangitis2009Inngår i: EUROPEAN JOURNAL OF INTERNAL MEDICINE, ISSN 0953-6205, Vol. 20, nr 2, s. 190-196Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Overlap syndrome is a term used for overlapping features of autoimmune hepatitis and primary sclerosing cholangitis or primary biliary cirrhosis and for autoimmune cholangitis. We describe a high prevalence of small duct primary sclerosing cholangitis among patients with overlapping autoimmune hepatitis and primary sclerosing cholangitis.

    Methods: We sought to retrieve all patients with overlap syndrome between primary sclerosing cholangitis and autoimmune hepatitis in six university hospitals in Sweden. The revised autoimmune hepatitis scoring system proposed by the International Autoimmune Hepatitis Group was used to establish the diagnosis autoimmune hepatitis. Endoscopic retrograde cholangiography and/or magnetic resonance cholangiography were used to separate the primary sclerosing cholangitis cases diagnosed through liver biopsy into small and large primary sclerosing cholangitis. A histologocial diagnosis compatible with both autoimmune hepatitis and primary sclerosing cholangitis was required for inclusion.

    Results: 26 patients fulfilled our criteria for histological overlap of autoimmune hepatitis and primary sclerosing cholangitis, 7 (27%) of which had small duct primary sclerosing cholangitis. The reliability of the diagnosis small duct primary sclerosing cholangitis was supported by a very close similarity between small and large duct primary sclerosing cholangitis patients in clinical and laboratory data, and by a poor response to immunosuppressive therapy in the small duct primary sclerosing cholangitis patients. Patients with large duct overlap syndrome had a good response to immunosuppressive therapy. In both groups, our limited experience from ursodeoxycholic acid was largely poor.

    Conclusions: Small duct primary sclerosing cholangitis is prevalent in the overlap syndrome between autoimmune hepatitis and primary sclerosing cholangitis.

  • 241.
    Ose, L
    et al.
    Univ Oslo, Rikshosp, Dept Med, Lipid Clin, N-0027 Oslo, Norway Laakariasema Koe Oy, FIN-00100 Helsinki, Finland Seinajoki Hlth Ctr, FIN-60220 Seinajoki, Finland Univ Sjukhuset, Med Kliniken, S-58185 Linkoping, Sweden Uppsala Univ, Dept Geriatr, S-75125 Uppsala, Sweden Sahlgrenska Sjukhuset, Med Kliniken, S-41345 Gothenburg, Sweden.
    Luurila, O
    Univ Oslo, Rikshosp, Dept Med, Lipid Clin, N-0027 Oslo, Norway Laakariasema Koe Oy, FIN-00100 Helsinki, Finland Seinajoki Hlth Ctr, FIN-60220 Seinajoki, Finland Univ Sjukhuset, Med Kliniken, S-58185 Linkoping, Sweden Uppsala Univ, Dept Geriatr, S-75125 Uppsala, Sweden Sahlgrenska Sjukhuset, Med Kliniken, S-41345 Gothenburg, Sweden.
    Eriksson, J
    Olsson, Anders
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Lithell, H
    Univ Oslo, Rikshosp, Dept Med, Lipid Clin, N-0027 Oslo, Norway Laakariasema Koe Oy, FIN-00100 Helsinki, Finland Seinajoki Hlth Ctr, FIN-60220 Seinajoki, Finland Univ Sjukhuset, Med Kliniken, S-58185 Linkoping, Sweden Uppsala Univ, Dept Geriatr, S-75125 Uppsala, Sweden Sahlgrenska Sjukhuset, Med Kliniken, S-41345 Gothenburg, Sweden.
    Widgren, B
    Univ Oslo, Rikshosp, Dept Med, Lipid Clin, N-0027 Oslo, Norway Laakariasema Koe Oy, FIN-00100 Helsinki, Finland Seinajoki Hlth Ctr, FIN-60220 Seinajoki, Finland Univ Sjukhuset, Med Kliniken, S-58185 Linkoping, Sweden Uppsala Univ, Dept Geriatr, S-75125 Uppsala, Sweden Sahlgrenska Sjukhuset, Med Kliniken, S-41345 Gothenburg, Sweden.
    Cerivastatin gender effect: Sub-analyses of results from a multinational, randomised, double-blind study2000Inngår i: Current Medical Research and Opinion, ISSN 0300-7995, E-ISSN 1473-4877, Vol. 16, nr 2, s. 80-87Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    We previously reported the results of a multicentre, randomised, double-blind, parallel-group study comparing the efficacy, and safety of cerivastatin 0.4 mg/day and cerivastatin 0.2 mg/day in patients with primary hypercholesterolaemia. Exploratory analysis in this study suggested a gender difference ill the 0.4 wry group: mean low-density lipoprotein cholesterol (LDL-C) decreased by 44.4 +/- 8.9% in women, compared with a mean decrease of 37.0 +/- 0.9% in men (p < 0.046). This paper reports the results of further sub-analyses from this study. Overall in the per-protocol (PP) population. 71.5% (n = 73) of women taking cerivastatin 0.4 mg had all LDL-C decrease of > 40%, compared with 38.0% (n = 76) of men taking the same dose. In the cerivastatin 0.2 mg PP population, 34% (n = 17) of women had an LDL-C decrease of > 40%, compared with 19% (n = Ig) of men. Mean LDL-C/HDL-C ratio decreased by 43% from baseline to the end of the study in the cerivastatin 0.4 mg PP group: -41.3% in males la. -48.3% in females. In the cerivastatin 0.2 mg group, the decrease in LDL-C/HDL-C ratio from baseline to endpoint did not markedly differ between genders: -37.0% for males vs. -37.3% for females. Categorial analysis of the LDL-C/HDL-C ratio found that 90% of PP patients taking cerivastatin 0.4 mg, and 84% of PP patients taking cerivastatin 0.2 my, had a low CHD risk (defined as a LDL-C/HDL-C ratio less than or equal to 3) after 8 weeks of treatment. The 6th and 95th percentiles of the distribution of LDL-C reduction from baseline revealed that 90% of PP patients taking cerivastatin 0.4 mg had all LDL-C reduction of between 22% and 56%. The mean LDL-C reduction for this 90% subset of patients uas 40.1%. The same analysis for PP patients taking cerivastatin 0.2 my found that 90% had all LDL-C reduction of between 13% and 49%. The mean LDL-C reduction in this 90% subset of patients was 31.5%. Of the patients raking cerivastatin 0.4 mg and valid for treatment according to National Cholesterol( Education Program (NCEP) criteria, 71% (149/211) achieved NCEP targets for LDL-C at Week 16.

  • 242.
    Packard, C
    et al.
    Glasgow Royal Infirm, Glasgow G4 0SF, Lanark, Scotland Linkoping Univ Hosp, Clin Res Ctr, S-58185 Linkoping, Sweden.
    Olsson, Anders
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Management of hypercholesterol - aemia in the patient with diabetes2002Inngår i: International journal of clinical practice (Esher), ISSN 1368-5031, E-ISSN 1742-1241, s. 27-32Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Coronary heart disease (CHD) is the leading cause of death in patients with type 2 diabetes. The hyperglycaemia that characterises this disease is often accompanied by a cluster of other risk factors, such as dyslipidaemia and hypertension, and effective management of the patient with diabetes requires treatment directed at correcting all of the abnormalities that increase cardiovascular risk. Approximately 90% of patients with diabetes have type 2 disease, and dyslipidaemia in these patients is characterised by elevated plasma triglycerides and very-low-density lipoproteins (VLDL), by reduced high-density lipoprotein cholesterol (HDL-C), and by a shift in LDL distribution towards small, dense particles. All of these lipid abnormalities are important risk factors for CHD. Retrospective subgroup analysis and prospective studies have shown that lipid-lowering therapy can slow the progression of atherosclerosis and reduce the risk for cardiovascular events in patients with diabetes, and both the National Cholesterol Education Program Adult Treatment Panel III and American Diabetes Association have established aggressive treatment goals for lipid-lowering therapy in these patients. All of the major medications used to treat hyperlipidaemia in other populations (niacin, fibrates, bile acid sequestrants and statins) have been used effectively to improve the plasma lipid profile in patients with diabetes. Statins are generally accepted as first-line treatment for these patients, although fibrates also have an important role in patients with pronounced hypertriglyceridaemia. Statins significantly reduce low-density lipoprotein cholesterol (LDL-C) in a broad range of patients. These agents also have substantial effects on plasma triglycerides and, in patients with hypertriglyceridaemia, lower very-low-density lipoprotein cholesterol (VLDL-C) to approximately the same extent as LDLC. In this regard, the new agent rosuvastatin has been shown, in recent trials, to produce greater decreases in these lipoproteins than currently marketed compounds. Aggressive use of agents that attack the lipid abnormalities characteristic of patients with type 2 diabetes has the potential to significantly reduce CHD risk in these individuals.

  • 243.
    Pedersen, T R
    et al.
    Ullevål University Hospital.
    Faergeman, O
    Århus University Hospital.
    Kastelein, JJP
    Academic Hospital Amsterdam.
    Olsson, Anders
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Tikkanen, MJ
    Helsinki University Central Hospital.
    Holme, I
    Ullevål University Hospital.
    Larsen, ML
    Århus University Hospital.
    Bendiksen, FS
    Hamar, Norway.
    Lindahl, C
    Pfizer Sweden.
    Szarek, M
    Pfizer Inc, New York.
    Tsai, J
    Pfizer Inc, New York.
    High-dose atorvastatin vs usual dose simvastatin for secondary prevention after myocardial infarction - The IDEAL study: A randomized controlled trial2005Inngår i: Journal of the American Medical Association (JAMA), ISSN 0098-7484, E-ISSN 1538-3598, Vol. 294, nr 19, s. 2437-2445Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Context Evidence suggests that more intensive lowering of low-density lipoprotein cholesterol (LDL-C) than is commonly applied clinically will provide further benefit in stable coronary artery disease. Objective To compare the effects of 2 strategies of lipid lowering on the risk of cardiovascular disease among patients with a previous myocardial infarction (MI). Design, Setting, and Participants The IDEAL study, a prospective, randomized, open-label, blinded end-point evaluation trial conducted at 190 ambulatory cardiology care and specialist practices in northern Europe between March 1999 and March 2005 with a median follow-up of 4.8 years, which enrolled 8888 patients aged 80 years or younger with a history of acute MI. Interventions Patients were randomly assigned to receive a high dose of atorvastatin (80 mg/d; n=4439), or usual-dose simvastatin (20 mg/d; n=4449). Main Outcome Measure Occurrence of a major coronary event, defined as coronary death, confirmed nonfatal acute MI, or cardiac arrest with resuscitation. Results During treatment, mean LDL-C levels were 104 (SE, 0.3) mg/dL in the simvastatin group and 81 (SE, 0.3) mg/dL in the atorvastatin group. A major coronary event occurred in 463 simvastatin patients (10.4%) and in 411 atorvastatin patients (9.3%) (hazard ratio [HR], 0.89; 95% Cl, 0.78-1.01; P=.07). Nonfatal acute MI occurred in 321 (7.2%) and M7 (6.0%) in the 2 groups (HR, 0.83; 95% Cl, 0.71-0.98; P=.02), but no differences were seen in the 2 other components of the primary end point. Major cardiovascular events occurred in 608 and 533 in the 2 groups, respectively (HR, 0.87; 95% Cl, 0.77-0.98; P=.02). Occurrence of any coronary event was reported in 1059 simvastatin and 898 atorvastatin patients (HR, 0.84; 95% Cl, 0.76-0.91; Pless than.001). Non-cardiovascular death occurred in 156 (3.5%) and 143 (3.2%) in the 2 groups (HR, 0.92; 95% Cl, 0.73-1.15; P=.47). Death from any cause occurred in 374 (8.4%) in the simvastatin group and 366 (8.2%) in the atorvastatin group (HR, 0.98; 95% Cl, 0.85-1.13; P=.81). Patients in the atorvastatin group had higher rates of drug discontinuation due to nonserious adverse events; transaminase elevation resulted in 43 (1.0%) vs 5 (0.1%) withdrawals (Pless than.001). Serious myopathy and rhabdomyolysis were rare in both groups. Conclusions In this study of patients with previous MI, intensive lowering of LDL-C did not result in a significant reduction in the primary outcome of major coronary events, but did reduce the risk of other composite secondary end points and nonfatal acute MI. There were no differences in cardiovascular or all-cause mortality. Patients with MI may benefit from intensive lowering of LDL-C without an increase in noncardiovascular mortality or other serious adverse reactions.

  • 244.
    Pedersen, Terje R
    et al.
    Oslo University Hospital.
    Cater, Nilo B
    Pfizer Inc.
    Faergeman, Ole
    Arhus University Hospital.
    Kastelein, John J P
    Acad Hospital Amsterdam.
    Olsson, Anders
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Tikkanen, Matti J
    Helsinki University Hospital.
    Holme, Ingar
    Oslo University Hospital.
    Lytken Larsen, Mogens
    Arhus University Hospital.
    Lindahl, Christina
    Pfizer Sweden.
    Szarek, Michael
    Pfizer Inc.
    Comparison of Atorvastatin 80 mg/day Versus Simvastatin 20 to 40 mg/day on Frequency of Cardiovascular Events Late (Five Years) After Acute Myocardial Infarction (from the Incremental Decrease in End Points Through Aggressive Lipid Lowering [IDEAL] Trial)2010Inngår i: AMERICAN JOURNAL OF CARDIOLOGY, ISSN 0002-9149, Vol. 106, nr 3, s. 354-359Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Previous studies have demonstrated that benefits of intensive statin therapy compared to standard statin therapy begin shortly after an acute event and are continued up to 2 years of follow-up. However, whether efficacy and safety of intensive statin therapy in patients with a recent cardiac event are maintained in longer-term follow-up has not been evaluated. We conducted a post hoc analysis of a subgroup of 999 patients who had a first acute myocardial infarction (MI) andlt;2 months before randomization in a prospective, open-label, blinded end-point evaluation trial of 8,888 patients with a history of MI that compared intensive statin therapy (atorvastatin 80 mg) to standard statin therapy (simvastatin 20 to 40 mg) over approximately 5 years of follow-up. We analyzed the same composite end point used in the Pravastatin or Atorvastatin Evaluation and Infection Therapy (PROVE IT) trial (death, MI, hospitalization for unstable angina, revascularization, and stroke). Rates of the composite end point were 44.7% (n = 226) in the simvastatin group and 37.9% (n = 187) in the atorvastatin group (hazard ratio 0.82, 95% confidence interval 0.67 to 0.99, p = 0.04). Although statistical power was smaller than that of the PROVE IT trial, the relative risk decrease observed at 5 years is consistent with that in the 2-year follow-up in PROVE IT. The 2 treatment regimens were well tolerated. In conclusion, our analysis provides support for the strategy of placing patients with recent MI on intensive statin therapy and maintaining the high dose over the long term, beyond 2 years.

  • 245.
    Pedersen, T.R.
    et al.
    Center of Preventive Medicine, Ullevål University Hospital, Oslo, Norway.
    Faergeman, O.
    Department of Medicine-Cardiology A, Århus University Hospital, Århus, Denmark.
    Kastelein, J.J.P.
    Academic Hospital Amsterdam, Amsterdam, Netherlands.
    Olsson, Anders
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Tikkanen, M.J.
    Medical Clinic, Helsinki University Hospital, Helsinki, Finland.
    Holme, I.
    Center of Preventive Medicine, Ullevål University Hospital, Oslo, Norway.
    Larsen, M.L.
    Department of Medicine-Cardiology A, Århus University Hospital, Århus, Denmark.
    Bendiksen, F.S.
    Bendiksen, F.S..
    High-dose statins and the IDEAL study: Reply2006Inngår i: Journal of the American Medical Association (JAMA), ISSN 0098-7484, E-ISSN 1538-3598, Vol. 295, nr 21, s. 2478-2479s. 2478-2479Artikkel i tidsskrift (Annet vitenskapelig)
    Abstract [en]

    [No abstract available]

  • 246.
    Pedersen, T.R.
    et al.
    Center for Preventive Medicine, Ullevål University Hospital, Oslo, Norway, Center for Preventive Medicine, Building K, Ulleval Univ. Hosp., N-0407 Oslo, N..
    Faergeman, O.
    Department of Medicine-Cardiology A, Århus University Hospital, Århus, Denmark.
    Kastelein, J.J.P.
    Academic Hospital Amsterdam, Amsterdam, The Netherlands.
    Olsson, Anders
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Tikkanen, M.J.
    Medical Clinic, Helsinki University Hospital, Helsinki, Finland.
    Holme, I.
    Center for Preventive Medicine, Ullevål University Hospital, Oslo, Norway.
    Larsen, M.L.
    Department of Medicine-Cardiology A, Århus University Hospital, Århus, Denmark.
    Bendiksen, F.S.
    Hamar, Lysaker, Norway.
    Lindahl, C.
    Pfizer Sweden, Täby, Sweden.
    Palmer, G.
    Pfizer Inc., New York, New York, USA.
    Design and baseline characteristics of the Incremental Decrease in End Points through Aggressive Lipid Lowering study2004Inngår i: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 94, nr 6, s. 720-724Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The Incremental Decrease in End Points through Aggressive Lipid Lowering (IDEAL) study is an investigator-initiated trial designed to determine whether additional clinical benefit might be gained through a strategy that decreases levels of low-density lipoprotein cholesterol levels better than those currently achieved with established statin therapy in patients who have coronary heart disease. IDEAL is a multicenter prospective, randomized, open-label, blinded, end point classification study. Patients who had myocardial infarction were randomized to prescription treatment with 80 mg/day of atorvastatin or 20 mg/day of simvastatin (the dose was increased to 40 mg/day at week 24 in those patients whose plasma total cholesterol remained >5.0 mmol/L, or 190 mg/dl, or whose low-density lipoprotein cholesterol remained >3.0 mmol/L, or 115 mg/dl). The primary clinical outcome variable is the time to initial occurrence of a major coronary event, which is defined as nonfatal acute myocardial infarction, coronary death, or resuscitated cardiac arrest. The study is designed to have a power of 90% to detect a relative decrease of 20% in the atorvastatin-group compared with the simvastatin-group in the number of major events caused by coronary heart disease over ~5.5 years. The 8,888 randomized patients had the following characteristics: mean age 61.7 ± 9.5 years, 19.1% women (mean age 64.0 ± 9.5 years), baseline total cholesterol 5.1 ± 1.0 mmol/L (197 mg/dl), low-density lipoprotein cholesterol 3.2 ± 0.9 mmol/L (124 mg/dl), and high-density lipoprotein cholesterol 1.2 ± 0.3 mmol/L (46 mg/dl). Drug treatment before randomization consisted of statins in 77% of patients, aspirin in 78.9%, ß blockers in 75.1%, and angiotensin-converting enzyme inhibitors in 30%. © 2004 by Excerpta Medica, Inc.

  • 247.
    Pedersen, T.R.
    et al.
    Aker Hospital, University of Oslo, Oslo, Norway.
    Wilhelmsen, L.
    Sahlgrenska Hospital, University of Gothenburg, Gothenburg, Sweden.
    Faergeman, O.
    Færgeman, O., Århus University Hospital, Århus, Denmark.
    Strandberg, T.E.
    Helsinki University Hospital, Helsinki, Finland.
    Thorgeirsson, G.
    Landspitalinn University Hospital, Reykjavik, Iceland.
    Troedsson, L.
    MSD Scandinavia, Stockholm, Sweden.
    Kristianson, J.
    MSD Scandinavia, Stockholm, Sweden.
    Berg, K.
    Ullevål Hospital, University of, Oslo, Norway.
    Cook, T.J.
    Merck Research Laboratories, Rahway, NJ, United States.
    Haghfelt, T.
    Odense University Hospital, Odense, Denmark.
    Kjekshus, J.
    National Hospital, University of Oslo, Oslo, Norway.
    Miettinen, T.
    Helsinki University Hospital, Helsinki, Finland.
    Olsson, Anders
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Pyorala, K.
    Pyörälä, K., Kuopio University Hospital, Kuopio, Finland, Nordic Sch. Pub. H., Gothenburg, Sweden.
    Wedel, H.
    Aker Hospital, University of Oslo, Oslo, Norway.
    Follow-up study of patients randomized in The Scandinavian Simvastatin Survival Study (4S) of cholesterol lowering2000Inngår i: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 86, nr 3, s. 257-262Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The Scandinavian Simvastatin Survival Study (4S) and other randomized clinical trials have demonstrated that cholesterol-lowering treatment with statins improves prognosis in patients with coronary atherosclerosis compared with placebo. The effect of therapy with statins beyond the typical 5 to 6 years' duration of the trials, in particular regarding the risk of cancer, has not been investigated. This study examines the long-term effects of simvastatin for up to 8 years on cause-specific mortality in patients with coronary heart disease (CHD). We performed an observational, government registry-based study of mortality in the groups originally randomized to simvastatin or placebo in the 4S over an additional 2-year follow-up period, so that the median total follow-up period was 7.4 years (range 6.9 to 8.3 in surviving patients). Randomization took place at outpatient clinics at 94 clinical centers in Denmark, Finland, Iceland, Norway, and Sweden from 1988 to 1989. Of 4,444 patients with CHD, 2,223 and 2,221 were randomized to treatment with placebo or simvastatin therapy, respectively. Patients received treatment with simvastatin, starting at 20 mg/day, with titration to 40 mg/day at 12 or 24 weeks if total cholesterol was >5.2 mmol/L (200 mg/dl), or placebo. After the double-blind period, most patients in both treatment groups received simvastatin as open-label prescription. Of the 1,967 patients originally treated with placebo and surviving the double-blind period, 97 (4.9%) died during the following 2 years. In the group randomized to simvastatin the corresponding number was 74 of the 2,039 survivors (3.6%). Adding these deaths to those occurring during the original trial, the total was 353 (15.9%) and 256 (11.5%) deaths in the groups originally randomized to placebo and simvastatin, respectively. The relative risk was 0.70 (95% confidence interval 0.60 to 0.82, p = 0.00002). The total number of cancer deaths was 68 (3.1%) in the placebo group and 52 (2.3%) in the simvastatin group (relative risk 0.73, 95% confidence interval 0.51 to 0.05, p = 0.087), and the numbers of noncardiovascular and other deaths were similar in both groups. We therefore conclude that treatment with simvastatin for up to 8 years in patients with CHD is safe and yields continued survival benefit. Copyright (C) 2000 Excerpta Medica Inc.

  • 248.
    Persson, Karin
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Farmakologi. Linköpings universitet, Hälsouniversitetet.
    Sauma, Lilian
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Safholm, Annette
    Linköpings universitet, Institutionen för medicin och hälsa, Farmakologi. Linköpings universitet, Hälsouniversitetet.
    Xu, Lihua
    Linköpings universitet, Institutionen för klinisk och experimentell medicin. Linköpings universitet, Hälsouniversitetet.
    Li, Wei
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Yuan, Ximing
    Linköpings universitet, Institutionen för klinisk och experimentell medicin. Linköpings universitet, Hälsouniversitetet.
    LDL and UV-oxidized LDL induce upregulation of iNOS and NO in unstimulated J774 macrophages and HUVEC2009Inngår i: Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), ISSN 0903-4641, E-ISSN 1600-0463, Vol. 117, nr 1, s. 1-9Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Oxidized low-density lipoprotein (LDL) diminishes NO production from activated macrophages. The interaction between LDL and inactivated macrophages is neglected and controversial. This study examines the effect of LDL, 7-oxysterols and iron compounds on NO production in unstimulated J774 macrophages. J774 cells and human umbilical vein endothelial cells (HUVEC) were either incubated for 24 h with native LDL (LDL) or ultraviolet (UV)-oxidized LDL (UVoxLDL), in the absence or presence of an inducible nitric oxide synthase (iNOS)- or an endothelial constitutive nitric oxide synthase (eNOS)-inhibitor. J774 cells were also incubated with lipopolysaccharide (LPS), in the absence or presence of an iNOS- or an eNOS-inhibitor. Nitrite was analysed as a marker of NO production. The mRNA levels of iNOS were evaluated by reverse transcriptase polymerase chain reaction. LDL and UVoxLDL significantly increased NO production from unstimulated J774 macrophages. This increase in NO was accompanied by enhanced expression of iNOS mRNA, and was inhibited by the iNOS inhibitor. Furthermore, NO production was elevated and angiotensin-converting enzyme (ACE) activity was reduced in HUVEC following the exposure to LDL and UVoxLDL. In conclusion, LDL may serve as an important inflammatory activator of macrophages and HUVEC, inducing inducible nitric oxide production but diminishing ACE. After its oxidation, this function of LDL may be further enhanced and may contribute to the regulation and progression of atheroma formation.

  • 249.
    Pihl-Lesnovska, K
    et al.
    n/a.
    Hjortswang, Henrik
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Gastroenterologi och hepatologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Ek, Anna-Christina
    Linköpings universitet, Institutionen för medicin och hälsa, Omvårdnad. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Närsjukvården i centrala Östergötland, Akutkliniken.
    Hollman Frisman, Gunilla
    Linköpings universitet, Institutionen för medicin och hälsa, Omvårdnad. Linköpings universitet, Hälsouniversitetet.
    Quality of life among individuals with Crohn's disease.2008Inngår i: Conference on Transition, 2008Konferansepaper (Fagfellevurdert)
  • 250. Prytz, Hanne
    et al.
    Keiding, Susanne
    Björnsson, Einar
    Broomé, Ulrika
    Almer, Sven
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Gastroenterologi och hepatologi. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Castedal, Maria
    Lajord Munk, Ole
    Dynamic FDG-PET is useful for detection of cholangiocarcinoma in patients with PSC listed for liver transplantation2006Inngår i: Hepatology, ISSN 0270-9139, E-ISSN 1527-3350, Vol. 44, nr 6, s. 1572-1580Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Five to 15% of patients with primary sclerosing cholangitis (PSC) develop cholangiocarcinoma (CC) with a median survival of 5 to 7 months, an outcome not significantly improved by liver transplantation. However, if CC is found incidentally during the procedure or in the explanted liver, 5-year survival rates of 35% are reported. A noninvasive method to detect CC small enough to allow for intended curative surgery is needed. Unfortunately, computed tomography (CT) and ultrasonography (US) have poor sensitivity for detection of CC in PSC, however, positron emission tomography (PET) using 2-[ 18F]fluoro-2-deoxy-D-glucose (FDG) differentiates well between CC and nonmalignant tissue. We examined whether PET findings are valid using a blinded study design comparing pretransplantation FDG-PET results with histology of explanted livers. Dynamic FDG-PET was performed in 24 consecutive patients with PSC within 2 weeks after listing for liver transplantation and with no evidence of malignancy on CT, magnetic resonance imaging, or ultrasonography. The PET Center staff was blinded to clinical findings, and surgeons and pathologists were blinded to the PET results. Three patients had CC that was correctly identified by PET. PET was negative in 1 patient with high-grade hilar duct dysplasia. In 20 patients without malignancies, PET was false positive in 1 patient with epitheloid granulomas in the liver. In conclusion, dynamic FDG-PET appears superior to conventional imaging techniques for both detection and exclusion of CC in advanced PSC. FDG-PET may be useful for screening for CC in the pretransplant evaluation of patients with PSC. Copyright © 2006 by the American Association for the Study of Liver Diseases.

234567 201 - 250 of 338
RefereraExporteraLink til resultatlisten
Permanent link
Referera
Referensformat
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • oxford
  • Annet format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annet språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf