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Sepsiste LDL kolesterol mortalite ilişkisi

Year 2018, Volume: 3 Issue: 3, 111 - 119, 06.12.2018

Abstract

Amaç: Sepsis inflamasyonun sebep olduğu fizyolojik, biyokimyasal ve biyolojik anormallikler ile
karakterize bir klinik sendromdur. Sepsisin erken d
öneminde tanı için kullanılan bazı laboratuvar ve klinik parametreleri vardır (laktat. prokalsitonin, crp. ates. kan basıncı, solunum sayısı, şuur durumu vb). Fakat bu parametrelerin hiç birisi erken dönemde tanı koydurucu değildir. Çalışmamızda sepsisli hastalarda LDL kolesterol
seviyelerindeki d
üşmeyi ve LDL kolesteroldeki bu düşmenin mortaliteyi göstermede bir belirteç olarak kullanılıp kullanılamayacağını araştırdık.

Materyal
ve Metod:
1 ocak - 31 aralık 2011 tarihleri arasında Kayseri Eğitim ve Araştırma Hastanesi İç Hastalıkları Yoğun Bakım Servisine sepsis tanısı ile yatırılan 84 hasta hastane kayıtlarından retrospektif olarak tarandı. Sepsisli ölen ve yaşayan hastalar arasındaki total kolesterol, HDL kolesterol, LDL kolesterol seviyeleri
kar
şılaştırıldı.

Bulgular: Hastaların erkek kadın oranı %44 ve %56, hastaların ortalama yaşı 71,49±11,07 idi. Yaşayan ve ölen hastaların yaş ortalamaları; yaşayan hastalar 68,19±13,88, ölen hastalar 72,97±9,31 idi (p=0,019). Bu hastaların 58 i kaybedildi. Yirmialtı hasta yaşadı. Ölen hastaların %70 inde LDL kolesterol seviyeleri 70mg /dl
nin alt
ında, yaşayan hastaların %30 unda LDL kolesterol seviyeleri 70 mg/dl
nin alt
ında idi.Yaşayan hastaların %64 ünde LDL kolesterol 70 mg/dl üzerinde, ölen hastaların %36 sında LDL kolesterol 70 mg/dl nin üzerinde idi. İki grup arasında LDL kolesterol seviyelerine göre belirgin fark vardı. Ancak bu istatistiksel olarak anlamlı değildi (p=0,577).







Sonuç:Sepsisli hastalarda TC, HDL, LDLC normal
populasyondan daha d
üşüktür.Bu çalışmada sepsisli kaybedilen hastalarda LDL
kolesterol seviyeleri sepsisli ya
şayan hastalardan belirgin olarak daha düşük bulundu. Fakat bu fark istatistiksel olarak anlamlı değildi.LDL kolesterol seviyeleri 70 mg/dl nin altında olan 25 (% 70) hasta öldü.LDL kolesterol seviyesi 70 mg/dl nin altında olan 12 (%30) hasta yaşadı.Bu fark istatistiksel olarak anlamlı değildi. LDL kolesterol seviyeleri 70 mg/ dl nin üzerinde olan 25 (% 64) hasta yaşadı ve LDL kolesterol seyeleri 70 mg/dl nin üzerinde olan 14 (%36) hasta kaybedildi. Fakat bu fark istatistiksel
olarak anlaml
ı değildi.Bu küçük tek merkezli çalışma bu konuda son kararı vermek için yeterli değildir. Kesin karar verebilmek için daha ileri çalışmalara ihtiyaç vardır.

References

  • Ferri, F., Ferri's Clinical Advisor 2017 5 books in 1. 1 ed. 2017.2. Rivers, E., et al., Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med, 2001. 345(19): p. 1368-77.3. Jacob, J.A., NEw sepsis diagnostic guidelines shift focus to organ dysfunction. JAMA, 2016. 315(8): p. 739-740.4. Schuetz P, Birkhahn R, Sherwin R, et al. Serial Procalcitonin Predicts Mortality in Severe Sepsis Patients: Results From the Multicenter Procalcitonin MOnitoring SEpsis (MOSES) Study. Crit Care Med 2017; 45:781.5. Cecil, R.L., L. Goldman, and A. Schafer, Goldman's Cecil Medicine. 24 ed. 2012, Philadelphia: Elsevier/Saunders.6. Neviere, R., ed. Sepsis syndromes in adults: Epidemiology, definitions, clinical presentation, diagnosis, and prognosis. ed. P.E. Parsons and G. Finlay. 2016, UpToDate: Waltham, MA.7. Nassaji, M. and R. Ghorbani, Plasma lipid levels in patients with acute bacterial infections. Turkish Journal of Medical Sciences, 2012. 42(3): p. 465-469.8. Murch, O., et al., Lipoproteins in inflammation and sepsis. I. Basic science. Intensive Care Med, 2007. 33(1): p. 13-24.9. Kwiterovich, P.O., Jr., The metabolic pathways of high-density lipoprotein, low-density lipoprotein, and triglycerides: a current review. Am J Cardiol, 2000. 86(12A): p. 5L-10L.10. Carpentier, Y.A. and O. Scruel, Changes in the concentration and composition of plasma lipoproteins during the acute phase response. Curr Opin Clin Nutr Metab Care, 2002. 5(2): p. 153-8.
  • 11. Alvarez, C. and A. Ramos, Lipids, lipoproteins, and apoproteins in serum during infection. Clin Chem, 1986. 32(1 Pt 1): p. 142-5.12. van Leeuwen, H.J., et al., Lipoprotein metabolism in patients with severe sepsis. Crit Care Med, 2003. 31(5): p. 1359-66.13. Fraunberger, P., et al., Reduction of circulating cholesterol and apolipoprotein levels during sepsis. Clin Chem Lab Med, 1999. 37(3): p. 357-62.14. Berbee JF, Havekes LM, Rensen PC. Apoliporoteins modulate the inflammatory response to lipopoly-saccharide. J Endotoxin Res 2005;11:97–103.15. Frauberger P, Pilz G, Cremer P, Werdan K, Walli AK. Association of serum tumor necrosis factor levels with decrease of cholesterol during septic shock.Shock 1998; 10:359–363. 16.Kaplan M, Aviram M. Oxidized low density lipoprotein: atherogenic and proinflammatory characteristics during macrophage foam cell formation: an inhibitory role for nutritional antioxidants and serum paraoxonase. Clin Chem Lab Med 1999;37:777–787.
  • 17. Navab M, Berliner JA, Subbanagounder G, Hama S, Lusis AJ, Castellani LW, Reddy S, Shih D, Shi W, Watson AD, Van Lenten BJ, Vora D, Fogelman AM. HDL and the inflammatory response induced by LDL-derived oxidized phospholipids.Arterioscler Thromb Vasc Biol 2001;21:481–488.
  • 18. Delgado Rodriguez M, Medina Cuadros M, Martinez Gallego G, et al: Total cholesterol, HDL-cholesterol, and risk of nosocomial infection: A prospective study in surgical patients. Infect Control Hosp Epidemiol 1997; 18:9–1819.Cabana VG, Lukens JR, Rice KS, et al: HDL content and composition in acute phase response in three species: Triglyceride enrichment of HDL a factor in its decrease. J Lipid Res 1996; 37:2662–267420. Hardardottir I, Grunfeld C, Feingold KR: Effects of endotoxin and cytokines on lipid metabolism. Curr Opin Lipidol 1994; 5:207–215
Year 2018, Volume: 3 Issue: 3, 111 - 119, 06.12.2018

Abstract

References

  • Ferri, F., Ferri's Clinical Advisor 2017 5 books in 1. 1 ed. 2017.2. Rivers, E., et al., Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med, 2001. 345(19): p. 1368-77.3. Jacob, J.A., NEw sepsis diagnostic guidelines shift focus to organ dysfunction. JAMA, 2016. 315(8): p. 739-740.4. Schuetz P, Birkhahn R, Sherwin R, et al. Serial Procalcitonin Predicts Mortality in Severe Sepsis Patients: Results From the Multicenter Procalcitonin MOnitoring SEpsis (MOSES) Study. Crit Care Med 2017; 45:781.5. Cecil, R.L., L. Goldman, and A. Schafer, Goldman's Cecil Medicine. 24 ed. 2012, Philadelphia: Elsevier/Saunders.6. Neviere, R., ed. Sepsis syndromes in adults: Epidemiology, definitions, clinical presentation, diagnosis, and prognosis. ed. P.E. Parsons and G. Finlay. 2016, UpToDate: Waltham, MA.7. Nassaji, M. and R. Ghorbani, Plasma lipid levels in patients with acute bacterial infections. Turkish Journal of Medical Sciences, 2012. 42(3): p. 465-469.8. Murch, O., et al., Lipoproteins in inflammation and sepsis. I. Basic science. Intensive Care Med, 2007. 33(1): p. 13-24.9. Kwiterovich, P.O., Jr., The metabolic pathways of high-density lipoprotein, low-density lipoprotein, and triglycerides: a current review. Am J Cardiol, 2000. 86(12A): p. 5L-10L.10. Carpentier, Y.A. and O. Scruel, Changes in the concentration and composition of plasma lipoproteins during the acute phase response. Curr Opin Clin Nutr Metab Care, 2002. 5(2): p. 153-8.
  • 11. Alvarez, C. and A. Ramos, Lipids, lipoproteins, and apoproteins in serum during infection. Clin Chem, 1986. 32(1 Pt 1): p. 142-5.12. van Leeuwen, H.J., et al., Lipoprotein metabolism in patients with severe sepsis. Crit Care Med, 2003. 31(5): p. 1359-66.13. Fraunberger, P., et al., Reduction of circulating cholesterol and apolipoprotein levels during sepsis. Clin Chem Lab Med, 1999. 37(3): p. 357-62.14. Berbee JF, Havekes LM, Rensen PC. Apoliporoteins modulate the inflammatory response to lipopoly-saccharide. J Endotoxin Res 2005;11:97–103.15. Frauberger P, Pilz G, Cremer P, Werdan K, Walli AK. Association of serum tumor necrosis factor levels with decrease of cholesterol during septic shock.Shock 1998; 10:359–363. 16.Kaplan M, Aviram M. Oxidized low density lipoprotein: atherogenic and proinflammatory characteristics during macrophage foam cell formation: an inhibitory role for nutritional antioxidants and serum paraoxonase. Clin Chem Lab Med 1999;37:777–787.
  • 17. Navab M, Berliner JA, Subbanagounder G, Hama S, Lusis AJ, Castellani LW, Reddy S, Shih D, Shi W, Watson AD, Van Lenten BJ, Vora D, Fogelman AM. HDL and the inflammatory response induced by LDL-derived oxidized phospholipids.Arterioscler Thromb Vasc Biol 2001;21:481–488.
  • 18. Delgado Rodriguez M, Medina Cuadros M, Martinez Gallego G, et al: Total cholesterol, HDL-cholesterol, and risk of nosocomial infection: A prospective study in surgical patients. Infect Control Hosp Epidemiol 1997; 18:9–1819.Cabana VG, Lukens JR, Rice KS, et al: HDL content and composition in acute phase response in three species: Triglyceride enrichment of HDL a factor in its decrease. J Lipid Res 1996; 37:2662–267420. Hardardottir I, Grunfeld C, Feingold KR: Effects of endotoxin and cytokines on lipid metabolism. Curr Opin Lipidol 1994; 5:207–215
There are 4 citations in total.

Details

Primary Language Turkish
Journal Section Makale
Authors

Ali Çetinkaya 0000-0001-8485-0982

Deniz Avcı 0000-0001-9220-194X

Publication Date December 6, 2018
Acceptance Date December 5, 2018
Published in Issue Year 2018 Volume: 3 Issue: 3

Cite

Vancouver Çetinkaya A, Avcı D. Sepsiste LDL kolesterol mortalite ilişkisi. JAMER. 2018;3(3):111-9.