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2005 | 5 | 3 | 194-199
Article title

Homocysteina jako czynnik ryzyka uszkodzenia naczyń

Content
Title variants
EN
Homocysteine as a risk factor of vascular damage
Languages of publication
EN PL
Abstracts
EN
Physiologic role of homocysteine, one of sulfur-containing amino acids, is fairly well understood. During the last few years we are witnessing a trend to correlate hyperhomocysteinemia with blood vessel damage and pathogenesis of atheromatosis. Its role as a risk factor in cerebrovascular accidents (CVA) has been highlighted. In 100 patients with ischemic brain stroke, confirmed by neuroimaging studies (CT and/or MRI) and Doppler sonography of cerebral arteries, we have determined serum levels of homocysteine, vitamin B12 and folic acid. The same tests were performed in 40 controls with no pyramidal signs. Our results show a significant elevation of homocysteine level in CVA patients. In 28% of patients, the difference as compared with the control group was significant, thus indicating that hyperhomocysteinemia may constitute an independent risk factor for stroke. Sonography revealed the presence of vascular lesions and the number of vessels involved, while CT and/or MRI studies visualized areas of brain ischemia. High level of homocysteine did not correlate directly with the number of vessels involved. Noteworthy is that elevated homocysteine level may be controlled by supplementation with group B vitamins and folic acid. The level of homocysteine may be elevated in such neurologic diseases as dementia and Parkinson’s disease. Another noteworthy issue is hyperhomocysteinemia associated with prolonged administration of antiepileptic drugs in persons with epilepsy.
PL
Rola homocysteiny – aminokwasu siarkowego jest w organizmie znana. W ostatnich latach próbowano łączyć hiperhomocysteinemię z uszkodzeniem naczyń krwionośnych i patogenezą miażdżycy. Zwrócono uwagę na jej rolę jako czynnika ryzyka w udarze mózgu. U 100 chorych z udarem niedokrwiennym mózgu – potwierdzonym w badaniu neuroobrazowym (CT i/lub NMR głowy) oraz w przeprowadzonym metodą Dopplera badaniu tętnic domózgowych (USG) – oznaczano w surowicy poziom homocysteiny oraz witaminy B12 i kwasu foliowego. U 40 osób z grupy kontrolnej (bez objawów piramidowych) dokonywano tych samych oznaczeń. Okazało się, że poziom homocysteiny w surowicy krwi był podwyższony w sposób istotny statystycznie. U 28% różnica ta była znaczna w porównaniu z grupą kontrolną, co wskazuje, że hiperhomocysteinemia stanowi niezależny czynnik ryzyka udaru mózgu. Badania USG pozwoliły na ustalenie zmian i ilości zajętych tętnic, z kolei badanie CT lub/i NMR ujawniało obszary niedokrwienia. Wysoki poziom homocysteiny nie korelował bezpośrednio z ilością zajętych naczyń. Interesujący jest fakt, że podwyższony poziom homocysteiny można regulować poprzez suplementację witaminami z grupy B i kwasem foliowym. Poziom homocysteiny bywa podwyższony w takich chorobach układu nerwowego, jak otępienie czy choroba Parkinsona. Zwraca uwagę hiperhomocysteina występująca w przebiegu długotrwałej terapii lekami przeciwpadaczkowymi u osób chorujących z powodu epilepsji.
Discipline
Publisher

Year
Volume
5
Issue
3
Pages
194-199
Physical description
Contributors
  • Oddział Kliniczny Epileptologii, II Katedra Chorób Układu Nerwowego UM, Oddział Neurologii WSS im. M. Kopernika w Łodzi
  • Oddział Kliniczny Epileptologii, II Katedra Chorób Układu Nerwowego UM, Oddział Neurologii WSS im. M. Kopernika w Łodzi
References
  • 1. Cebalska B.: Choroby metaboliczne układu nerwowego. W: Czochańska J. (red.): Neurologia dziecięca. PZWL, Warszawa 1985: 229-244.
  • 2. Rees M.M., Rodgers G.M.: Homocysteinemia: association of a metabolic disorder with vascular disease and thrombosis. Thromb. Res. 1993; 71: 337-359.
  • 3. Boushey C.J., Beresford SA., Omenn G.S., Motulsky A.G.: A quantitative assessment of plasma homocysteine as a risk factor for vascular disease. Probable benefits of increasing folic acid intakes. JAMA 1995; 274: 1049-1057.
  • 4. Eikelboom J.W., Hankey G.J., Anand S.S. iwsp.: Association between high homocyst(e)ine and ischemic stroke due to large- and small-artery disease but not other etiologic subtypes of ischemic stroke. Stroke 2000; 31: 1069-1075.
  • 5. Stamler J.S., Osborne J.A., Jaraki O. i wsp.: Adverse vascular effects of homocysteine are modulated by endothelium-derived relaxing factor and related oxides of nitrogen. J. Clin. Invest. 1993; 91: 308-318.
  • 6. Freyburger G., Labrouche S., Sassoust G. i wsp.: Mild hyperhomocysteinemia and hemostatic factors in patients with arterial vascular diseases. Thromb. Haemost. 1997; 77: 466-471.
  • 7. Sung J.J., Sanderson J.E.: Hyperhomocysteinaemia, Helicobacter pylori, and coronary heart disease. Heart 1996; 76: 305-307.
  • 8. Lalouschek W, Aull S., Serles W. i wsp.: Genetic and non-genetic factors influencing plasma homocysteine levels in patients with ischemic cerebrovascular disease and in healthy control subjects. J. Lab. Clin. Med. 1999; 133: 575-582.
  • 9. Selhub J., Jacques PF., Rosenberg I.H. i wsp.: Serum total homocysteine concentrations in the third National Health and Nutrition Examination Survey (1991-1994): population reference ranges and contribution of vitamin status to high serum concentrations. Ann. Intern. Med. 1999; 131: 331-339.
  • 10. Lindgren A., Brattstrom L., Norrving B. i wsp.: Plasma homocysteine in the acute and convalescent phases after stroke. Stroke 1995; 26: 795-800.
  • 11. Evans R.W., Shaten B.J., Hempel J.D. i wsp.: Homocyst(e)ine and risk of cardiovascular disease in the Multiple Risk Factor lntervention Trial. Arterioscler. Thromb. Vasc. Biol. 1997; 17: 1947-1953.
  • 12. Clarke R., Frost C., Leroy V. i wsp.; for the Homocysteine Lowering Trialists’ Collaboration: Lowering blood homocysteine with folic acid based supplements: meta-analysis of randomised trials. BMJ 1998; 316: 894-898.
  • 13. Giles WH., Croft J.B., Greenlund K.J. i wsp.: Total homocyst(e)ine concentration and the likelihood of nonfatal stroke: results from the Third National Health and Nutrition Examination Survey, 1988-1994. Stroke 1998; 29: 2473-2477.
  • 14. Okamura T, Kitamura A., Moriyama Y. i wsp.: Plasma level of homocysteine is correlated to extracranial carotidartery atherosclerosis in non-hypertensive Japanese. J. Cardiovasc. Risk 1999; 6: 371-377.
  • 15. Adamkiewicz B.: Hiperhomocysteinemia a ryzyko udaru mózgu. Rozprawa doktorska. UM, Łódź 2003.
  • 16. Miller J.W., Green R., Mungas D.M. i wsp.: Homocysteine, vitamin B6, and vascular disease in AD patients. Neurology 2002; 58: 1471-1475.
  • 17. Clarke R., Smith A.D., Jobst K.A. i wsp.: Folate, vitamin B12, and serum total homocysteine levels in confirmed Alzheimer disease. Arch. Neurol. 1998; 55: 1449-1455.
  • 18. Leblhuber F., Walii J., Widner B. i wsp.: Hyperhomocysteinemia and immune activation in Alzheimer’s disease. J. Neural Transm. 2000: S63-S64.
  • 19. Bottiglieri T., Laundy M., Crellin R. i wsp.: Homocysteine, folate, methylation, and monoamine metabolism in depression. J. Neurol. Neurosurg. Psychiatry 2000; 69: 228-232.
  • 20. O K., Lynn E.G., Chung Y.H. i wsp.: Homocysteine stimulates the production and secretion of cholesterol in hepatic cells. Biochim. Biophys. Acta 1998; 1393: 317-324.
  • 21. Harker L.A., Ross R., Slichter S.J., Scott C.R.: Homocystine-induced arteriosclerosis. The role of endothelial cell injury and platelet response in its genesis. J. Clin. lnvest. 1976; 58: 731-741.
  • 22. Wall R.T, Harlan J.M., Harker L.A., Striker G.E.: Homocysteine-induced endothelial cell injury in vitro: a model for the study of vascular injury. Thromb. Res. 1980; 18: 113-121.
  • 23. Cooke J.P, Tsao PS.: Is NO an endogenous antiatherogenic molecule? Arterioscler. Thromb. 1994; 14: 653-655.
  • 24. Woo K.S., Chook P., Lolin Y.I. i wsp.: Hyperhomocyst(e)inemia is a risk factor for arterial endothelial dysfunction in humans. Circulation 1997; 96: 2542-2544.
  • 25. Vermeer S.E., van Dijk E.J., Koudstaal PJ. i wsp.: Homocysteine, silent brain infarcts, and white matter lesions: the Rotterdam Scan Study. Ann. Neurol. 2002; 51: 285-289.
  • 26. Kim N.K., Choi B.O., Jung W.S. i wsp.: Hyperhomocysteinemia as an independent risk factor for silent brain infarction. Neurology 2003; 61: 1595-1599.
  • 27. Longstreth W.T. Jr, Katz R., Olson J. i wsp.: Plasma total homocysteine levels and cranial magnetic resonance imaging findings in elderly persons: the Cardiovascular Health Study. Arch. Neurol. 2004; 61: 67-72.
  • 28. Hankey G.J.: Is homocysteine a causal and treatable risk factor for vascular diseases of the brain (cognitive impairment and stroke)? Ann. Neurol. 2002; 51: 279-281.
  • 29. VITATOPS Trial Study Group: The VITATOPS (Vitamins to Prevent Stroke) Trial: rationale and design of an international, large, simple, randomised trial of homocysteine-lowering multivitamin therapy in patients with recent transient ischaemic attack or stroke. Cerebrovasc. Dis. 2002: 13: 120-126.
  • 30. Diaz-Arrastia R.: Homocysteine and neurologic disease. Arch. Neurol. 2000; 57: 1422-1427.
Document Type
article
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YADDA identifier
bwmeta1.element.psjd-0da75c9c-e4ba-4bdd-b83a-0cfe7243239f
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