Author/Editor     Žemva, Aleš
Title     Homocysteine - a new marker of cardiovascular risk
Type     članek
Source     In: Štiblar-Martinčič D, Petrovič D, editors. Cardiovascular diseases. Proceedings of the 32nd memorial meeting devoted to professor Janez Plečnik, International symposium in memory of professor Rene Favaloro; 2001 Dec 6-8; Ljubljana. Ljubljana: Medical faculty,
Publication year     2001
Volume     str. 221-5
Language     eng
Abstract     Homocysteine is formed by methylation of amino acid methionine. Plasma homocysteine increases through life. In the adult population fasting homocysteine concentrations of 5 -15 pmol/1 are classified as normal, whereas values of 16 -30 micro mol/l, 31 -100 micro mol/1, and more than 100 pmol/1 are classified as moderate, intermediate, and severe hyperhomocysteinemia, respectively. Elevated homocysteine concentrations are found in 7% of population and in almost 30% of patients with vascular disease. Homocysteine concentrations are determined by nutritional factors (deficiency of vitamins B6, B12, and folic acid) and by mutations in the genes for enzymes involved in homocysteine metabolism, such as the common 5,10methyentetrahydrofolate reductase (MTHFR) 677C-->T mutation. Smoking, high consumption of coffee and alcohol increase homocysteine. Plasma levels of homocysteine are elevated in renal failure, myocardial infarction, stroke, rheumatoid arthritis, diabetes mellitus, psoriasis and neoplastic diseases. Even moderately elevated levels of homocysteine increase the risk of atherosclerosis and cardiovascular death. Elevated homocysteine may contribute to 10% of population coronary heart disease risk. Elevated homocysteine is involved in the pathogenesis of atherosclerosis by inducing endothelial injury, platelet activation, smooth muscle proliferation, and oxidation of LDL and endothelial-leukocyte interaction. In many cases, a change in life-style may be sufficient to lower homocysteine levels. Individuals with homocysteine levels > 12 micro mol/l should be encouraged to increase intake of foods rich in folic acid such as vegetables and fruit. (Abstract truncated at 2000 characters).
Descriptors     HOMOCYSTEINE
ATHEROSCLEROSIS
CORONARY DISEASE
VITAMIN B 12 DEFICIENCY
PYRIDOXINE DEFICIENCY
FOLIC ACID DEFICIENCY