Avtor/Urednik | Rogel, Polona; Žemva, Aleš | |
Naslov | Homocistein - dejavnik tveganja za srčno-žilne bolezni | |
Prevedeni naslov | Homocysteine - cardiovascular risk factor | |
Tip | članek | |
Vir | Slov Kardiol | |
Vol. in št. | Letnik 2, št. 1 | |
Leto izdaje | 2005 | |
Obseg | str. 56-64 | |
Jezik | slo | |
Abstrakt | Homocysteine is an intermediate product of metabolism of methionine. Folic acid, vitamin B12, and vitamin B6 deficiencies inhibit breakdown of homocysteine, and increase homocysteine concetration in cells and in the blood. Numerous studies showed relationship between mild hyperhomocysteinemia and cardiovascular disease. Hyperhomocysteinemia is responsible for about 10% of cardiovascular risk. Mild elevations of homocysteine (>12 micro mol/l) are found in 5 to 10% of general population and in 40% of patients with cardiovascular disease. Hyperhomocysteinemia is associated with procoagulant state. Vascular damage is mostly due to oxidative stress caused by hyperhomocysteinemia. Drugs, diseases, and lifestyle have an impact on homocysteine metabolism. Folic acid deficiency is the most common cause of hyperhomocysteinemia. An adequate intake of at least 400 mg of folate per day is difficult to maintain. Diagnosis and treatment of hyperhomocysteinemia is needed in high-risk individuals and in patients with manifested cardiovascular disease. Target level of homocysteine is below 10 micro mol/l. Reduction of homocysteine may prevent up to 25% of cardiovascular events. Supplementation is effective in patients at risk and in those with known cardiovascular disease. The results of ongoing randomized intervention trials must be awaited, before screening for and treatment of hyperhomocysteinemia can be recommended for general popula tion. | |
Izvleček | Homocistein nastane iz aminokisline metionin. Pomanjkanje folne kisline in vitaminov skupine B moti delovanje encimov, ki sodelujejo pri razgradnji homocisteina. Ker se zaradi tega količina homocisteina v celicah poveča, homocistein prestopa v kri, kjer se njegova koncentracija zviša. Številne študije so pokazale povezavo med hiperhomocisteinemijo in srčno-žilnim tveganjem. Hiperhomocisteinemija predstavlja 10% vsega srčno-žilnega tveganja. Blaga hiperhomocisteinemija (>12 mikro mol/l) je prisotna pri 5-10 % celotne populacije in pri 40% bolnikov s srčno-žilno boleznijo. Hiperhomocisteinemija povečuje nagnjenje k strjevanju krvi. Domnevajo, da so žilne poškodbe, ki jih sproži homocistein, posledica oksidativnega stresa. Na presnovo homocisteina vplivajo zdravila, bolezni, fiziološke spremenljivke in življenjske navade. Pomanjkanje folne kisline je najpogostejši vzrok hiperhomocisteinemije. Potrebujemo 400 mg folata na dan, kar je težko doseči, tudi če uživamo uravnoteženo prehrano. Osebam z velikim tveganjem in izraženo srčno-žilno boleznijo moramo izmeriti koncentracijo homocisteina in jo znižati, če je previsoka. Raven homocisteina želimo znižati pod 10 mikro mol/l. Z znižanjem ravni homocisteina lahko preprečimo do 25% srčno-žilnih dogodkov. Folna kislina in vitamini skupine B zmanjšajo srčno-žilno tveganje tako pri ogroženih osebah kot pri tistih, ki srčno-žilno okvaro že imajo. Pri zdravi populaciji presejalno merjenje homocisteina in uporaba vitaminov nista upravičeni, dokler ne bodo na voljo rezultati randomiziranih intervencijskih kliničnih študij. | |
Deskriptorji | CARDIOVASCULAR DISEASES HOMOCYSTEINE HYPERTENSION SMOKING RISK FACTORS |