İzole Hiperkolesterolemili Olgularda Terapötik Yaşam Şekli Değişikliği ve HMG-KoA Redüktaz İnhibitörü Tedavisinin Kan TWEAK (TNF-related weak inducer of apoptosis) Düzeyi Üzerine Etkisi

Year 2018, Volume: 5 Issue: 3, 24 - 30, 04.12.2018

Gokhan Ozgur İlker Tascı Serkan Tapan Gurkan Celebı Ali Selcuk Battal Altun Gurhan Taskın Alper Sonmez Bilgin Bahadir Basgoz Gokhan Erdem

Abstract

İzole
hiperkolesterolemi genel popülasyonda sık görülen bir durumdur. Tedavide terapötik
yaşam tarzı değişikliği ve/veya statin tedavisi altın standarttır. TWEAK, TNF
süper familya-sından bir sitokindir ve akut dönemde doku rejenerasyonunda rol
oynar, ayrıca kronik dö-nemde doku hasarında da rol oynar. Bu çalışmada, ilk 12
haftalık yaşam tarzı değişikliği ve 12 haftalık statin tedavisine yanıt olarak
izole LDL kolesterol yüksekliği olan hastaların plazma TWEAK düzeylerini
araştırdık. Sonuç olarak, terapötik yaşam tarzı değişikliğinden sonra hedef LDL
seviyelerine ulaşabilen dislipidemi hastalarında plazma sTWEAK düzeyi
artmıştır. Bununla birlikte, dislipideminin statin ile düzeltilmesi, plazma
sTWEAK seviyesinde herhangi bir değişiklik gözlenmemiştir.

Keywords

Hidroksimetilglutaril KoA Redüktaz İnhibitörleri, Hiperkolesterolemi, Sitokin TWEAK, Yaşam Tarzı Değişikliği

The Effects of Lifestyle Modification and HMG-Coa Reductase Inhibitor Treatment on Blood Tumor Necrosis Factor-Like Weak Inducer of Apoptosis (TWEAK) Levels Among Patients with Isolated Hypercholesterolemia

Abstract

Isolated
hypercholesterolemia is a frequent condition in the general population. It is managed
mostly by therapeutic lifestyle intervention and/or statin treatment. TWEAK is
a cytokine from the TNF superfamily and plays a role in tissue regeneration in
acute period; it is also involved in tissue damage in chronic period. In this
study, we investigated plasma TWEAK levels of participants with isolated LDL
cholesterol elevation in response to first 12 weeks of lifestyle modification,
and 12 weeks of statin treatment. In conclusion, plasma sTWEAK level increased
in dyslipidemia patients who were able to reach target LDL levels after
therapeutic lifestyle modification. However, correcting dyslipidemia with
statin was not associated with any change in plasma sTWEAK level.

Keywords

Hydroxymethylglutaryl-CoA Reductase Inhibitors, Hypercholesterolemia, Cytokine TWEAK, Lifestyle Modification

References

• 1. Tracy RP. Inflammation in cardiovascular disease: cart, horse or both--revisited. Arterioscler Thromb Vasc Biol. 2002;22(10):1514-5.
• 2. Bienvenu J WJ, Aguzzi F. C-reactive protein. In: Ritchie RF NO, editor. Serum proteins in clinical medicine. Portland: Maine Printing Group; 1996. p. 7.01.–7..6. 3. Pepys MB. C-reactive protein fifty years on. Lancet (London, England). 1981;1(8221):653-7.
• 4. Kinlay S, Schwartz GG, Olsson AG, et al. High-dose atorvastatin enhances the decline in inflammatory markers in patients with acute coronary syndromes in the MIRACL study. Circulation. 2003;108(13):1560-6.
• 5. Nissen SE, Tuzcu EM, Schoenhagen P, et al. Effect of intensive compared with moderate lipid-lowering therapy on progression of coronary atherosclerosis: a randomized controlled trial. Jama. 2004;291(9):1071-80.
• 6. Ridker PM. Rosuvastatin in the primary prevention of cardiovascular disease among patients with low levels of low-density lipoprotein cholesterol and elevated high-sensitivity C-reactive protein: rationale and design of the JUPITER trial. Circulation. 2003;108(19):2292-7.
• 7. Okutani D. The role of long pentraxin 3, a new inflammatory mediator in inflammatory responses. Nihon Rinsho Men'eki Gakkai kaishi = Japanese journal of clinical immunology. 2006;29(3):107-13.
• 8. Mantovani A, Garlanda C, Bottazzi B, et al. The long pentraxin PTX3 in vascular pathology. Vascul Pharmacol. 2006;45(5):326-30.
• 9. Ortega-Hernandez OD, Bassi N, Shoenfeld Y, Anaya JM. The long pentraxin 3 and its role in autoimmunity. Semin Arthritis Rheum. 2009;39(1):38-54.
• 10. Kotooka N, Inoue T, Fujimatsu D, et al. Pentraxin3 is a novel marker for stent-induced inflammation and neointimal thickening. Atherosclerosis. 2008;197(1):368-74.
• 11. Tong M, Carrero JJ, Qureshi AR, et al. Plasma pentraxin 3 in patients with chronic kidney disease: associations with renal function, protein-energy wasting, cardiovascular disease, and mortality. CJASN. 2007;2(5):889-97.
• 12. Imamura M, Kawasaki T, Savchenko AS, et al. Lipopolysaccharide induced expression of pentraxin 3 in human neutrophils and monocyte-derived macrophages. Cell Immunol. 2007;248(2):86-94.
• 13. Kotooka N, Inoue T, Aoki S, Anan M, Komoda H, Node K. Prognostic value of pentraxin 3 in patients with chronic heart failure. Int J Cardiol. 2008;130(1):19-22.
• 14. Peri G, Introna M, Corradi D, et al. PTX3, A prototypical long pentraxin, is an early indicator of acute myocardial infarction in humans. Circulation. 2000;102(6):636-41.
• 15. Kim SH, Lee WH, Kwon BS, Oh GT, Choi YH, Park JE. Tumor necrosis factor receptor superfamily 12 may destabilize atherosclerotic plaques by inducing matrix metalloproteinases. Jpn Circ J. 2001;65(2):136-8.
• 16. Wiley SR, Winkles JA. TWEAK, a member of the TNF superfamily, is a multifunctional cytokine that binds the TweakR/Fn14 receptor. Cytokine Growth Factor Rev. 2003;14(3-4):241-9.
• 17. Burkly LC, Michaelson JS, Hahm K, Jakubowski A, Zheng TS. TWEAKing tissue remodeling by a multifunctional cytokine: role of TWEAK/Fn14 pathway in health and disease. Cytokine. 2007;40(1):1-16.
• 18. Tasci I, Erdem G, Ozgur G, Tapan S, Dogru T, Genc H, et al. LDL-cholesterol lowering increases plasma apelin in isolated hypercholesterolemia. Atherosclerosis. 2009;204(1):222-8.
• 19. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia. 1985;28(7):412-9.
• 20. Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, And Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III). Jama. 2001;285(19):2486-97.
• 21. Durstine JL, Grandjean PW, Davis PG, Ferguson MA, Alderson NL, DuBose KD. Blood lipid and lipoprotein adaptations to exercise: a quantitative analysis. Sports Med. 2001;31(15):1033-62.
• 22. Yusuf S, Hawken S, Ounpuu S, et al. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. Lancet (London, England). 2004;364(9438):937-52.
• 23. Krauss RM, Eckel RH, Howard B, et al. AHA Dietary Guidelines: revision 2000: A statement for healthcare professionals from the Nutrition Committee of the American Heart Association. Circulation. 2000;102(18):2284-99.
• 24. Kreisberg RA, Oberman A. Medical management of hyperlipidemia/dyslipidemia. J Clin Endocrinol Metab. 2003;88(6):2445-61.
• 25. Williams PT. The relationships of vigorous exercise, alcohol, and adiposity to low and high high-density lipoprotein-cholesterol levels. Metabolism. 2004;53(6):700-9.
• 26. Rice T, Despres JP, Perusse L, et al. Familial aggregation of blood lipid response to exercise training in the health, risk factors, exercise training, and genetics (HERITAGE) Family Study. Circulation. 2002;105(16):1904-8.
• 27. Lakka TA, Lakka HM, Rankinen T, et al. Effect of exercise training on plasma levels of C-reactive protein in healthy adults: the HERITAGE Family Study. Eur Heart J. 2005;26(19):2018-25.
• 28. Jenkins DJ, Kendall CW, Marchie A, et al. Effects of a dietary portfolio of cholesterol-lowering foods vs lovastatin on serum lipids and C-reactive protein. Jama. 2003;290(4):502-10.
• 29. Yilmaz MI, Carrero JJ, Martin-Ventura JL, et al. Combined therapy with renin-angiotensin system and calcium channel blockers in type 2 diabetic hypertensive patients with proteinuria: effects on soluble TWEAK, PTX3, and flow-mediated dilation. CJASN. 2010;5(7):1174-81.
• 30. Munoz-Garcia B, Moreno JA, Lopez-Franco O, et al. Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) enhances vascular and renal damage induced by hyperlipidemic diet in ApoE-knockout mice. Arterioscler Thromb Vasc Biol. 2009;29(12):2061-8.
• 31. Schapira K, Burkly LC, Zheng TS, et al. Fn14-Fc fusion protein regulates atherosclerosis in ApoE-/- mice and inhibits macrophage lipid uptake in vitro. Arterioscler Thromb Vasc Biol. 2009;29(12):2021-7.
• 32. Munoz-Garcia B, Martin-Ventura JL, Martinez E, et al. Fn14 is upregulated in cytokine-stimulated vascular smooth muscle cells and is expressed in human carotid atherosclerotic plaques: modulation by atorvastatin. Stroke. 2006;37(8):2044-53.
• 33. Sanz AB, Sanchez-Nino MD, Izquierdo MC, et al. TWEAK, the facilitator of acute kidney injury. Nefrologia. 2008;28(6):587-92.
• 34. Chicheportiche Y, Bourdon PR, Xu H, et al. TWEAK, a new secreted ligand in the tumor necrosis factor family that weakly induces apoptosis. J Biol Chem. 1997;272(51):32401-10.