Assessment of prolactin associated platelet activation in ischemic stroke

Yıl 2012, , 1 - 6, 01.03.2012

Ayşegül Akagündüz Ege Şule Bilen Fikri Ak

https://doi.org/10.5799/ahinjs.01.2012.01.0101

Öz

Objectives: We aimed to investigate whether there were any relations between prolactin levels, prolactin associated platelet activation and ischemic stroke, and whether they had role in etiology of ischemic stroke. Materials and methods: Totally 57 patients with the diagnosis of acute ischemic stroke and 43 age and sex matched controls with no history of ischemic vascular diseases were included in the study. Prolactin levels, mean platelet volume (MPV) a marker of platelet activation, and platelet count, of the patients, after 12 hours of fasting, compared with the measurements of control group. Results: Patients had significantly higher prolactin levels. A correlation between prolactin levels and early measurements of MPV was not detected. While there was no difference in terms of MPV, the platelet count was significantly higher in the patient group. Conclusions: In the present study, the existence of an effect of prolactin on the mean platelet volume, or a relationship between early ischemic stroke and MPV could not be shown. However, in ischemic stroke patients, in early phase, presence of higher levels of prolactin and platelet count may be meaningful in etiology of ischemic events. Besides, presence of higher prolactin levels in early phase of ischemic stroke may lead to consider the potential role of prolactin elevation in ischemic stroke pathogenesis.

Anahtar Kelimeler

Ischemic stroke, prolactin, mean platelet volume, platelet count

İskemik inmede prolaktin ilişkili platelet aktivasyonunun değerlendirilmesi

Öz

Amaç: İskemik inme ile prolaktin seviyeleri, prolaktin ilişkili platelet aktivasyonu arasında ilişki olup olmadığı ve iskemik inme etyolojisinde rolleri olup olmadığının araştırılmasını amaçladık. Gereç ve yöntem: Çalışmaya akut iskemik inme tanısı almış olan 57 hasta ile iskemik vasküler hastalık hikayesi olmayan, yaş ve cinsiyet uyumlu 43 kontrol olgusu dahil edildi. Hastaların 12 saat açlığı takiben değerlendirilen prolaktin seviyeleri, platelet sayısı ve platelet aktivasyonunun bir göstergesi olan ortalama platelet hacmi (OPH) kontrol grubunun ölçümleri ile karşılaştırıldı. Bulgular: Hastaların prolaktin seviyeleri anlamlı şekilde yüksekti. Prolaktin seviyeleri ile erken OPH ölçümleri arasında bir ilişki bulunmadı. OPH açısından bir fark yok iken platelet sayısı hasta grubunda anlamlı şekilde yüksekti. Sonuç: Bu çalışmada prolaktinin ortalama platelet hacmi üzerinde bir etkisinin varlığı veya erken iskemik inme ve OPH arasında bir ilişki gösterilememiştir. Ancak iskemik inmeli hastalarda, erken dönemde yüksek prolaktin seviyesi ve yüksek platelet sayısı varlığı iskemik olayların etyolojisinde anlamlı olabilir. Bunun yanı sıra iskemik inmenin erken döneminde yüksek prolaktin seviyesi bulunması iskemik inmenin patogenezinde prolaktin artışının rolü olabileceğini düşündürebilir.

Anahtar Kelimeler

İskemik inme, prolaktin, ortalama platelet hacmi, platelet sayısı

Kaynakça

• Biller J, Love BB, Schneck MJ. Ischemic cerebrovas- cular disease.In Bradley WJ, Daroff RB, Fenichel GM, Jankovic J, eds. Neurology in Clinical Practice 5th edn. Butterworth-Heinemann . Elsevier, 2008:1165- 1220.
• Ruggeri ZM.; Platelets in atherothrombosis. Nat Med 2002;8(11):1227-34.
• Gawaz M, Langer H, May AE. Platelets in inflammation and atherogenesis. J Clin Invest 2005;115(12):3378- 84.
• Bath P, Algert C, Chapman N, Neal B. Association of mean platelet volume with risk of stroke among 3134 individuals with history of cerebrovascular dis- ease. PROGRESS Collaborative Group. Stroke 2004;35(3):622-6.
• Fateh-Moghadam S, Htun P, Tomandl B et al. Hyperre- sponsiveness of platelets in ischemic stroke. Thromb Haemost 2007;97(6):974-8.
• Fisher M, Levine PH, Fullerton AL et al. Marker proteins of platelet activation in patients with cerebrovascular disease. Arch Neurol 1982;39(11):692-5.
• Fisher M, Francis R. Altered coagulation in cerebral ischemia. Platelet, thrombin, and plasmin activity. Arch Neurol 1990;47(10):1075-9.
• Joseph R, D’Andrea G, Oster SB, Welch KM. Whole blood platelet function in acute ischemic stroke. Im- portance of dense body secretion and effects of anti- thrombotic agents. Stroke 1989;20(1):38-44.
• Tohgi H, Suzuki H, Tamura K, Kimura B. Platelet vol- ume, aggregation, and adenosine triphosphate re- lease in cerebral thrombosis. Stroke 1991;22(1):17-21
• Serebruany VL, Malinin AI, Oshrine BR et al. Lack of uniform platelet activation in patients after ischemic stroke and choice of antiplatelet therapy. Thromb Res 2004;113(3-4):197-204.
• Wallaschofski H, Donné M, Eigenthaler M et al. PRL as a novel potent cofactor for platelet aggregation. J Clin Endocrinol Metab 2001;86(12):5912-9
• Wallaschofski H, Kobsar A, Sokolova O, Eigenthaler M, Lohmann T. Co-activation of platelets by prolactin or leptin-pathophysiological findings and clinical impli- cations. Horm Metab Res 2004;36(1):1-6.
• Wilson JL, Hareendran A, Hendry A, et al. Reliabil- ity of the modified rankin scale across multiple raters: benefits of a structured interview. Stroke 2005;36: 777–81.
• Raaz D, Wallaschofski H, Stumpf C et al. Increased prolactin in acute coronary syndromes as putative Co-activator of ADP-stimulated P-selectin expression. Horm Metab Res 2006;38(11):767-72.
• Wallaschofski H, Kobsar A, Koksch M et al. Prolac- tin receptor signaling during platelet activation. Horm Metab Res 2003;35(4):228-35.
• Schwarz S, Schwab S, Klinga K, Maser-Gluth C, Bet- tendorf M. Neuroendocrine changes in patients with acute space occupying ischaemic stroke. J Neurol Neurosurg Psychiatry 2003;74(6):725-7.
• Van den Berghe G, de Zegher F, Bouillon R. Clinical review 95: Acute and prolonged critical illness as dif- ferent neuroendocrine paradigms. J Clin Endocrinol Metab 1998;83(6):1827-34.
• Greisenegger S, Endler G, Hsieh K, Tentschert S, Mannhalter C, Lalouschek W. Is elevated mean plate- let volume associated with a worse outcome in pa- tients with acute ischemic cerebrovascular events? Stroke 2004;35(7):1688-91.
• Kinlough-Rathbone RL, Mustard JF, Packham MA, Harfenist EJ. Factors influencing the deaggregation of chymotrypsin-treated human platelets aggregated by fibrinogen. Thromb Haemost 1983 28;49(3):196-8.
• O’Malley T, Langhorne P, Elton RA, Stewart C. Plate- let size in stroke patients. Stroke 1995;26(6):995-9.
• Jackson SR, Carter JM. Platelet volume: laboratory measurement and clinical application. Blood Rev 1993;7(2):104-13.
• D’Erasmo E, Aliberti G, Celi FS, Romagnoli E, Vecci E, Mazzuoli GF. Platelet count, mean platelet volume and their relation to prognosis in cerebral infarction. J Intern Med 1990;227(1):11-4.
• Shah AB, Beamer N. Enhanced in vivo platelet activa- tion in subtypes of ischemic stroke. Coull BM. Stroke 1985;16(4):643-7.