Journals / Türk Beyin Damar Hastalıkları Dergisi / 2000 / Cilt: 6 - Sayı: 2

Plasma concentrations of soluble E-selectin and P-selectin in acute middle cerebral artery infarction: A special impact to the short-term prognosis and infarct topography

Akut orta serebral arter alanı infarktlarında serum selektin düzeyleri: Kısa dönem prognozu ve infarkt topografisi ile ilişkisi

Pages
47–54
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

These results indicate that endothelial cells dysfunction shows a correlation with the size and clinical severity of cerebral infarction and may imply some prospective aspects on the prognosis.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:To define the pathophysiological role of selectins in acute ischemic stroke pathogenesis, sE-selectin and sP-selectin concentrations during the first 24 hours following event were measured by ELISA in 42 patients with cerebral infarction located in the territory of middle cerebral artery (MCA) and 13 age-matched symptom-free controls.
📊
Key Findings & Data:MCA infarcts were classified into four categories according to Ueda system as isolated lenticulostriate (basal ganglia: type ı, n=8), extensive cortical-subcortical )lobar: type n, n=12), large hemispheric (malign: type m, n=7), and localized cortical-subcortical (lobular: type iV, n=15).
💡
Conclusion & Impact:These results indicate that endothelial cells dysfunction shows a correlation with the size and clinical severity of cerebral infarction and may imply some prospective aspects on the prognosis.
🔬Design:Research Article
📍Scope:2099 Verileri
⚙️Variables:E-selektin · Serebral arterler · Beyin iskemisi

Abstract

To define the pathophysiological role of selectins in acute ischemic stroke pathogenesis, sE-selectin and sP-selectin concentrations during the first 24 hours following event were measured by ELISA in 42 patients with cerebral infarction located in the territory of middle cerebral artery (MCA) and 13 age-matched symptom-free controls. MCA infarcts were classified into four categories according to Ueda system as isolated lenticulostriate (basal ganglia: type ı, n=8), extensive cortical-subcortical )lobar: type n, n=12), large hemispheric (malign: type m, n=7), and localized cortical-subcortical (lobular: type iV, n=15). The groups with various type MCA territory infarction and the controls were not differ with age, gender, prevalence of hypertension, diabetes mellitus, smoking, coronary artery disease, congestive heart failure, stroke etiological subtype (according to modified TOAST classification system as cardioembolic, large artery atherothrombotic, mixed, undetermined and other), bilateral carotid doppler ultrasonography, electrocardiography, transthoracic echocardiography and blood sampling interval. Hospital case fatality ratio and stroke severity graded by NıHSS were higher in the malign MCA group (p=0.0167). There is no difference among groups with simultaneous blood glucose and cholesterol concentrations, hemoglobin, the percents of neutrophyl, monocyte and thrombocyte counts whereas the leukocyte counts were found to be higher in basal ganglia, lobar and malign MCA infarctions than controls (p=0.0002). The mean sE-selectin levels were significantly higher in patients with large hemispheric type infarction (50.7±23.2 hg/ml) than other type infarcts (basal ganglia: 21.6+6.7, lobar: 26.2±10.8, lobular: 24.3±16.4) and the control group (21.9±9.2) (p=0.0005). There was no significant difference in sP-selectin concentrations among MCA infarction type and controls (Basal ganglia: 53.5±16.9, lobar: 63.5±31.8, malign: 83.8±46.5, lobular: 66.1±42.4, and controls: 46.4±25.1, p=0.2099. Each selectin levels were well correlated stroke severity assessed by NiH stroke scale (r=0.51, p=0.0001 for sEsel and r=0.36, p=0.0210 for sPsel). The patients with atrial fibrillation (AF, n=11) tended to have lower sP-selectin concentrations (59.1±33.2 versus 85.16±41.3, p=0.0575). whereas their sE-selectin levels were found to be similar (38.1±20.9 versus 25.4±15.5) in comparison with the patients without AF. A weak correlation was determined between the sPsel levels and the degree of carotid artery disease (p=0.0685). The other clinical and laboratory parameters had no significant effects on selectin levels, in patients dead during hospitalization (n=8), sEsel concentrations were higher than patients survived (42.3±15.3 versus 25.6±16.9, p=0.0140). These results indicate that endothelial cells dysfunction shows a correlation with the size and clinical severity of cerebral infarction and may imply some prospective aspects on the prognosis.

Özet

Bu çalışmada 42 orta serebral arter (MCA) alanı infarktında, ilk 24 saatte sistemik E-selektin (sEsel) ve P-selektin (sPsel) düzeyleri, 13 kontrolle karşılaştırılarak bu faktörlerin iskemik inmedeki rolü incelenmiştir. MCA alanı infarktları Ueda sistemine göre izole lentikülostriat (bazal ganglia; 8), yaygın kortikal+subkortikal (lober; 12), tüm (malign; 7) ve izole kortikal+subkortikal (lobuler; 15) olarak 4 gruba ayrılmıştır. Bu gruplar ve kontrol grubu arasında yaş, cinsiyet, hipertansiyon, DM, sigara içimi, koroner arter hastalığı, konjestif kalp yetmezliği, inme tipi (modifiye TOAST sistemine göre kardiyoembolik, büyük arter aterotrombotik, miks, bulunamamış olan ve diğer olarak sınırlanmıştır), ekokardiyografi, karotis doppler USG, EKG bulguları, kan örneği alınma zamanları açısından fark yoktur. N1HSS ile derecelendirilen inme klinik şiddeti ve hastanede ölüm oranı malign MCA grubunda daha yüksektir (p=0.0167). Gruplar arasında simültane kan şekeri, kolesterol düzeyi, hemoglobin, % nötrofil, % monosit, trombosit sayısı açısından fark yok iken lökosit sayısı bazal ganglia, lober ve malign tip infarktlarda kontrol grubuna göre yüksek bulunmuştur (p=0.0002). sEsel düzeyi malign MCA infarktlarında (50.7±23.2 hg/ml) hem diğer tip infarktlardan (bazal ganglia: 21.6+6.7, lober: 26.2±10.8, lobuler: 24.3±16.4) hem de kontrol grubundan (21.9±9.2) anlamlı olarak yüksektir (p=0.0005). sPsel düzeyleri ise infarkt gruplarında (bazal ganglia: 53.5±16.9, lober: 63.5±31.8, malign: 83.8±46.5, lobuler: 66.1±42.4) kontrol grubundan (46.4±25.1) farklı değildir (p=0.2099). inme klinik şiddeti (NIHSS) ile sEsel (r=0.51, p=0.0001) ve sPsel (r=0.36, p=0.0210) arasında anlamlı (+) korelasyon saptanmıştır. AF'lu hasta (n=ll) subgrubunda sEsel diğer hastalardan farksız iken (38.1±20.9'e 25.4±15.5), sPsel düzeyi daha düşük olmaya eğilimlidir (59.1±33.2'ye 85.16±41.3, p=0.0575). Karotis aterosklerozu derecesi ile sPsel düzeyi arasında zayıf bir ilişki saptanmıştır (p=0.0685). Diğer klinik ve laboratuar parametreleri selektin düzeylerine etkimemektedir. Hastanede ölen hastalarda (n=8) sEsel düzeyi (42.3±15.3) sağ kalanlardan (25.6±16.9) daha yüksektir (p=0.0140). Bu sonuçlar akut iskemik inmede endotel disfonksiyonunun infarktın büyüklüğü ile değiştiğini ve prognostik önemi olduğunu işaret etmektedir.

🔖

Cite This Article

TOPÇUOĞLU, M. A., VRSEVSA, Y., ÖZCEBE, O. İ., SARIBAŞ, O. (2000). Plasma concentrations of soluble E-selectin and P-selectin in acute middle cerebral artery infarction: A special impact to the short-term prognosis and infarct topography. Türk Beyin Damar Hastalıkları Dergisi, Cilt: 6 - Sayı: 2, 47–54. https://ajindex.com/articles/409150

References (21)

  1. Adams DH, Shaw 5. Leukocyte endothelial interactions and regulation of lukocyte migration. Lancet 1994; 343: 831-836
  2. McEver RP, Moore KL, Cummings RD. Leukocyte; trafficking mediaated by selectin-carbohydrate interactions. J Biol Chem 1995:270:11025-11028
  3. Frenette PS, Wagner DD. Adhesion molecules-Part 1. New Engl J Med 1996; 334:1527-1529
  4. Frenette PS, Denisa D, Wagner DD. Adhesion molecules-Part 2: Blood vessels and blood cells. New Engl J Med 1996; 335: 43-45
  5. Bevilacqua MP, Nelson RM. Selectins. J Clin ınvest 1993; 91: 379-387
  6. Kansas GS. Selectins and their ligands: Current concepts and controversies. Blood 1996; 88:3259-3287
  7. Kim JS. Cytokines and adhesion molecules in stroke and related diseases. J Neurol Sci 1996-137: 69-78
  8. Becker KJ. ınflammation and acute stroke. Cur Opin Neurol 1998; 11:45-49
  9. Ten Cate JW, van der Poll T, Levi et al. Cytokines: Triggers of clinical thrombotic disease. Thromb Haemost 1997; 78:415-419
  10. Adhesion Molecules. http://www.bi-bioproducts.de/ products/data.html 11. Güç D. Adezyon molekülleri. Hacettepe Tıp Dergisi 1997; 28 (2): 72-77
  11. DeGraba TJ. The role of inflammation after stroke-Utility of pursuing anti-adhesion molecule therapy. Neurology 1998; 51 (suppl-3): 62-68
  12. Bednar MM, Cordell EC, Balazy M, Falck JR. Antineutrophil strategies. Neurology 1997;49 (suppl-4): 20-22
  13. Topçuoğlu MA, Kayahan K, Sarıbaş O. İskemik inmelerde yaş-etyoloji ilişkisi (697 hasta analizi)
  14. Ulusal Nöroloji Kongresi Kitabı- Ufuk Matbaacılık-1996; 730-736
  15. Ueda S, Fujitsu K, Inomori S, Kuwabara T. Thrombotic occlusion of the middler cerebral artery. Stroke-1992; 23: 1761-1766
  16. Zenker G, Koltringer P, Bone G et al. Lipoprotein(a) as a strong indicator for cerebrovascular disease. Stroke 1986; 17: 942-945
  17. Brickner ME. Cardioembolic stroke. Am J Med 1996; 100: 465-474
  18. Thiagarajan RR, Winn RK, Harlan JM. The role of leukocyte and endothelial adhesion molecules in ischemia-reperfusion injury. Thromb Haemost 1997; 78: 310-314
  19. Wu G, LI F, LI P, Ruan C. Detection of plasma alpha-granule membrane protein GMP-140 using radiolabeled monoclonal antibodies in thrombotîc diseases. Haemostasis 1993; 23: 121-128
  20. Faasbender K, Mossner R, Motsch L, Kischka U, Grau A, Hennerici M. Circulating selectin and immunglubin type adhesion molecules in acute isehemic stroke. Stroke 1995; 26: 1361-1364
  21. Frijns CJM, Kapelle LJ, Van Gijn J, Nieuwenhuis HK, Sixma JJ, Fijnheer R. Soluble adhesion