Homocysteine levels and platelet aggregation in patients with cerebral circulatory disorders


Cite item

Full Text

Abstract

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.

About the authors

Z Sabaliauskiene

Pecпyбликaнcкая вильнюсская университетская больница

Email: Z.Sabaliauskiene@gmail.com

P Gribauskas

Институт кардиологии Каунасского медицинского университета

Email: prangryb@med.kmu.lt

V Gaigalaite

Вильнюсский университет

Email: gaigalaitevirginija@gmail.com

J Ptašekas

ЗАО "Диагноститнес системос" (Диагностические системы)

Email: diagnostinessistemos@mail.lt

V Ojeraitene

Вильнюсский университет

Email: violeta.ozeraitiene@mf.vu.lt

D Kalibatene

Вильнюсский университет

Email: danute.kalibatiene@mf.vu.lt

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.

Copyright (c) 2013 Consilium Medicum

Creative Commons License
This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.
 
 


This website uses cookies

You consent to our cookies if you continue to use our website.

About Cookies