Preferences help
enabled [disable] Abstract
Number of results
2006 | 6 | 1 | 62-66
Article title

Udział homocysteiny w patologii niektórych chorób neurologicznych

Title variants
Role of homocysteine in the pathology of some neurological diseases
Languages of publication
Lately the role of homocysteine in pathology of diseases, also neurological, seems to be very interesting. Homocysteine is an amino acid containing thiol group, produced in body by demethylation of methionine. An important role in its metabolism play vitamins from group B (vitamin B6 and B12), folic acid and enzymes: reductase and synthetase. The level of homocysteine depends on genetic and congenital factors. Normal concentration of homocysteine in serum for people under 60 years old is 5-15 μmol/l, for older it is higher. Recently there was found the correlation between the excess of homocysteine and the risk of vascular diseases, dementia. It is also interesting if the level of homocysteine changes in patients with Parkinson’s disease. It can also be teratogenic. It was found that in epileptic patients the level of homocysteine is higher. Antiepileptic drugs which induce cytochrome P450 cause increase in homocysteine levels.
Ostatnio obserwuje się duże zainteresowanie homocysteiną i jej rolą w patologii chorób, także neurologicznych. Homocysteina jest siarkowym aminokwasem zawierającym grupę tiolową, powstającym w organizmie w wyniku demetylacji metioniny. W jej metabolizmie ważną rolę odgrywają witaminy z grupy B (witamina B6 i B12), kwas foliowy oraz enzymy z grupy reduktaz i syntetaz. Poziom homocysteiny zależny jest od czynników wrodzonych i nabytych. Prawidłowy poziom homocysteiny w surowicy krwi dla osób poniżej 60. roku życia wynosi 5-15 mmol/l, dla ludzi starszych dopuszcza się wyższy. Stwierdzono zależność między podwyższonym poziomem homocysteiny a ryzykiem chorób naczyniowych czy otępiennych. Zainteresowanie wzbudziło również zachowanie się poziomu homocysteiny u pacjentów z chorobą Parkinsona. Podwyższony poziom homocysteiny może mieć też działanie teratogenne. Niedawno zwrócono uwagę, że u pacjentów leczonych lekami przeciwpadaczkowymi poziom homocysteiny może być podwyższony. Leki przeciwpadaczkowe indukujące cytochrom P450 powodują wzrost stężenia homocysteiny w surowicy.
Physical description
  • Oddział Neurologii, Wojewódzki Szpital Specjalistyczny im. M. Kopernika, ul. Pabianicka 62, 93-513 Łódź, tel. 0 691 917 307
  • 1. Gibson J.B., Carson N.A., Neill D.W.: Pathological findings in homocystinuria. J. Clin. Pathol. 1964; 17: 427-437.
  • 2. Schimke R.N., McKusickV.A., Huang T, Pollack A.D.: Homocystinuria. Studies of 20 families with 38 affected members. JAMA 1965; 193: 711-719.
  • 3. McCully K.S.: Vascular pathology of homocysteinemia: implications for the pathogenesis of arteriosclerosis. Am. J. Pathol. 1969; 56: 111-128.
  • 4. Ueland P.M., Refsum H., Stabler S.P. i wsp.: Total homocysteine in plasma or serum: methods and clinical applications. Clin. Chem. 1993; 39: 1764-1779.
  • 5. Lussier-Cacan S., Xhignesse M., Piolot A. i wsp.: Plasma total homocysteine in healthy subjects: sex-specific relation with biological traits. Am. J. Clin. Nutr. 1996; 64: 587-593.
  • 6. Refsum H., Ueland PM., Nygard O., Vollset S.E.: Homocysteine and cardiovascular disease. Annu. Rev. Med. 1998: 49: 31-62.
  • 7. Andersson A., Brattstrom L., Israelsson B. i wsp.: Plasma homocysteine before and after methionine loading with regard to age, gender, and menopausal status. Eur. J. Clin. Invest. 1992; 22: 79-87.
  • 8. American Society of Human Genetics/American College of Medical Genetics Test and Technology Transfer Committee Working Group: ASHG/ACMG statement. Measurement and use of total plasma homocysteine. Am. J. Hum. Genet. 1998; 63: 1541-1543.
  • 9. Clarke R., Daly L., Robinson K. i wsp.: Hyperhomocysteinemia: an independent risk factor for vascular disease. N. Engl. J. Med. 1991; 324: 1149-1155.
  • 10. Goyette P., Frosst P., Rosenblatt D.S., Rozen R.: Seven novel mutations in the methylenetetrahydrofolate reductase gene and genotype/phenotype correlations in severe methylenetetrahydrofolate reductase deficiency. Am. J. Hum. Genet. 1995; 56: 1052-1059.
  • 11. Diaz-Arrastia R.: Homocysteine and neurologic disease. Arch. Neurol. 2000; 57: 1422-1427.
  • 12. Selhub J., Jacques P.F., Wilson P.W. i wsp.: Vitamin status and intake as primary determinants of homocysteinemia in an elderly population. JAMA 1993; 270: 2693-2698.
  • 13. Stolzenberg-Solomon R.Z., Miller E.R. 3rd, Maguire M.G. i wsp.: Association of dietary protein intake and coffee consumption with serum homocysteine concentrations in an older population. Am. J. Clin. Nutr. 1999; 69: 467-475.
  • 14. Ueland P.M., Refsum H.: Plasma homocysteine, a risk factor for vascular disease: plasma levels in health, disease, and drug therapy. J. Lab. Clin. Med. 1989; 114: 473-501.
  • 15. Bostom A.G., Gohh R.Y., Tsai M.Y. i wsp.: Excess prevalence of fasting and postmethionine-loading hyperhomocysteinemia in stable renal transplant recipients. Arterioscler. Thromb. Vasc. Biol. 1997; 17: 1894-1900.
  • 16. Ono H., Sakamoto A., Eguchi T i wsp.: Plasma total homocysteine concentrations in epileptic patients taking anticonvulsants. Metabolism 1997; 46: 959-962.
  • 17. James G.K., Jones M.W., PudekM.R.: Homocyst(e)ine levels in patients on phenytoin therapy. Clin. Biochem. 1997; 30: 647-649.
  • 18. Schwaninger M., Ringleb P., Winter R. i wsp.: Elevated plasma concentrations of homocysteine in antiepileptic drug treatment. Epilepsia 1999; 40: 345-350.
  • 19. Verrotti A., Pascarella R., Trotta D. i wsp.: Hyperhomocysteinemia in children treated with sodium valproate and carbamazepine. Epilepsy Res. 2000; 41: 253-257.
  • 20. Apeland T, Mansoor M.A., Strandjord R.E., Kristensen O.: Homocysteine concentrations and methionine loading in patients on antiepileptic drugs. Acta Neurol. Scand. 2000; 101:217-223.
  • 21. Apeland T, Mansoor M.A., Strandjord R.E.: Antiepileptic drugs as independent predictors of plasma total homocysteine levels. Epilepsy Res. 2001; 47: 27-35.
  • 22. Karabiber H., Sonmezgoz E., Ozerol E. i wsp.: Effects of valproate and carbamazepine on serum levels of homocysteine, vitamin B12, and folic acid. Brain Dev. 2003; 25: 113-115.
  • 23. van der Mooren M.J., Wouters M.G., Blom H.J. i wsp.: Hormone replacement therapy may reduce high serum homocysteine in postmenopausal women. Eur. J. Clin. Invest. 1994; 24: 733-736.
  • 24. Kang S.S., Wong PW, Zhou J.M., Cook H.Y.: Total homocysteine in plasma and amniotic fluid of pregnant women. Metabolism 1986; 35: 889-891.
  • 25. 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.
  • 26. Adamkiewicz B.: Hiperhomocysteinemia a ryzyko udaru mózgu. Aktualn. Neurol. 2002; 2: 236-244.
  • 27. Perry I.J., Refsum H., Morris R.W i wsp.: Prospective study of serum total homocysteine concentration and risk of stroke in middle-aged British men. Lancet 1995; 346: 1395-1398.
  • 28. Ridker P.M., Manson J.E., Buring J.E. i wsp.: Homocysteine and risk of cardiovascular disease among postmenopausal women. JAMA 1999; 281: 1817-1821.
  • 29. Bostom A.G., Rosenberg I.H., Silbershatz H. i wsp.: Nonfasting plasma total homocysteine levels and stroke incidence in elderly persons: the Framingham Study. Ann. Intern. Med. 1999; 131: 352-355.
  • 30. Bots M.L., Launer L.J., Lindemans J. i wsp.: Homocysteine and short-term risk of myocardial infarction and stroke in the elderly: the Rotterdam Study. Arch. Intern. Med. 1999; 159: 38-44.
  • 31. D’Angelo A., Selhub J.: Homocysteine and thrombotic disease. Blood 1997; 90: 1-11.
  • 32. Fassbender K., Mielke O., Bertsch T. i wsp.: Homocysteine in cerebral macroangiography and microangiopathy. Lancet 1999; 353: 1586-1587.
  • 33. Toole J.F., Malinow M.R., Chambless L.E. i wsp.: Lowering homocysteine in patients with ischemic stroke to prevent recurrent stroke, myocardial infarction, and death: the Vitamin Intervention for Stroke Prevention (VISP) randomized controlled trial. JAMA 2004; 291: 565-575.
  • 34. Lindenbaum J., Healton E.B., Savage D.G. i wsp.: Neuropsychiatric disorders caused by cobalamin deficiency in the absence of anemia or macrocytosis. N. Engl. J. Med. 1988; 318: 1720-1728.
  • 35. Goodwin J.S., Goodwin J.M., Garry P.J.: Association between nutritional status and cognitive functioning in a healthy elderly population. JAMA 1983; 249: 2917-2921.
  • 36. Riggs K.M., Spiro A. 3rd, Tucker K., Rush D.: Relations of vitamin B-12, vitamin B-6, folate, and homocysteine to cognitive performance in the Normative Aging Study. Am. J. Clin. Nutr. 1996; 63: 306-314.
  • 37. Williams J.H., Pereira E.A., Budge M.M., Bradley K.M.: Minimal hippocampal width relates to plasma homocysteine in community-dwelling older people. Age Ageing 2002; 31: 440-444.
  • 38. Seshadri S., Beiser A., Selhub J. i wsp.: Plasma homocysteine as a risk factor for dementia and Alzheimer’s disease. N. Engl. J. Med. 2002; 346: 476-483.
  • 39. Rogers J.D., Sanchez-Saffon A., Frol A.B., Diaz-Arrastia R.: Elevated plasma homocysteine levels in patients treated with levodopa: association with vascular disease. Arch. Neurol. 2003; 60: 59-64.
  • 40. Yasui K., Nakaso K., Kowa H. i wsp.: Levodopa-induced hyperhomocysteinaemia in Parkinson’s disease. Acta Neurol. Scand. 2003; 108: 66-67.
  • 41. O’Suilleabhain EE., Sung V, Hernandez C. i wsp.: Elevated plasma homocysteine level in patients with Parkinson disease: motor, affective, and cognitive associations. Arch. Neurol. 2004; 61: 865-868.
  • 42. Kubova H., Folbergrova J., Mares P.: Seizures induced by homocysteine in rats during ontogenesis. Epilepsia 1995; 36: 750-756.
  • 43. Sokołowska D., Wendorf J.: Wpływ karbamazepiny na metabolizm kwasu foliowego u dzieci. Epileptologia 2003; 11 (supl. 1): 48-49.
  • 44. Morrell M.J.: Guidelines for the care of women with epilepsy. Neurology 1998; 51 (5 supl. 4): S21-S27.
  • 45. Steegers-Theunissen R.P, Boers G.H., Trijbels FJ. i wsp.: Maternal hyperhomocysteinemia: a risk factor for neural-tube defects? Metabolism 1994; 43: 1475-1480.
  • 46. van der Put N.M., Steegers-Theunissen R.P, Frosst P i wsp.: Mutated methylenetetrahydrofolate reductase as a risk factor for spina bifida. Lancet 1995; 346: 1070-1071.
  • 47. Steegers-Theunissen R.P, Boers G.H., Blom H.J. i wsp.: Neural tube defects and elevated homocysteine levels in amniotic fluid. Am. J. Obstet. Gynecol. 1995; 172: 1436-1441.
Document Type
Publication order reference
YADDA identifier
JavaScript is turned off in your web browser. Turn it on to take full advantage of this site, then refresh the page.