Hubungan Profil Lipid dan Kadar High-Sensitivity C-Reactive Protein dengan Outcome Pasien Stroke Iskemik Akut

Stefanus Erdana Putra, Fauzi Novia Isnaening Tyas, Muhammad Hafizhan, Raden Ajeng Hanindia Riani Prabaningtyas, Diah Kurnia Mirawati

Abstract

Pendahuluan: Stroke adalah penyebab utama kecacatan jangka panjang dengan dampak klinis dan sosial ekonomi yang signifikan di seluruh dunia. Hiperlipidemia dan inflamasi memainkan peranan penting dalam patofisiologi stroke iskemik. Meskipun high-sensitivity C-Reactive Protein (hs-CRP) dan kadar lipid merupakan penentu risiko penyakit pembuluh darah, kekuatan penggunaan biomarker ini dalam penentuan prognosis stroke iskemik belum dapat dipastikan. Penelitian ini bertujuan untuk mengetahui hubungan kadar hs-CRP dan profil lipid pada pasien stroke iskemik akut di Rumah Sakit Universitas Sebelas Maret dan memahami hubungan antara biomarker tersebut dengan outcome jangka pendek.

Metode penelitian: Penelitian cross-sectional dilakukan pada 34 pasien dengan serangan stroke iskemik pertama kali. Profil lipid dan hs-CRP diukur pada hari pertama masuk rumah sakit. Defisit neurologis diukur menggunakan National Institutes of Health Stroke Scale (NIHSS) dan outcome diukur menggunakan Barthel Index pada hari ke-7 perawatan di unit stroke. Selanjutnya, kadar serum hs-CRP dan profil lipid dianalisis korelasinya dengan defisit neurologis dan outcome jangka pendek.

Hasil penelitian: Pasien stroke iskemik memiliki kadar hs-CRP, kolesterol total (TC), trigliserida (TG), low-density lipoprotein (LDL) yang lebih tinggi; serta kadar high-density lipoprotein (HDL) yang lebih rendah dari kriteria normal. Berdasarkan uji korelasi Pearson, LDL memiliki korelasi signifikan dengan NIHSS (r = 0,447; p = 0,008) sedangkan hs-CRP memiliki korelasi signifikan yang lebih kuat dengan Barthel Index daripada NIHSS (r = -0,412; p = 0,015). TC dan HDL juga memiliki korelasi signifikan dengan NIHSS.

Kesimpulan: Penelitian ini menunjukkan bahwa profil lipid dan hs-CRP dapat digunakan sebagai prediktor prognosis outcome stroke iskemik akut.

 

Introduction: Stroke is the leading cause of long-term disability with significant clinical and socioeconomic impact worldwide. Hyperlipidemia and inflammation play major roles in ischemic stroke. While high-sensitivity C-Reactive Protein (hs-CRP) and lipid levels are established risk determinants for vascular disease, the relative strength of these biomarkers for ischemic stroke is uncertain. The purpose of this study is to investigate the association of hs-CRP levels and lipid profile in acute ischemic stroke patients and understand correlation between those markers and short-term outcome.

Methods: This was a cross-sectional study of 34 first-timer ischemic stroke patients. Lipid profiles and hs-CRP were measured on admission day. The neurological deficit was quantified using National Institutes of Health Stroke Scale (NIHSS) and outcome was quantified using Barthel Index at the 7th day in stroke unit. Serum level of hs-CRP and lipid profile were estimated and correlated with neurological deficit and short-term outcome.

Results: Ischemic stroke patients had higher levels of hs-CRP, total cholesterol (TC), triglyceride (TG), low-density lipoprotein (LDL); and lower level of high-density lipoprotein (HDL) than normal criteria. Based on Pearson correlation test, LDL had significant correlation with NIHSS (r=0.447; p=0.008) while hs-CRP had stronger significant correlation with Barthel Index than NIHSS (r=-0.412; p=0.015). TC and HDL also had significant correlation with NIHSS.

Conclusions: This research suggests that lipid profile and hs-CRP can be used as predictors of prognosis for acute ischemic stroke outcome. Keywords: Barthel index, C-reactive protein, National Institutes of Health Stroke Scale, lipid profile, ischemic stroke.

Keywords

Barthel Index; C-Reactive Protein; National Institutes of Health Stroke Scale; profil lipid; stroke iskemik

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References

Kustiowati, E. 2003. Trombosis di bidang neurologi: stroke iskemik. Semarang: Bagian Neurologi Universitas Diponegoro.

Kementerian Kesehatan Republik Indonesia. 2018. Laporan Hasil Riset Kesehatan Dasar Indonesia Tahun 2018. Jakarta: Kementerian Kesehatan Republik Indonesia.

Dinata CA, Safrita Y, Sastri S. 2013. Gambaran Faktor Resiko dan Tipe Stroke pada Pasien Rawat Inap di Bagian Penyakit Dalam RSUD Kabupaten Solok Selatan Periode 1 Januari 2010-31 Juni 2012. Jurnal Kesehatan Andalas; 2(2):16-22.

Aguiar FJB, Ferreira-Junior M, Sales MM, Cruz-Neto LM, Fonseca LAM, Sumita NM, et al. 2013. C-reactive Protein: Clinical Applications and Proposals for a Rational Use. Associacao Medica Brasileira; 59(1):85-92.

Zhou Y, Han W, Gong D, Man C, Fan Y. 2015. Hs-CRP in Stroke: A Meta Analysis. Clinica Chemica Act.; 26(1):15-24.

Misbach J, Ali W. 2001. Stroke in Indonesia: a first large prospective hospital-based study of acute stroke in 28 hospitals in Indonesia. Journal of Clinical Neuroscience; 8(3):245-249.

Napoli M, Papa F, Bocola V. 2001. Prognostic influence of increased C-reactive protein and fibrinogen levels in ischemic stroke. Stroke; 32(1):133-138.

Rost NS, Wolf PA, Kase CS, Kelly-Hayes M, Silbershatz H, Massaro JM, et al. 2001. Plasma concentration of C-reactive protein and risk of ischemic stroke and transient ischemic attack: the Framingham study. Stroke; 32(11):2575-2579.

Wakugawa Y, Kiyohara Y, Tanizaki Y, Kubo M, Ninomiya T, Hata J, et al. 2006. C-reactive protein and risk of first-ever ischemic and hemorrhagic stroke in a general Japanese population: the Hisayama Study. Stroke; 37(1):27-32

Sabatine MS, Morrow DA, Jablonski KA, Rice MM, Warnica JW, Domanski MJ, et al. 2007. Prognostic significance of the Centers for Disease Control/American Heart Association high-sensitivity C-reactive protein cut points for cardiovascular and other outcomes in patients with stable coronary artery disease. Circulation; 115(12): 1528-1536.

Hulthe J, Wikstrand J, Mattsson-Hulten L, Fagerberg B. 2002. Circulating ICAM-1 (intercellular cell-adhesion molecule 1) is associated with early stages of atherosclerosis development and with inflammatory cytokines in healthy 58-year-old men: the Atherosclerosis and Insulin Resistance (AIR) study. Clin Sci (Lond); 103(2):123-129.

Chen C, Nan B, Lin P, Yao Q. 2008. C-reactive protein increases plasminogen activator inhibitor-1 expression in human endothelial cells. Thromb Res; 122(1):125-133.

Ridker PM, Cook N. 2004. Clinical usefulness of very high and very low levels of C-reactive protein across the full range of Framingham risk scores. Circulation; 109:1955–1959.

Dandona P. 2008. Effects of antidiabetic and antihyperlipidemic agents on C-reactive protein. Mayo Clin Proc; 83:333–342.

Dhamoon MS, Moon YP, Paik MC, Boden-Albala B, Rundek T, Sacco RL, et al. 2009. Long-term functional recovery after first ischemic stroke: the Northern Manhattan Study. Stroke; 40(8):2805–2811.

Chang KC, Tseng MC, Tan TY, Liou CW. 2006. Predicting 3-month mortality among patients hospitalized for first-ever acute ischemic stroke. J Formos Med Assoc; 105(4):310–317.

Young FB, Weir CJ, Lees KR. 2005. GAIN International Trial Steering Committee and Investigators. Comparison of the National Institutes of Health Stroke Scale with disability outcome measures in acute stroke trials. Stroke; 36:2187–2192.

Lyden PD, Lau GT. 1991. A critical appraisal of stroke evaluation and rating scales. Stroke; 22:1345–1352.

Bahadursingh S, Beharry K, Maharaj K, Mootoo C, Sharma P, Singh J, et al. 2009. C-reactive protein: adjunct to cardiovascular risk assessment. West Indian Med J; 58(6):551–555.

Audebert HJ, Rott MM, Eck T, Haberl RL. 2004. Systemic inflammatory response depends on initial stroke severity but is attenuated by successful thrombolysis. Stroke; 35(9):2128–2133.

Feinberg WM, Erickson LP, Bruck D, Kittelson J. 1996. Hemostatic markers in acute ischemic stroke. Association with stroke type,severity, and outcome. Stroke; 27(8):1296–300.

Pepys MB, Hirschfield GM, Tennent GA, Gallimore JR, Kahan MC, Bellotti V, et al. 2006. Targeting C-reactive protein for the treatment of cardiovascular disease. Nature; 440(7):1217–1221.

Amarenco P, Labreuche J. 2009. Lipid management in the prevention of stroke: review and updated meta-analysis of statins for stroke prevention. Lancet Neurol; 8:453-463.

Gorelick PB, Mazzone T. Plasma lipids and stroke. 1999. J Cardiovasc Risk; 6(4):217-221.

Konishi M, Iso H, Komachi Y, Iida M, Shimamoto T, Jacobs DR Jr., et al. 1993. Associations of serum total cholesterol, different types of stroke, and stenosis distribution of cerebral arteries. The Akita Pathology Study. Stroke; 24(7):954-964.

Navab M, Berliner JA, Subbanagounder G. 2001. HDL and the inflammatory response induced by LDL-derived oxidized phospholipids. Arterioscler Thromb Vasc Biol; 21:481-488.

Lapergue B, Moreno JA, Dang BQ. 2010. Protective effect of high-density lipoprotein-based therapy in a model of embolic stroke. Stroke; 41:1536–1542.

Chen J, Cui X, Zacharek A. 2007. Niaspan increases angiogenesis and improves functional recovery after stroke. Ann Neurol; 7:49–58.

Adibhatla RM, Hatcher JF. 2010. Lipid oxidation and peroxidation in CNS health and disease: from molecular mechanisms to therapeutic opportunities. Antioxid Redox Signal; 12:125-169.

Pedro-Botet J, Senti M, Nogues X, Rubies-Prat J, Roquer J, D'Olhaberriague L, et al. 1992. Lipoprotein and apolipoprotein profile in men with ischemic stroke. Role of lipoprotein (a), triglyceride-rich lipoproteins, and apolipoprotein E polymorphism. Stroke; 23(11):1556-1562.

Hachinski V, Graffagnino C, Beaudry M, Bernier G, Buck C, Donner A, et al. 1996. Lipids and stroke: a paradox resolved. Arch Neurol; 53(4):303-308.

Kar AM, Garg RK, Gaur SPS. 1993. Serum Lipids and Stroke. Neurol India; 41(1):1-5.

Willey JZ, Xu Q, Boden-Albala B, Paik MC, Moon YP, Sacco RL, et al. 2009. Lipid profile components and risk of ischemic stroke: the Northern Manhattan Study (NOMAS). Arch Neurol; 66(11):1400-1406.

Butterworth RJ, Marshall WJ, Bath PMW. 1997. Changes in serum lipid measurements following acute ischaemic stroke. Cerebrovasc Dis; 7:10–13.

Tan CE, Squires L, Caslake MJ. 1995. Relationship between very low and low density lipoprotein subfractions in normolipaemic men and women. Arterioscler Thromb Vasc Biol; 13:1839–1848.

Kempf M: Effect of nutrition on combined hyperlipidaemia. 1997. Ann Endocrinol; 58:292–296.

Bittner V. 2008. Impact of Gender and Life Cycle on Triglyceride Levels. Omaha Nebraska: Medscape Family Medicine (CME).

Poehlman ET, Toth MJ, Ades PA, and Rosen CJ. 1997. Menopause-associated changes in plasma lipids, insulin-like growth factor I and blood pressure: a longitudinal study. European Journal of Clinical Investigation; 27(4):322–326.

Carroll MD, Lacher DA, Sorlie PD. 2005. Trends in serum lipids and lipoproteins of adults, 1960–2002. Journal of the American Medical Association; 294(14):1773–1781.

Devaraj S, Du Clos TW, Jialal I. 2005. Binding and internalization of C-reactive protein by Fcgamma receptors on human aortic endothelial cells mediates biological effects. Arterioscler Thromb Vasc Biol; 25(7):1359-1363.

Muir KW, Weir CJ, Alwan W, Squire IB, Lees KR. 1999. C-reactive protein and outcome after ischemic stroke. Stroke; 30(5): 981-985.

DOI: https://doi.org/10.13057/smj.v3i2.43779

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