THE EVALUATION OF PLASMA HOMOCYSTEINE AND CRP LEVELS IN SUBJECTS WITH STROKE

Yıl 2012, Cilt: 6 Sayı: 2, 44 - 49, 21.08.2012

Kübranur Karatoprak

Öz

Background and Aim: Higher homocysteine and CRP levels are risk factors for endothelial dysfunction and atherosclerosis. Several studies have shown that homocysteine and CRP levels are increased in patients with stroke. In this study, we aimed to assess homocysteine and CRP levels in cases with stroke.
Materials and Methods: A total of 48 healthy controls and 119 patients diagnosed with stroke in the Neurology Department of Ankara Numune Training and Research Hospital between January and June 2012 were inluded in the study. In the blood samples of all individuals homocysteine levels were determined by HPLC and triglyceride, total cholosterol, HDL and CRP concentrations were measured by Roche P800 otoanalyzer. Serum ferritin, vitamin B12 and folat levels were analyzed by Roche Cobas e-601. Statistical Package for the Social Sciences (SPSS, version 13.0, Chicago, IL, USA) was used to evaluate the data.
Results: Levels of homocysteine and CRP were significantly higher in the stroke patients than in the control group (p<0.01). Serum HDL cholesterol concentrations were lower in the stroke patients than in the control group (p<0.05). Other parameters were not significantly different when compared the groups.
Conclusions: It is shown that plasma levels of homocysteine and CRP are associated with cerebrovascular diseases. In this study, the concentrations of homocysteine and CRP were higher in patients with stroke. These data suggest that stroke and homocysteine and CRP levels are related. These parameters may be used to establish the risk of cerebrovascular diseases.

Anahtar Kelimeler

Homocysteine, CRP, stroke.

STROK HASTALARININ HOMOSİSTEİN ve CRP DÜZEYLERİNİN İNCELENMESİ

Öz

Giriş ve Amaç: Homosistein ve CRP yüksekliği, endotel disfonksiyonu ve ateroskleroz riskini arttırmaktadır. Yüksek CRP ve homosistein düzeylerinin iskemik strok ve koroner iskemik hastalıklar için bir risk faktörü olduğu öne sürülmektedir. Biz bu çalışmada strok tanısı almış hastaların homosistein ve CRP düzeylerini incelemeyi amaçladık.

Materyal ve Metod: Ocak-Haziran 2012 tarihleri arasında Ankara Numune Eğitim ve Araştırma Hastanesi Nöroloji Kliniği’ne başvuran 119 strok tanısı almış hasta ve 48 sağlıklı gönüllü çalışmaya dahil edilmiştir. Alınan kan örneklerinden homosistein düzeyleri HPLC ile, trigliserit, total kolesterol, HDL ve CRP düzeyleri Roche P800 otoanalizöründe, serum ferritin, B12 vitamini ve folat düzeyleri ise Roche Cobas e-601 cihazında çalışıldı. Statistical Package for the Social Sciences (SPSS, version 13.0, Chicago, IL, USA) programı ile veriler değerlendirildi.
Bulgular: Strok grubunun homosistein ve CRP düzeyleri sağlıklı kontrol grubuna göre anlamlı derecede yüksekti (p<0.01). Hasta grubunun HDL kolesterol düzeyleri ise kontrol grubuna göre anlamlı derecede düşüktü (p<0.05). Hasta ve kontrol grubu diğer parametreler açısından karşılaştırıldığında istatistiksel olarak anlamlı bir farklılık yoktu.

Tartışma: Plazma homosistein ve CRP düzeylerinin serebrovasküler hastalık ile ilişkili olduğu gösterilmiştir. Bu çalışmada strok hastalarının homosistein ve CRP düzeyleri kontrol grubuna göre anlamlı derecede yüksek bulunmuştur. Elde ettiğimiz veriler bize homosistein ve CRP düzeylerinin strok ile ilişkili olduğunu ve bu parametrelerin strok riskini önceden belirlemede kullanılabileceğini düşündürmektedir.

Anahtar Kelimeler

Homosistein, CRP, strok

Kaynakça

• 1. Adams RD, Victor M, Ropper AH. The neurology of aging. In: Adams RD, Victor M, Ropper AH, eds. Principles of Neurology. New York, NY: McGraw-Hill; 1997:608- 620.
• 2. Kumral K, Kumral E: Santral Sinir Sisteminin Damarsal Hastalıkları. İzmir: Ege Üniversitesi Tıp Fakültesi Yayınları;1993:4-446.
• 3. Adams Jr HP, Bendixen BH, Kappelle J, Biller J, Love BB, Gordon DL, Marsh EE and the TOAST Investigators. Classification of subtype of acute ischemic stroke. Definition for use in multicenter clinical trial. Stroke 1993 ;24:35-41.
• 4. Rumack C M, Wilson S R, Charboneau J W. Diagnostic Ultrasound . Second Edition, New York: Mosby; 1998: 885-916.
• 5. Berkow R, Fletcher A J , Chir B. The Merck Manual of Diagnosis and Therapy . Sixteenth Edition, Rahway, NJ: Merck and Co Inc; 1992:406-414.
• 6. Gonzales FC , Doan T H, Han S S, et all. Vascular Imaging : Angiography and the New Modalites. Extracranial Vascular Angiogaphy. Radiolagic Clinics of North America 1986; 24: 419451.
• 7. Antonella L, Luigi MB, et al. Inflammation as a Possible link between Coronary and Carotid Plaque Instability. Circulation 2004; 109: 3158-3164.
• 8. Taveras JM. Neuroradiology. In: Brain Vascular Disorders. 3rd ed. Philadelphia, Pa: Williams and Wilkins; 1996: 401-570.
• 9. Pasterkamp G, Schoneveld AH , van der Wal AC, Hijnen DJ, van Wolveren WJ, Plomp S, Tepen HL, Borst C. Inflammation of atherosclerotic cap and shoulder of the plaque is a common and locally observed feature in unruptured plaques of femoral and coronary arteries . Arterioscler Thromb and Vasc Biol 1999;19:54-58.
• 10. Jander S, Sitzer M, Schumann R. Inflammation in high-grade carotid stenosis: a possible role for macrofages and T cells in plague destabilization Stroke 1998; 29: 1625-1630.
• 11. Ridker PM, Cushman M, Stampfer MJ. Inflammation , aspirin and the risk of cardiovaskular disease in apparently healthy men. N Engl J Med 1997; 336: 973-979.
• 12. Ridker PM, Rifai N, Clearfield M, Downs JR, Weis SE, Miles JS, Gotto AM Jr. Measurement of C reactive protein for the targeting of statin therapy in the primary prevention of acute coronary events. N Engl J Med 2001; 344: 1959-1965.
• 13. Kılıçturgay K. İnflamasyonun akut faz cevabıyla izlenmesi. İmmünoloji 2000;24:226-7.
• 14. Pepys MB, Berger A. The Renaissance of C-Reactive Protein. Brit Med J 2001; 322: 4-5.
• 15. Price DT, Loscalso J. Cellular Adhesion Molecules and Atherogenesis. Am J Med 1999; 107: 85-97.
• 16. Makris M. Hyperhomocysteinemia and thrombosis. Clin Lab Haematol 2000; 22 :133-143.
• 17. Gouallie BC. Focus on homocysteine and vitamins involved in its metobo-lism. Second edition. France:Springer Verlag; 2000: 14-16.
• 18. Lim U Cassano PA. Homocysteine and blood pressure in the third national health and nutrition examination survey, 1988–1994 Am. J. Epidemiol. 2002;156:1105- 1113.
• 19. Özdemir G, Özkan S, Uzuner N, ve ark. Türkiye’de beyin damar hastalıkları için major risk faktörleri. Türk Çok Merkezli Strok Çalışması. Türk Beyin Damar Hastalıkları Dergisi 2000; 2: 31-5.
• 20. Palasik W, Fiszer U, Lechowicz W, Czartoryska B, Krzesiewicz M, Lugowska A. Assessment of relations between clinical outcome of ischemic stroke and activity of inflammatory processes in the acute phase based on examination of selected parameters. Eur Neurol 2005; 53: 188-93.
• 21. Atanassova PA, Angelova E, Tz-vetanov P, Semerdjieva M, Dimitrov BD. Modelling of increased homocysteine in ischaemic stroke: post-hoc cross-sectional matched case-control analysis in young patients. Arq Neu-ropsiquiatr 2007;65:24-31.
• 22. Whitehead AS, Bruns GA, Markham AF, Colten HR, Woods DE Isolation of human C-reactive protein complementary DNA and localization of the gene to chromosome 1. Science 1983; 221: 69-71.
• 23. Castell JV, Gomez-lechon MJ, David M, Farba R, Trullenque R, Heinrich PC. Acute-phase response of human hepatocytes: Regulation of acute-phase protein synthesis by interleukin-6. Hepatology 1990; 12:1179-1186.
• 24. Cleland SJ, Sattar N, Petrie JR, Forouhi NG, Elliott HL, Connell JMC. Endothelial dysfunction as a possible link between C-reactive protein levels and cardiovascular disease. Clin Sci (Lond) 2000; 98:531-535.
• 25. Fichtlscherer S, Rosenberger G, Walter DH, Breuer S, Dimmeler S, Zeiher AM Elevated C-Reactive Protein Levels and Impaired Endothelial Vaso-reactivity in Patients With Coronary Artery Disease. Circulation 2000; 102:1000-1006.
• 26. Cermak J, Key NS, Bach RR, Balla J, Jacob HS, Vercellotti GM. C-reactive protein induces human peripheral blood monocytes to synthesize tissue factor. Blood 1993; 82: 513-20.
• 27. Chang CY, Chen JY, Ke D, Hu ML. Plasma levels of lipophilic antioxidant vitamins in acute ischemic stroke patients: correlation to inflammation markers and neurological deficits. Nutrition 2005; 21: 987-93.
• 28. Rost NS, Wolf PA, Kase CS, Kelly-Hayes M, Silbershatz H, Massaro JM, et al. Plasma concentration of C-reactive protein and risk of ischemic stroke and transient ischemic attack: the Framingham study. Stroke 2001; 32: 2575-9.
• 29. KIM, Suk Jae, et al. Are stroke biomarkers seeing brain vessels in patients with ischemic stroke? A C-reactive protein and homocysteine study. Stroke, 2011 42.5: 1464-1468.
• 30. Graeme J Hankey, et al, clinical usefulness of plazma homocysteine in vascular dissease. MJA 2004;181:314-318.
• 31. Stanfer MJ, Malino MR et al A Prospective Study of Plasma homocystine and risk of myocardial infarction in US physicians. JAMA 1992;268:877-881.
• 32. Lim U Cassano PA. Homocysteine and blood pressure in the third national health and nutrition examination survey, 1988–1994 Am J Epidemiol 2002; 156:1105- 1113. 3. Celermajer DS, Surensen K, Ryalls M, Robinson J, Thomas O, Leonard JV, Deanfield JE Impaired endothelial function occurs in the systemic arteries of children with homozygous homo-cystinuria but not in their heterozygous parents. J Am Coll Cardiol 1993; 22:854-858.
• 34. Van Den Berg M, Boers GH, Franfen DG, et al. Hyperhomocyseinemia and endotheliai dysfunction in young pa- tients with peripheral dysfunction in young patients with peripheral arterial occlusive disease. Eur J Clin Invest 1995; 25:176-181.
• 35. Misra HP. Generation of superoxide free radical during the outooxidation of thiols. J Biol Chem 1974; 249:2151-2155.
• 36. KIM, Suk Jae, et al. Plasma fasting and nonfasting triglycerides and high-density lipoprotein cholesterol in atherosclerotic stroke: Different profiles according to low-density lipoprotein cholesterol. Atherosclerosis 2012, 223.2: 463-467.