Hyperhomocysteïnemie: verschil tussen versies

:*{{en}}J Am Coll Cardiol. 2006 Mar 21;47(6):1108-16. TITLE Cardiovascular morbidity and mortality in the Atherosclerosis and Folic Acid Supplementation Trial (ASFAST) in chronic renal failure: a multicenter, randomized, controlled trial.CONCLUSIONS: High-dose folic acid does not slow atheroma progression or improve cardiovascular morbidity or mortality in patients with CRF.▼

:*{{en}}N Engl J Med. 2006 Apr 13;354(15):1567-77. TITLE: Homocysteine lowering with folic acid and B vitamins in vascular disease. CONCLUSIONS: Supplements combining folic acid and vitamins B6 and B12 did not reduce the risk of major cardiovascular events in patients with vascular disease. (ClinicalTrials.gov number, NCT00106886; Current Controlled Trials number, ISRCTN14017017.). Copyright 2006 Massachusetts Medical Society.▼

:5 *{{en}}Heart. 2005 Sep;91(9):1213-4. Compound (MeSH Keyword), Substance (MeSH Keyword), Cited in PMC, LinkOut. Secondary prevention with folic acid: results of the Goes extension study.▼

:*{{en}}Int J Cardiol. 2004 Feb;93(2-3):175-9. TITLE: Efficacy of folic acid when added to statin therapy in patients with hypercholesterolemia following acute myocardial infarction: a randomised pilot trial. CONCLUSIONS: In this medium-size pilot study, folic acid did not demonstrate any beneficial additive effects on cardiovascular mortality or morbidity in post-MI patients with hypercholesterolemia who were treated with statin therapy. Larger trials, possibly targeting at selected populations, must be awaited before definitive conclusions regarding the potentially favourable effects of folic acid supplementation in secondary prevention can be drawn.▼

:*{{en}}JAMA. 2004 Feb 4;291(5):565-75. TITLE: Lowering homocysteine in patients with ischemic stroke to prevent recurrent stroke, myocardial infarction, and death: the Vitamin Intervention for Stroke Prevention (VISP) randomized controlled trial. CONCLUSIONS: In this trial, moderate reduction of total homocysteine after nondisabling cerebral infarction had no effect on vascular outcomes during the 2 years of follow-up. However, the consistent findings of an association of total homocysteine with vascular risk suggests that further exploration of the hypothesis is warranted and longer trials in different populations with elevated total homocysteine may be necessary.▼

:*{{en}}J Am Coll Cardiol. 2003 Jun 18;41(12):2105-13. TITLE: Secondary prevention with folic acid: effects on clinical outcomes. CONCLUSIONS: Within two years, folic acid does not seem to reduce clinical end points in patients with stable coronary artery disease (CAD) while on statin treatment. Homocysteine might therefore merely be a modifiable marker of disease. Thus, low-dose folic acid supplementation should be treated with reservation, until more trial outcomes become available.▼

:*{{en}}Eur J Clin Invest. 2003 Mar;33(3):209-15. TITLE: Homocysteine-lowering treatment with folic acid plus vitamin B6 lowers urinary albumin excretion but not plasma markers of endothelial function or C-reactive protein: further analysis of secondary end-points of a randomized clinical trial. CONCLUSIONS: Homocysteine-lowering vitamin treatment in healthy siblings of patients with premature atherosclerotic disease is associated with a decreased urinary albumin-to-creatinine ratio, but not with other markers of endothelial dysfunction, or in plasma C-reactive protein. The clinical significance of these findings remains to be determined.▼

:*{{en}}Blood. 2007 Jan 1;109(1):139-44. TITLE: Homocysteine lowering by B vitamins and the secondary prevention of deep vein thrombosis and pulmonary embolism: A randomized, placebo-controlled, double-blind trial. CONCLUSIONS: The results of our study do not show that homocysteine lowering by B vitamin supplementation prevents recurrent venous thrombosis.▼

:*{{en}}N Engl J Med. 2006 Apr 13;354(15):1578-88. TITLE: Homocysteine lowering and cardiovascular events after acute myocardial infarction. CONCLUSIONS: Treatment with B vitamins did not lower the risk of recurrent cardiovascular disease after acute myocardial infarction. A harmful effect from combined B vitamin treatment was suggested. Such treatment should therefore not be recommended. (ClinicalTrials.gov number, NCT00266487.). Copyright 2006 Massachusetts Medical Society.▼

:*{{en}}Eur J Clin Invest. 2006 May;36(5):333-9. TITLE: No effect of homocysteine-lowering therapy on vascular inflammation and haemostasis in peripheral arterial occlusive disease. CONCLUSION: Although homocysteine is associated with vascular disease risk in the general population and in particular with PAOD, marked lowering of homocysteine concentrations by folic acid and B-vitamin supplementation does not influence inflammatory responses involving usCRP, IL-6, IL-8, IL-18 and MCP-1, nor tissue factor. These results provide evidence against a major effect of hyperhomocysteinaemia on vascular chronic inflammation or coagulation in patients with symptomatic peripheral arterial occlusive disease. </small>▼