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Forhøjet p-homocystein--en risikofaktor for trombose

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In the healthy population P-homocysteine increases with age and the level is higher in men aged 30-60 years as compared to women of the same age group. Most often, elevated P-homocysteine is caused by genetic defects, vitamin deficiency (folic acid, B6- and B12-vitamin) or renal failure. Based on retrospective as well as prospective studies, it can be concluded that elevated P-homocysteine is a risk factor for arterial as well as venous thrombosis. Severely elevated P-homocysteine is capable of causing premature arteriosclerosis, whereas slightly elevated levels may also be involved. A slightly positive correlation has been found between P-homocysteine on one hand, and smoking, blood pressure and cholesterol on the other, whereas physical activity is slightly negatively correlated to P-homocysteine. Altered function of endothelial cells and coagulation has been demonstrated in relation to elevated P-homocysteine, but the pathogenetic mechanisms have not been fully elucidated. Usually, an elevated P-homocysteine is normalised by folic acid supplementation, although additional treatment with vitamin B6 may be required. Presumably, the risk of thrombosis is thereby reduced, but future controlled studies may reveal whether this holds true.
Bidragets oversatte titelIncreased p-homocysteine--a risk factor for thrombosis
OriginalsprogDansk
TidsskriftUgeskrift for Laeger
Vol/bind160
Nummer30
Sider (fra-til)4405-10
Antal sider6
ISSN0041-5782
StatusUdgivet - 20 jul. 1998

    Forskningsområder

  • Adult, Age Factors, Aged, Arteriosclerosis, Female, Folic Acid, Homocysteine, Humans, Male, Middle Aged, Pyridoxine, Risk Factors, Sex Factors, Thrombosis

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