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Journals / Muğla Sıtkı Koçman Üniversitesi Tıp Dergisi / 2018 / Cilt: 5 - Sayı: 3

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

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

Gokhan OZGUR
İlker TASCI
Serkan TAPAN
Gurkan CELEBI
Ali SELCUK
Battal ALTUN
Gurhan TASKIN
Alper SONMEZ
Bilgin Bahadir BASGOZ
Gokhan ERDEM
Pages
24–30
Publication Date
2018-12-04
DOI
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AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

In conclusion, plasma sTWEAK level increased in dyslipidemia patients who were able to reach target LDL levels after therapeutic lifestyle modification.

📌 3 Key Takeaways

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Objective & Hypothesis:Isolated hypercholesterolemia is a frequent condition in the general population.
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Key Findings & Data: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.
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Conclusion & Impact:In conclusion, plasma sTWEAK level increased in dyslipidemia patients who were able to reach target LDL levels after therapeutic lifestyle modification.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Hidroksimetilglutaril KoA Redüktaz İnhibitörleri · Hiperkolesterolemi · Sitokin TWEAK

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.

Özet

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.

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Cite This Article

OZGUR, G., TASCI, İ., TAPAN, S., CELEBI, G., SELCUK, A., ALTUN, B., TASKIN, G., SONMEZ, A., BASGOZ, B. B., ERDEM, G. (2018). 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. Muğla Sıtkı Koçman Üniversitesi Tıp Dergisi, Cilt: 5 - Sayı: 3, 24–30. https://ajindex.com/articles/692228

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References (15)

  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