Homocysteine levels and platelet aggregation in patients with cerebral circulatory disorders


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AIM: To reveal platelet functional changes manifesting as abnormal rate of platelet aggregation in patients with acute cerebral circulatory disorders (ischemic stroke, transient ischemic attack), to evaluate the effect of homocysteine (Hc) on platelet aggregation, depending on the degree of cerebral blood flow disturbances, patients' gender and age, and to estimate the diagnostic value of their associations/MATERIAL AND METHODS: 50 patients aged 33 to 98 years (mean age, 63.7±2.1 years; 20 men and 30 women) with acute cerebral circulatory disorders (18 with transient ischemic attack and 32 with ischemic stroke) were examined. The diagnosis was verified by the results of computed tomography and other clinical examinations. Adenosine diphosphate-, epinephrine-, and collagen-induced platelet aggregation was assessed in platelet-rich plasma; serum Hc concentrations were also studied/RESULTS: Comparison of platelet aggregation and Hc concentration revealed a statistically significant correlation between platelet aggregation with collagen and elevated Hc levels (r=0.376; p<0.01). There was no statistically significant correlation with other inducers. Blood Hc concentrations increased with advancing age (r=0.357; p=0.015). No statistically significant correlation was found between age and platelet aggregation (p>0.05). The levels of Hc were statistically significantly higher as cerebral circulatory disorders progressed/CONCLUSION: There was a statistically significantly relationship between collagen-induced platelet aggregation and Hc concentration. The Hc levels were statistically significantly related to the severity of cerebral circulatory disorders and age.

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Уровень гомоцистеина и показателей агрегации тромбоцитов у больных c нарушением мозгового кровообращения. - Резюме. Цель исследования. Выявить изменения функции тромбоцитов, выражающиеся в отклонениях интенсивности их агрегации, у больных с острыми нарушениями кровообращения в головном мозге (ишемический инсульт, преходящee нарушение мозгового кровообращения - ПНМК) и оценить воздействие концентрации гомоцистеина (Гц) на агрегацию тромбоцитов (АгТ) в зависимости от степени нарушения кровообращения, пола, возраста больных, а также оценить диагностическое значение их взаимосвязи. Материалы и методы. Обследовали 50 больных в возрасте от 33 до 98 лет (средний возраст 63,7±2,1 года, 20 мужчин, 30 женщин) с болезнью кровеносных сосудов в остром периоде (18 больных с ПНМК и 32 с ишемическим инсультом). Диагноз подтвержден результатами компьютерной томографии и других клинических исследований. Оценена АгТ, вызванная аденозиндифосфатом, адреналином и коллагеном, в богатой тромбоцитами плазме, а также изучена концентрация Гц в сыворотке крови. Результаты. При сравнении АгТ и концентрации Гц отмечена статистически значимая корреляция между АгТ с коллагеном и увеличением количества Гц (r=0,376; p<0,01). с другими индукторами статистически значимой корреляции нет. С увеличением возраста больных содержание Гц в крови повышалось (r=0,357; p=0,015). Статистически значимой корреляции между возрастом и АгТ не получено (p>0,05). Количество Гц статистически значимо увеличивалось по мере прогрессирования нарушения мозгового кровообращения. Заключение. АгТ вызванная коллагеном, и концентрация Гц статистически значимо взаимосвязаны. Количество Гц статистически значимо зависело от тяжести нарушения мозгового кровообращения и возраста больных.
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References

  1. Born G.V.R. Aggregation of blood platelets by adenosine diphosphate and its reversal. Nature 1962; 194: 927-929.
  2. Shipchandler M.T., Moore E.G. Rapid, fully automated measurement of plasma homocyst(e)ine with the Abbott IMX analyser. Clin Chem 1995; 41: 991-994.
  3. Ueland P.M., Refsum H., Beresford S.A. et al. The controversy over homocysteine and cardiovascular risk. Am J Clin Nutr 2000; 72 (2): 333- 334.
  4. Milosevič-Tosič M., Borota J. Hyperhomocysteinemia - a risk factor for development of occlusive vascular diseases. Med Pregl 2002; 55 (9-10): 385-391.
  5. Dionisio N., Jardin I., Salido G.M., Rosado J.A. Homocysteine, intracellular signaling and thrombotic disorders. Curr Med Chem 2010; 17 (27): 3109-3119.
  6. Garalienė V. The main determinants of endothelial dysfunction. Medicina (Kaunas) 2006; 42 (5): 362-369.
  7. Alam M.M., Mohammad A.A., Shualb U. et al. Homocysteine reduces endothelial progenitor cells in stroke patients throught apoptosis. J Cereb Blood Flow Metab 2009; 29 (1): 157-165.
  8. Mohan I.V., Jagroop I.A., Mikhailidis D.P. et al. Homocysteine activates platelets in vitro. Clin Appl Thromb Hemost 2008; 14: 8-18.
  9. Karolczak K., Olas B. Mechanizm of action of homocysteine and its thiolactone in hemostasis system. Physiol Res 2009; 58 (5): 623-633.
  10. Luo F., Liu X., Wang S., Chen H. Effect of homocysteine on platelet activation induced by collagen. Nutrition 2006; 22 (1): 69-75.
  11. Riba R., Nicolaou A., Troxler M. et al. Altered platelet reactivity in peripheral vascular disease complicated with elevated plasma homocysteine levels. Atherosclerosis 2004; 175 (1): 69-75.
  12. Bigalke B., Schuster A., Sopova K. et al. Platelets in atherothrombosis - diagnostic and prognostic value of platelet activation in patients with atherosclerotic diseases. Curr Vasc Pharmacol 2012; 10 (5): 589-596.
  13. Santarelli L., Gabrielli M., Cremonini F. et al. Atrophic gastritis as a cause of hyperhomocysteinaemia. Aliment Pharmacol Ther 2004; 19 (1): 107-111.
  14. Zoccali C., Jager K.J. Hyperhomocysteinemia: a renal and cardiovascular risk factor? Nat Rev Nephrol 2010; 6 (12): 695-696.
  15. Goldstein L.B., Adams R., Alberts M.J. et al. Primary Prevention of ischemic stroke: a guideline from the American Heart Assotiation/American Stroke Assotiation Stroke Counsil: cosponsored by the Atherosclerotic Peripheral Vascular Disease Interdisciplinary Working Group. Stroke 2006; 37 (6): 1583-1633.
  16. Manolescu B.N., Oprea E., Farcasanu I.C. et al. Homocysteine and vitamin therapy in stroke prevention and treatment: a review. Acta Biochim Pol 2010; 57 (4): 467-477.
  17. Origlia C., Pescarmona G., Capizzi A. et al. Platelet cGMP inversely correlates with age in healthy subjects. J Endocrinol Invest. 2004; 27 (2): 1-4.
  18. Aronow W.S. Association Between Plasma Homocysteine and Vascular Atherosclerotic Disease in Older Persons. Prevent Cardiol 2000; 3 (2): 89-91.

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