Wpływ simwastatyny na stężenie białka C-reaktywnego i profil lipidowy u chorych w ostrej fazie niedokrwiennego udaru mózgu w zależności od polimorfizmu -717A>G genu CRP

Dariusz Kotlęga, Monika Białecka, Mateusz Kurzawski, Marek Droździk, Monika Gołąb-Janowska, Sylwester Ciećwież, Przemysław Nowacki

Abstrakt


Wstęp: Patogeneza i ryzyko wystąpienia udaru niedokrwiennego mózgu związane są z obecnością zmian zapalnych biorących udział w rozwoju miażdżycy. Powszechnie stosowanym wykładnikiem procesu zapalnego jest stężenie białka C-reaktywnego (CRP) w surowicy. Poziom CRP wykorzystuje się w ocenie ryzyka wystąpienia i rokowania w chorobach sercowo-naczyniowych oraz w udarze. Stężenie CRP podlega wpływom czynników genetycznych, takich jak polimorfizm genetyczny, oraz środowiskowym, wśród których znajduje się stosowanie statyn. Celem pracy było ustalenie potencjalnego wpływu simwastatyny na stężenie CRP i profil lipidowy w udarze z uwzględnieniem wariantu polimorfizmu -717A>G genu CRP.

Materiały i metody: Do badania włączono 125 chorych hospitalizowanych z powodu udaru niedokrwiennego mózgu. Na podstawie kryteriów włączenia i wyłączenia do I grupy zakwalifikowano 95, a do grupy II – 30 chorych. Pacjenci z grupy I otrzymywali simwastatynę wdawce 40 mg od 1. doby, natomiast w grupie II nie stosowano tego leczenia. U wszystkich chorych oznaczono stężenie CRP i profil lipidowy w 1. i 10. dobie hospitalizacji oraz oznaczono wariant polimorfizmu -717A>G genu CRP.

Wyniki: W grupie I i II odnotowano istotny wzrost stężenia CRP, pomimo leczenia simwastatyną. U osób w grupie I i II nie stwierdzono istotnego wpływu poszczególnych wariantów polimorfizmu -717A>G genu CRP na zmianę stężenia CRP i profilu lipidowego pomiędzy 1. a10. dobą hospitalizacji.

Wnioski: Simwastatyna nie wpływa na stężenie CRP w ostrej fazie udaru mózgu w zależności od jakiegokolwiek wariantu polimorfizmu -717A>G genu CRP. Zastosowanie simwastatyny w ostrej fazie udaru niedokrwiennego mózgu wyraźnie wpływa na profil lipidowy, przy czym efekt nie jest zależny od wariantów polimorfizmu -717A>G genu CRP.

 


Słowa kluczowe


stroke; genetic polymorphism; C-reactive protein; lipids; atherosclerosis; statins

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Bibliografia


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DOI: http://dx.doi.org/10.21164/pomjlifesci.246

Copyright (c) 2017 Dariusz Kotlęga, Monika Białecka, Mateusz Kurzawski, Marek Droździk, Monika Gołąb-Janowska, Sylwester Ciećwież

URL licencji: https://creativecommons.org/licenses/by-nc-nd/3.0/pl/