Da li pentraksin -3 doprinosi sniženju koncentracije lipoproteina niske gustine i terapiji statinima?

Pentraksina -3 i lipoprotein niske gustine nakon terapije statinima

  • Vesna Vuković-Dejanović Institut za rehabilitaciju, Beograd
  • Vesna Spasojević-Kalimanovska Univerzitet u Beogradu - Farmaceutski fakultet, Katedra za medicinsku biohemiju
  • Dimitra Kalimanovska-Oštrić Univerzitetski klinički centar Srbije, Institut za kardiovaskularne bolesti
  • Nataša Bogavac Stanojević Univerzitet u Beogradu - Farmaceutski fakultet, Katedra za medicinsku biohemiju
Ključne reči: Pentraksin-3, hsCRP, statini, koronarna angiografija, multiplikativna interakcija, LDL-C

Sažetak


Pokazano je da statini snižavaju koncentracije inflamatornih markera, posebno visoko osetljivog C reaktivnog proteina (hsCRP), pri čemu je sniženje zavisno od doze leka. Pentraksin-3 (PTX3) je još jedan važan inflamatorni biomarker iz porodice pentraksina koji ima prognostičke karakteristike i olakšava dijagnozu kardiovaskularnih bolesti. U ovoj studiji je ispitivan efekat terapije statinima na koncentracije PTX3 i hsCRP, kao i sinergistički efekat  terapije, koncentracija PTX3 i hsCRP u snižavanju LDL-C. U studiju je uključeno 90 pacijenata kojima je koronarnom angiografijom procenjeno suženje koronarnih krvnih sudova. Rezultati su pokazali da statini smanjuju koncentraciju PTX3 (p=0,031). Koncentracije PTX3 i hsCRP značajno se razlikuju između grupa sa subkliničkim (p=0,011) i teškim oblikom stenoze (p=0,009). Primenom multiple logističke regresione analize uočena je veza između terapije statinima i niskih koncentracija PTX3 i LDL-C. Verovatnoća da će terapija statinima postići ciljne vrednosti LDL-C bila je najveća kod pacijenata sa niskim vrednostima PTX3 (OR=3,683, p=0,040), dok je multiplikativna interakcija bila 23,3. Efekat statina na sniženje PTX3 bio je veći u odnosu na efekat koji ostvaruje na hsCRP. Može se sugerisati da je terapija statinima bila uspešnija kod pacijenata sa niskim vrednostima PTX3.

Reference

Grundy SM, Stone NJ, Bailey AL, Beam C, Birtcher KK, Blumenthal RS, et al. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol. 2019 Jun;73(24):e285–e350.

Mach F, Baigent C, Catapano AL, Koskinas KC, Casula M, Badimon L, et al. 2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk: The Task Force for the management of dyslipidaemias of the European Society of Cardiology (ESC) and European Atherosclerosis Society (EAS). European Heart Journal. 2020;41:111-8.

Shavva VS, Mogilenko DA, Nekrasova EV, Trulioff AS, Kudriavtsev IV, Larionova EE, et al. Tumor necrosis factor α stimulates endogenous apolipoprotein A-I expression and secretion by human monocytes and macrophages: role of MAP-kinases, NF-κB, and nuclear receptors PPARα and LXRs. Mol Cell Biochem. 2018 Nov;448(1-2):211-23.

Liberale L, Carbone F, Montecucco F, Sahebkar A.. Statins reduce vascular inflammation in atherogenesis: A review of underlying molecular mechanisms. Int J Biochem Cell Biol. 2020 May;122:105735.

Margaritis M, Channon KM, Antoniades C. Statins as regulators of redox state in the vascular endothelium: beyond lipid lowering. Antioxid Redox Signal. 2014;20(8):1198-215.

Hognestad A, Aukrust P, Wergeland R, Stokke O, Gullestad L, Semb AG, et al. Effects of Conventional and Aggressive Statin Treatment on Markers of Endothelial Function and Inflammation. Clin Cardiol. 2004;27:199–203.

Nissen S, Turzu M, Schoenhagen P, Crowe T, Sasiela W, Tsai J, et al. Statin therapy, LDL cholesterol, C-reactive protein, and coronary artery disease. N Engl J Med. 2005;352:29-38.

Singh S, Suresh M, Voleti B, Agrawal A. The conection between C-reactive protein and atherosclerosis. Ann Med. 2008;40(2):110-20.

Morikawa S, Takabe W, Mataki C, Wada Y, Izumi A, Saito Y, et al. Global analysis of RNA expression profile in human vascular cells treated with statins. J Atheroscl Thromb. 2004;11(2):62-72.

Baetta R, Lento S, Ghilardi S, Barbati E, Corsini A, Tremoli E, et al . Atorvastatin reduces long pentraxin 3 expression in vascular cells by inhibiting protein geranylgeranylation. Vasc Pharmacol. 2015;67-69:38-47.

Kim J, McEvoy JW, Nasir K, Budoff MJ, Arad Y, Blumenthal RS, et al. Critical Review of High-Sensitivity C-Reactive Protein and Coronary Artery Calcium for the Guidance of Statin Allocation Head-to-Head Comparison of the JUPITER and St. Francis Heart Trials. Circ Cardiovasc Qual Outcomes. 2014;7(2):315-22.

Pearson TA, Mensah GA, Alexander RW, Anderson JL,Cannon RO, Criqui M, et al. Markers of inflammation and cardiovascular disease: application to clinical and public health practice: a statement for healthcare professionals from the Centers for Disease Control and Prevention and the American Heart Association. Circulation. 2003;107:499–511.

World Medical Association Declaration of Helsinki: Ethical principles for medical research involving human subjects. JAMA. 2013;310(20):2191-4.

Warnick GR, Benderson J, Albers JJ. Dextran sulfate-Mg2+ precipitation procedure for quantitation of high-densitylipoprotein cholesterol. Clin Chem. 1982;28:1379–88.

Friedewald WT, Levy RI, Fredrickson DS. Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. Clin Chem. 1972;18:499–502.

Jacobson TA, Ito MK, Maki KC, Orringer CE, Bays HE, Jones PH, et al. National Lipid Association recommendations for patient-centered management of dyslipidemia: Part 1 – Full report. J Clin Lipidol. 2015 Mar-Apr;9(2):129-69.

Tyler J, VanderWeele, Mirjam J, Knol. A Tutorial on Interaction. Epidemiol Methods. 2014;3(1):33–72.

Hiro T, Kimura T, Morimoto T, Miyauchi K, Nakagawa Y, Yamagishi M, et al. Effect of intensive statin therapy on regression of coronary atherosclerosis in patients with acute coronary syndrome. J Am Coll Cardiol. 2009;54:293-302.

Iwata A, Miura S, Tanaka T, Ike A, Sugihara M, Nishikawa H, et al. Plasma pentraxin-3 levels are associated with coronary plaque vulnerability and are decreased by statin. Coron Artery Dis. 2012;23(5):315-21.

Ohbayashi H, Miyazawa C, Miyamoto K, Sagara M, Yamashita T, Ouda R. Pitavastatin improves plasma pentraxin 3 and arterial stiffness in atherosclerotic patients with hypercholesterolemia. J Atheroscl Thromb. 2009;16(4):490-500.

Shindo A, Tanemura H, Yata K, Hamada K, Shibata M, Umeda Y, et al. Inflammatory biomarkers in atherosclerosis: pentraxin 3 can become a novel marker of plaque vulnerability. PLoS One. 2014;9:e100045.

Inoue K, Kodama T, Daida H. Pentraxin 3: A novel biomarker for inflammatory cardiovascular disease. Int J Vasc Med. 2012;2012:657025.

Zhao Y, Feng G, Wang Y, Yue Y, Zhao W. A key mediator, PTX3, of IKK/IκB/NF-κB exacerbates human umbilical vein endothelial cell injury and dysfunction. Int J Clin Exp Pathol. 2014;7(11):7699-707.

Lin R, Liu J, Peng N, Yang G, Gan W, Wang W. Lovastatin reduces nuclear factor κB activation induced by C-reactive protein in human vascular endothelial cells. Biol Pharm Bull. 2005;28(9):1630-4.

Rao A, Milbrandt E. To JUPITER and beyond: statins, inflammation, and primary prevention. Critical Care. 2010;14:310.

Albert MA, Danielson E, Rifai N, Ridker PM. Effect of statin therapy on C-reactive proteine levels: the pravastatin inflammation /CRP evaluation (PRINCE): a randomised trial and cohort study. JAMA. 2001;286(1):64-70.

Bosutti A, Grassi G, Zanetti M, Aleksova A, Zecchin M, Sinagra G, et al. Relation between the plasma levels of LDL-cholesterol and the expression of the early marker of inflammation long pentraxin PTX3 and the stress response gene p66 (ShcA) in pacemaker-implanted patients. Clin Exp Med. 2007;7(1):16-23.

Zanetti M, Zenti M, Barazzoni R, Zardi F, Semolic A, Messa MG, et al. HELP LDL apheresis reduces plasma pentraxin 3 in familial hypercholesterolemia. PLoS One. 2014 Jul 11;9(7):e101290.

Objavljeno
2022/04/28
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