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DACH-LIGA homocystein (german, austrian and swiss homocysteine society): consensus paper on the rational clinical use of homocysteine, folic acid and B-vitamins in cardiovascular and thrombotic diseases: guidelines and recommendations.

Abstract

About half of all deaths are due to cardiovascular disease and its complications. The economic burden on society and the healthcare system from cardiovascular disability, complications, and treatments is huge and getting larger in the rapidly aging populations of developed countries. As conventional risk factors fail to account for part of the cases, homocysteine, a "new" risk factor, is being viewed with mounting interest. Homocysteine is a sulfur-containing intermediate product in the normal metabolism of methionine, an essential amino acid. Folic acid, vitamin B12, and vitamin B6 deficiencies and reduced enzyme activities inhibit the breakdown of homocysteine, thus increasing the intracellular homocysteine concentration. Numerous retrospective and prospective studies have consistently found an independent relationship between mild hyperhomocysteinemia and cardiovascular disease or all-cause mortality. Starting at a plasma homocysteine concentration of approximately 10 micromol/l, the risk increase follows a linear dose-response relationship with no specific threshold level. Hyperhomocysteinemia as an independent risk factor for cardiovascular disease is thought to be responsible for about 10% of total risk. Elevated plasma homocysteine levels (>12 micromol/l; moderate hyperhomocysteinemia) are considered cytotoxic and are found in 5 to 10% of the general population and in up to 40% of patients with vascular disease. Additional risk factors (smoking, arterial hypertension, diabetes, and hyperlipidemia) may additively or, by interacting with homocysteine, synergistically (and hence over-proportionally) increase overall risk. Hyperhomocysteinemia is associated with alterations in vascular morphology, loss of endothelial anti-thrombotic function, and induction of a procoagulant environment. Most known forms of damage or injury are due to homocysteine-mediated oxidative stress. Especially when acting as direct or indirect antagonists of cofactors and enzyme activities, numerous agents, drugs, diseases, and lifestyle factors have an impact on homocysteine metabolism. Folic acid deficiency is considered the most common cause of hyperhomocysteinemia. An adequate intake of at least 400 microg of folate per day is difficult to maintain even with a balanced diet, and high-risk groups often find it impossible to meet these folate requirements. Based on the available evidence, there is an increasing call for the diagnosis and treatment of elevated homocysteine levels in high-risk individuals in general and patients with manifest vascular disease in particular. Subjects of both populations should first have a baseline homocysteine assay. Except where manifestations are already present, intervention, if any, should be guided by the severity of hyperhomocysteinemia. Consistent with other working parties and consensus groups, we recommend a target plasma homocysteine level of <10 micromol/l. Based on various calculation models, reduction of elevated plasma homocysteine concentrations may theoretically prevent up to 25% of cardiovascular events. Supplementation is inexpensive, potentially effective, and devoid of adverse effects and, therefore, has an exceptionally favorable benefit/risk ratio. The results of ongoing randomized controlled intervention trials must be available before screening for, and treatment of, hyperhomocysteinemia can be recommended for the apparently healthy general population.

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  • Publisher Full Text
  • Authors+Show Affiliations

    ,

    Landesklinik für Herzchirurgie, Landeskliniken Salzburg, Salzburg, Austria.

    , , , , , ,

    Source

    MeSH

    Austria
    Cardiovascular Diseases
    Female
    Folic Acid
    Germany
    Homocysteine
    Humans
    Hyperhomocysteinemia
    Male
    Risk Factors
    Switzerland
    Thrombosis
    Vitamin B 12
    Vitamin B 6

    Pub Type(s)

    Consensus Development Conference
    Guideline
    Journal Article
    Practice Guideline
    Review

    Language

    eng

    PubMed ID

    14656016

    Citation

    Stanger, Olaf, et al. "DACH-LIGA Homocystein (german, Austrian and Swiss Homocysteine Society): Consensus Paper On the Rational Clinical Use of Homocysteine, Folic Acid and B-vitamins in Cardiovascular and Thrombotic Diseases: Guidelines and Recommendations." Clinical Chemistry and Laboratory Medicine, vol. 41, no. 11, 2003, pp. 1392-403.
    Stanger O, Herrmann W, Pietrzik K, et al. DACH-LIGA homocystein (german, austrian and swiss homocysteine society): consensus paper on the rational clinical use of homocysteine, folic acid and B-vitamins in cardiovascular and thrombotic diseases: guidelines and recommendations. Clin Chem Lab Med. 2003;41(11):1392-403.
    Stanger, O., Herrmann, W., Pietrzik, K., Fowler, B., Geisel, J., Dierkes, J., & Weger, M. (2003). DACH-LIGA homocystein (german, austrian and swiss homocysteine society): consensus paper on the rational clinical use of homocysteine, folic acid and B-vitamins in cardiovascular and thrombotic diseases: guidelines and recommendations. Clinical Chemistry and Laboratory Medicine, 41(11), pp. 1392-403.
    Stanger O, et al. DACH-LIGA Homocystein (german, Austrian and Swiss Homocysteine Society): Consensus Paper On the Rational Clinical Use of Homocysteine, Folic Acid and B-vitamins in Cardiovascular and Thrombotic Diseases: Guidelines and Recommendations. Clin Chem Lab Med. 2003;41(11):1392-403. PubMed PMID: 14656016.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - DACH-LIGA homocystein (german, austrian and swiss homocysteine society): consensus paper on the rational clinical use of homocysteine, folic acid and B-vitamins in cardiovascular and thrombotic diseases: guidelines and recommendations. AU - Stanger,Olaf, AU - Herrmann,Wolfgang, AU - Pietrzik,Klaus, AU - Fowler,Brian, AU - Geisel,Jürgen, AU - Dierkes,Jutta, AU - Weger,Martin, AU - ,, PY - 2003/12/6/pubmed PY - 2004/2/10/medline PY - 2003/12/6/entrez SP - 1392 EP - 403 JF - Clinical chemistry and laboratory medicine JO - Clin. Chem. Lab. Med. VL - 41 IS - 11 N2 - About half of all deaths are due to cardiovascular disease and its complications. The economic burden on society and the healthcare system from cardiovascular disability, complications, and treatments is huge and getting larger in the rapidly aging populations of developed countries. As conventional risk factors fail to account for part of the cases, homocysteine, a "new" risk factor, is being viewed with mounting interest. Homocysteine is a sulfur-containing intermediate product in the normal metabolism of methionine, an essential amino acid. Folic acid, vitamin B12, and vitamin B6 deficiencies and reduced enzyme activities inhibit the breakdown of homocysteine, thus increasing the intracellular homocysteine concentration. Numerous retrospective and prospective studies have consistently found an independent relationship between mild hyperhomocysteinemia and cardiovascular disease or all-cause mortality. Starting at a plasma homocysteine concentration of approximately 10 micromol/l, the risk increase follows a linear dose-response relationship with no specific threshold level. Hyperhomocysteinemia as an independent risk factor for cardiovascular disease is thought to be responsible for about 10% of total risk. Elevated plasma homocysteine levels (>12 micromol/l; moderate hyperhomocysteinemia) are considered cytotoxic and are found in 5 to 10% of the general population and in up to 40% of patients with vascular disease. Additional risk factors (smoking, arterial hypertension, diabetes, and hyperlipidemia) may additively or, by interacting with homocysteine, synergistically (and hence over-proportionally) increase overall risk. Hyperhomocysteinemia is associated with alterations in vascular morphology, loss of endothelial anti-thrombotic function, and induction of a procoagulant environment. Most known forms of damage or injury are due to homocysteine-mediated oxidative stress. Especially when acting as direct or indirect antagonists of cofactors and enzyme activities, numerous agents, drugs, diseases, and lifestyle factors have an impact on homocysteine metabolism. Folic acid deficiency is considered the most common cause of hyperhomocysteinemia. An adequate intake of at least 400 microg of folate per day is difficult to maintain even with a balanced diet, and high-risk groups often find it impossible to meet these folate requirements. Based on the available evidence, there is an increasing call for the diagnosis and treatment of elevated homocysteine levels in high-risk individuals in general and patients with manifest vascular disease in particular. Subjects of both populations should first have a baseline homocysteine assay. Except where manifestations are already present, intervention, if any, should be guided by the severity of hyperhomocysteinemia. Consistent with other working parties and consensus groups, we recommend a target plasma homocysteine level of <10 micromol/l. Based on various calculation models, reduction of elevated plasma homocysteine concentrations may theoretically prevent up to 25% of cardiovascular events. Supplementation is inexpensive, potentially effective, and devoid of adverse effects and, therefore, has an exceptionally favorable benefit/risk ratio. The results of ongoing randomized controlled intervention trials must be available before screening for, and treatment of, hyperhomocysteinemia can be recommended for the apparently healthy general population. SN - 1434-6621 UR - https://www.unboundmedicine.com/medline/citation/14656016/DACH_LIGA_homocystein__german_austrian_and_swiss_homocysteine_society_:_consensus_paper_on_the_rational_clinical_use_of_homocysteine_folic_acid_and_B_vitamins_in_cardiovascular_and_thrombotic_diseases:_guidelines_and_recommendations_ L2 - https://www.degruyter.com/doi/10.1515/CCLM.2003.214 DB - PRIME DP - Unbound Medicine ER -