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Sökning: WFRF:(HJEMDAHL P)

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  • Forslund, T, et al. (författare)
  • Usage, risk, and benefit of weight-loss drugs in primary care
  • 2011
  • Ingår i: Journal of obesity. - : Hindawi Limited. - 2090-0716 .- 2090-0708. ; 2011, s. 459263-
  • Tidskriftsartikel (refereegranskat)abstract
    • Purpose. To investigate the use of the weight-loss drugs rimonabant, sibutramine, and orlistat in primary care and to characterize the patients receiving the drugs.Methods. In this retrospective, descriptive study, 300 randomly selected patients having started weight-loss drug treatment at 15 primary care centres were investigated using the patient's medical records and their complete drug purchase data.Results. Even though 48% of the patients specifically demanded drug treatment, 77% continued treatment less than one year. 28% of rimonabant patients and 32% of sibutramine patients had a history of depression or antidepressant treatment. 41% of sibutramine patients had a history of hypertension and/or cardiovascular disease. 36% had no documented weight after treatment initiation.Conclusions. These results suggest that weight-loss drug treatment was often initiated upon patient request but was of limited clinical benefit as it was managed in a large portion of Swedish primary carecenters.
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  • Quintana, M, et al. (författare)
  • Left ventricular function and cardiovascular events following adjuvant therapy with adenosine in acute myocardial infarction treated with thrombolysis - Results of the ATTenuation by Adenosine of Cardiac Complications (ATTACC) study
  • 2003
  • Ingår i: European Journal of Clinical Pharmacology. - : Springer Science and Business Media LLC. - 0031-6970 .- 1432-1041. ; 59:1, s. 1-9
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Reperfusion therapy for acute myocardial infarction (AMI) reduces mortality but is also associated with reperfusion injury. The present study tested the hypothesis that adjuvant therapy with a low anti-inflammatory dose of adenosine might prevent reperfusion injury and preserve left ventricular function. Methods: Six hundred and eight patients with ST-elevation AMI were randomised to receive infusions of adenosine (10 mug.kg(-1)min(-1)) or placebo (saline) to be started with thrombolysis and maintained for 6 h. The primary endpoint was global and regional left ventricular systolic and diastolic function, as assessed by two-dimensional and Doppler echocardiography before hospital discharge. The secondary end-point was all cause and cardiovascular mortality, and non-fatal myocardial infarction during 12 months of follow-up. Results: No beneficial effect of adenosine was found regarding echocardiographic indices of left ventricular systolic or diastolic function. Recruitment was stopped due to this apparent lack of effect after an interim analysis. However, after 12 months of follow-up, cardiovascular mortality was 8.9% with adenosine and 12.1% with placebo treatment [odds ratio (OR) 0.71, 95% confidence interval (C.I.) 0.4-1.2, P=0.2] among all patients and 8.4% vs 14.6% (OR 0.53, 95% C.I. 0.23-1.24, P=0.09) among patients with anterior AMI. All cause mortality differed similarly. Non-fatal AMI was not reduced similarly by adenosine treatment. Survival curves indicate that possible survival benefits are maintained after the first year of follow-up. Conclusions: Adenosine, given as adjunctive treatment with thrombolysis, did not provide detectable improvement of echocardiographic indices of left ventricular function when assessed before hospital discharge. Cardiovascular and all cause mortality appear to have been reduced by low-dose adenosine treatment, and the size of the effect appears to be clinically relevant (absolute risk reductions of approximate to4%). The power of the study regarding morbidity and mortality was, however, limited. The results are compatible with a beneficial anti-inflammatory effect of adenosine treatment on reperfusion injury after thrombolysis, which may be mediated by inhibition of leukocytes in peripheral blood. A larger trial is warranted to possibly establish beneficial effects of low-dose adenosine on survival after thrombolysis.
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  • Almquist, T., et al. (författare)
  • Lipid-lowering treatment and inflammatory mediators in diabetes and chronic kidney disease
  • 2014
  • Ingår i: European Journal of Clinical Investigation. - : Wiley. - 0014-2972 .- 1365-2362. ; 44:3, s. 276-284
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Inflammation may contribute to the high cardiovascular risk in diabetes mellitus (DM) and chronic kidney disease (CKD). Monocyte chemoattractant protein-1 (MCP-1) facilitates the recruitment of monocytes into atherosclerotic lesions and is involved in diabetic nephropathy. Interferon gamma (IFNγ) is important in atherosclerosis and increases the synthesis of chemokines including MCP-1. Lipid-lowering treatment (LLT) with statins may have anti-inflammatory effects, and ezetimibe cotreatment provides additional cholesterol lowering. Methods: After a placebo run-in period, the effects of simvastatin alone (S) or simvastatin + ezetimibe (S+E) were compared in a randomized, double-blind, cross-over study on inflammatory parameters. Eighteen DM patients with estimated glomerular filtration rate (eGFR) 15-59 mL/min × 1·73 m2 (CKD stages 3-4) (DM-CKD) and 21 DM patients with eGFR > 75 mL/min (DM only) were included. Results: At baseline, monocyte chemoattractant protein 1 (MCP-1) (P = 0·03), IFNγ (P = 0·02), tumour necrosis factor-α (TNFα) (P < 0·01) and soluble vascular adhesion molecule (sVCAM) (P = 0·001) levels were elevated in DM-CKD compared with DM-only patients. LLT with S and S+E reduced MCP-1 levels (P < 0·01 by anova) and IFNγ levels (P < 0·01) in DM-CKD patients but not in DM-only patients. Reductions were most pronounced with the combination treatment. Conclusions: DM patients with CKD stages 3-4 had increased inflammatory activity compared with DM patients with normal GFR. Lipid-lowering treatment decreased the levels of MCP-1 and IFNγ in DM patients with concomitant CKD, which may be beneficial with regard to the progression of both atherosclerosis and diabetic nephropathy.
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