Düşük Serum Serulapozmin Aktivitesi Aterosklerozun Göstergesi Olabilir: Kesitsel Bir Çalışma
Year 2015,
Volume: 12 Issue: 2, 200 - 205, 30.08.2015
Hatice Sezen
Emin Savik
,
Ahmet Kaymaz
Musluhittin Emre Erkus
,
İbrahim Halil Altiparmak
,
Abdullah Nurdağ
Abdusselam İlter
Nurten Aksoy
Abstract
Giriş
Daha önceki çalışmalarda serum seruloplazmin (Cp) seviyesi ile aterosklerotik kalp hastalığı arasında ilişki
bulunmuş ancak bu ilişkinin iskemi mi yoksa ateroskleroz mu kaynaklı olduğu araştırılmamıştır. Bu
çalışmanın amacı Cp aktivitesinin koroner ateroskleroz ve iskemi ile ilişkisini ayrı ayrı değerlendirerek
hangisine bağlı olduğunu araştırmaktır.
Materyal ve Metod
Koroner anjiyografi için alınan 90 hasta çalışmaya dâhil edildi. Hastalar koroner arter hastalığı (KAH): En az
1 ana koroner arterinde % 70 ve üzerinde darlık olan ve iskemi varlığı kanıtlanmış hastalar; nonkritik koroner
darlık (NOK): en az 1 ana koroner arterinde % 70'in altında darlığı olan ve açık iskemisi olmayan, normal
koroner arter (NKA): koronerlerinde herhangi bir aterosklerotik hastalık tespit edilemeyen ardışık 30 hasta
şeklinde gruplandı. Çalışmaya alınan tüm hastalardan enzimatik olarak ticari kitlerle lipid profili ve Erel
Metodu serum Cp aktivitesi ile ölçüldü.
Sonuçlar
Gruplar yaş cinsiyet, beden-kitle indeksi ve lipit profili yönünden benzerdi (p>0,05). Serum Cp aktivitesi
3 grup arasında anlamlı düzeyde farklı idi (p<0,05) ve hasta gruplarında NKA grubuna göre düşüktü. Alt
grup analizinde bu farkın NKA grubuyla diğer gruplar arasında olduğu görüldü. Pearson korelasyon
analizinde serum Cp aktivitesi ile total kolesterol ve düşük dansiteli lipoprotein kolesterol ile negatif ve
yüksek dansiteli lipoprotein kolesterol ile pozitif ilişkili olduğu görüldü. Linier regresyon analizinde bu
parametrelerden serum Cp aktivitesini sadece serum yüksek dansiteli lipoprotein kolesterol seviyesinin
etkilediği görüldü.Tartışma
Sonuç olarak, koroner ateroskleroz olan hastalarda serum Cp aktivitesi yüksek oksidatif stresi gösterecek
şekilde düşük olarak ölçüldü. İskemi olması ya da olmamasının sonucu etkilemediği gözlendi.
References
- 1.WHO Fact sheet N°310, Updated May 2014,
http://www.who.int/mediacentre/ factsheets/fs310/en/
2. Widimsky P, Wijns W, Fajadet J, de Belder M, Knot J,
Aaberge L, et al. Reperfusion therapy for ST elevation
acute myocardial infarction in Europe: description of the
current situation in 30 countries. Eur Heart J
2010;31:943-57.
1. ACC/AHA/ESC 2006 Guidelines for Management of
Patients With Ventricular Arrhythmias and the
Prevention of Sudden Cardiac Death Circulation
2006;114:385- 484.
2. Stone NJ, Robinson JG, Lichtenstein AH, Bairey
Merz CN, Blum CB, Eckel RH, et al. 2013 ACC/AHA
guideline on the treatment of blood cholesterol to reduce
atherosclerotic cardiovascular risk in adults: a report of
the American College of Cardiology/American Heart
Association Task Force on Practice Guidelines.
Circulation 2014;129: 1-45.
3.Hellman NE, Gitlin JD. Ceruloplasmin metabolism
and function. Annu Rev Nutr 2002;22:439-58.
4.Hellman NE, Kono S, Mancini GM, Hoogeboom AJ,
De Jong GJ, Gitlin JD. Mechanisms of copper
incorporation into human ceruloplasmin. J Biol Chem
2002;277(48):46632-8.
5.Correale M, Totaro A, Abruzzese S, Di Biase M,
Brunetti ND. Acute phase proteins in acute coronary
syndrome: an up-to-date. Cardiovasc Hematol Agents
Med Chem 2012;10(4):352-61.
6.Brunetti ND, Pellegrino PL, Correale M, De Gennaro
L, Cuculo A, Di Biase M. Acute phase proteins and
systolic dysfunction in subjects with acute myocardial
infarction. J Thromb Thrombolysis 2008;26(3):196-
202.
7.Kaur K, Bedi G, Kaur M, Vij A, Kaur I. Lipid
peroxidation and the levels of antioxidant enzymes in
coronary artery disease. Indian J Clin Biochem
2008;23(1):33- 7.
8.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.
9.Erel O. Automated measurement of serum ferroxidase
activity. Clin Chem 1998;44:2313-9.
10.Erel O. A novel automated method to measure total
antioxidant response against potent free radical reactions.
Biochem 2004;37:112-9.
13.Widimsky P, Wijns W, Fajadet J, de Belder M, Knot J,
Aaberge L, et al. Reperfusion therapy for ST elevation
acute myocardial infarction in Europe: description of the
current situation in 30 countries. Eur Heart J
2010;31:943-57.
14.Dendramis G, Paleologo C, Lo Presti A, Piraino D, Lo
Greco V, Grassedonio E, et al. Coronary artery ectasia:
etiopathogenesis, diagnosis and treatment. G Ital Cardiol
(Rome)2014;15(3):161-9.
15. Lenz T. [Current management ofrenal artery
stenosis]. Internist (Berl) 2013;54(12):1443-9.
16. Tanweer O, Wilson TA, Metaxa E, Riina HA, Meng H.
A comparative review of the hemodynamics and
pathogenesis of cerebral and abdominal aortic
aneurysms: lessons to learn from each other. J
Cerebrovasc Endovasc Neurosurg 2014;16(4):335-49.
17. Manea A, Simionescu M. Nox enzymes and oxidative
stress in atherosclerosis. Front Biosci 2012;4:651-70.
18. Peluso I, Morabito G, Urban L, Ioannone F, Serafini
M. Oxidative stress in atherosclerosis development: the
central role of LDL and oxidative burst. Endocr Metab
Immune Disord Drug Targets 2012;12(4):351-60.
19.Göçmen AY, Sahin E, Semiz E, Gümuşlü S. Is elevated
serum ceruloplasmin level associated with increased risk
of coronary artery disease? Can J Cardiol
2008;24(3):209-12.
20. Grammer TB, Kleber ME, Silbernagel G, Pilz S,
Scharnagl H, Lerchbaum E, et al. Copper, ceruloplasmin,
and long-term cardiovascular and total mortality (the
Ludwigshafen Risk and Cardiovascular Health Study).
Free Radic Res 2014;48(6):706-15.
21. Ziakas A, Gavrilidis S, Souliou E, Giannoglou G,
Stiliadis I, Karvounis H, et al. Ceruloplasmin is a better
predictor of the long-term prognosis compared with
Harran Üniversitesi Tıp Fakültesi Dergisi (Journal of
Harran University Medical Faculty) Cilt 12. Sayı
2, 2015fibrinogen, CRP, and IL-6 in patients with
severe unstable angina. Angiology 2009;60(1):50-9.
16. Brunetti ND, Pellegrino PL, Correale M, De Gennaro L,
Cuculo A, Di Biase M. Acute phase proteins and systolic
dysfunction in subjects with acute myocardial infarction. J
Thromb Thrombolysis 2008;26(3):196-202.
17. Brunetti ND, Correale M, Pellegrino PL, Cuculo A,
Biase MD. Acute phase proteins in patients with acute
coronary syndrome: Correlations with diagnosis,clinical
features, and angiographic findings. Eur J Intern Med
2007;18(2):109-17.
18. Lamb DJ, Leake DS. Acidic pH enables caeruloplasmin
to catalyse the modification of low density lipoprotein.
FEBS Lett 1994;338(2):122-26
19. Healy J, Tipton K. Ceruloplasmin and what it might do. J
Neural Transm 2007;114(6):777-81.
20. Jayakumari N, Ambikakumari V, Balakrishnan KG, Iyer
KS. Antioxidant status in relation to free radical production
during stable and unstable anginal syndromes.
Atherosclerosis 1992;94:183-90.
21. Biasucci LM, Santamaria M, Liuzzo G. Inflammation,
atherosclerosis and acute coronary syndromes. Minerva
Cardioangiol 2002;50(5):475-86.
22. Inoue K, Sugiyama A, Reid PC, Ito Y, Miyauchi K,
Mukai S, et al. Establishment of a high sensitivity plasma
assay for human pentraxin3 as a marker for unstable angina
pectoris. Arterioscler. Thromb. Vasc. Biol 2007;27(1):161-
7.
23.Mackness M, Mackness B. Paraoxonase 1 and
atherosclerosis: is the gene or the protein more important?
Free Radic Biol Med 2004;37(9):1317-23.
Low Serum Ceruloplasmin Activity May Be An Indicator Of Atherosclerosis: A Cross Sectional Study
Year 2015,
Volume: 12 Issue: 2, 200 - 205, 30.08.2015
Hatice Sezen
Emin Savik
,
Ahmet Kaymaz
Musluhittin Emre Erkus
,
İbrahim Halil Altiparmak
,
Abdullah Nurdağ
Abdusselam İlter
Nurten Aksoy
Abstract
Background
In previous studies, serum ceruloplasmin (Cp) level have been shown to be correlated with atherosclerotic
heart disease. But it has not been investigated which result from ischemia or atherosclerosis. The aim of this
study, serum Cp activity assess in coronary atherosclerosis and ischemia and investigate to which it is
connected.
Methods
90 patients taken for coronary angiography were included in the study. Patients divided three groups such as
coronary artery disease (CAD): at least one main coronary artery stenosis exceeding 70% and patients with
proven ischemia presence; noncritical coronary artery stenosis (NOC): at least one main coronary artery stenosis
less than 70% and no obvious ischemia, normal coronary artery (NKA): 30 consecutive patients with
normal coronary artery. Lipid profiles of all patients were measured. And serum Cp activity was measured by
Erel's method.
Results
Tree groups were similar in terms of age, gender, BMI and lipid profile (p> 0.05). Serum Cp activity was
significantly different among groups (p <0.05). CP activity was significantly lower in the patient group
compared to the NOC group. In the subgroup analysis this difference was observed among NKA group and
other groups. Pearson correlation analysis showed that serum Cp activity is the negative with total
cholesterol and low density lipoprotein cholesterol, positively correlated with high density lipoprotein
cholesterol (HDLK). Linier regression analysis showed that only HDLK effect serum Cp activity from these
parameters independently.
Conclusions
As a result, in patients with atherosclerosis, serum Cp activity was lower than in patients with normal
coronary arteries. The presence of ischemia did not affect the result.
References
- 1.WHO Fact sheet N°310, Updated May 2014,
http://www.who.int/mediacentre/ factsheets/fs310/en/
2. Widimsky P, Wijns W, Fajadet J, de Belder M, Knot J,
Aaberge L, et al. Reperfusion therapy for ST elevation
acute myocardial infarction in Europe: description of the
current situation in 30 countries. Eur Heart J
2010;31:943-57.
1. ACC/AHA/ESC 2006 Guidelines for Management of
Patients With Ventricular Arrhythmias and the
Prevention of Sudden Cardiac Death Circulation
2006;114:385- 484.
2. Stone NJ, Robinson JG, Lichtenstein AH, Bairey
Merz CN, Blum CB, Eckel RH, et al. 2013 ACC/AHA
guideline on the treatment of blood cholesterol to reduce
atherosclerotic cardiovascular risk in adults: a report of
the American College of Cardiology/American Heart
Association Task Force on Practice Guidelines.
Circulation 2014;129: 1-45.
3.Hellman NE, Gitlin JD. Ceruloplasmin metabolism
and function. Annu Rev Nutr 2002;22:439-58.
4.Hellman NE, Kono S, Mancini GM, Hoogeboom AJ,
De Jong GJ, Gitlin JD. Mechanisms of copper
incorporation into human ceruloplasmin. J Biol Chem
2002;277(48):46632-8.
5.Correale M, Totaro A, Abruzzese S, Di Biase M,
Brunetti ND. Acute phase proteins in acute coronary
syndrome: an up-to-date. Cardiovasc Hematol Agents
Med Chem 2012;10(4):352-61.
6.Brunetti ND, Pellegrino PL, Correale M, De Gennaro
L, Cuculo A, Di Biase M. Acute phase proteins and
systolic dysfunction in subjects with acute myocardial
infarction. J Thromb Thrombolysis 2008;26(3):196-
202.
7.Kaur K, Bedi G, Kaur M, Vij A, Kaur I. Lipid
peroxidation and the levels of antioxidant enzymes in
coronary artery disease. Indian J Clin Biochem
2008;23(1):33- 7.
8.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.
9.Erel O. Automated measurement of serum ferroxidase
activity. Clin Chem 1998;44:2313-9.
10.Erel O. A novel automated method to measure total
antioxidant response against potent free radical reactions.
Biochem 2004;37:112-9.
13.Widimsky P, Wijns W, Fajadet J, de Belder M, Knot J,
Aaberge L, et al. Reperfusion therapy for ST elevation
acute myocardial infarction in Europe: description of the
current situation in 30 countries. Eur Heart J
2010;31:943-57.
14.Dendramis G, Paleologo C, Lo Presti A, Piraino D, Lo
Greco V, Grassedonio E, et al. Coronary artery ectasia:
etiopathogenesis, diagnosis and treatment. G Ital Cardiol
(Rome)2014;15(3):161-9.
15. Lenz T. [Current management ofrenal artery
stenosis]. Internist (Berl) 2013;54(12):1443-9.
16. Tanweer O, Wilson TA, Metaxa E, Riina HA, Meng H.
A comparative review of the hemodynamics and
pathogenesis of cerebral and abdominal aortic
aneurysms: lessons to learn from each other. J
Cerebrovasc Endovasc Neurosurg 2014;16(4):335-49.
17. Manea A, Simionescu M. Nox enzymes and oxidative
stress in atherosclerosis. Front Biosci 2012;4:651-70.
18. Peluso I, Morabito G, Urban L, Ioannone F, Serafini
M. Oxidative stress in atherosclerosis development: the
central role of LDL and oxidative burst. Endocr Metab
Immune Disord Drug Targets 2012;12(4):351-60.
19.Göçmen AY, Sahin E, Semiz E, Gümuşlü S. Is elevated
serum ceruloplasmin level associated with increased risk
of coronary artery disease? Can J Cardiol
2008;24(3):209-12.
20. Grammer TB, Kleber ME, Silbernagel G, Pilz S,
Scharnagl H, Lerchbaum E, et al. Copper, ceruloplasmin,
and long-term cardiovascular and total mortality (the
Ludwigshafen Risk and Cardiovascular Health Study).
Free Radic Res 2014;48(6):706-15.
21. Ziakas A, Gavrilidis S, Souliou E, Giannoglou G,
Stiliadis I, Karvounis H, et al. Ceruloplasmin is a better
predictor of the long-term prognosis compared with
Harran Üniversitesi Tıp Fakültesi Dergisi (Journal of
Harran University Medical Faculty) Cilt 12. Sayı
2, 2015fibrinogen, CRP, and IL-6 in patients with
severe unstable angina. Angiology 2009;60(1):50-9.
16. Brunetti ND, Pellegrino PL, Correale M, De Gennaro L,
Cuculo A, Di Biase M. Acute phase proteins and systolic
dysfunction in subjects with acute myocardial infarction. J
Thromb Thrombolysis 2008;26(3):196-202.
17. Brunetti ND, Correale M, Pellegrino PL, Cuculo A,
Biase MD. Acute phase proteins in patients with acute
coronary syndrome: Correlations with diagnosis,clinical
features, and angiographic findings. Eur J Intern Med
2007;18(2):109-17.
18. Lamb DJ, Leake DS. Acidic pH enables caeruloplasmin
to catalyse the modification of low density lipoprotein.
FEBS Lett 1994;338(2):122-26
19. Healy J, Tipton K. Ceruloplasmin and what it might do. J
Neural Transm 2007;114(6):777-81.
20. Jayakumari N, Ambikakumari V, Balakrishnan KG, Iyer
KS. Antioxidant status in relation to free radical production
during stable and unstable anginal syndromes.
Atherosclerosis 1992;94:183-90.
21. Biasucci LM, Santamaria M, Liuzzo G. Inflammation,
atherosclerosis and acute coronary syndromes. Minerva
Cardioangiol 2002;50(5):475-86.
22. Inoue K, Sugiyama A, Reid PC, Ito Y, Miyauchi K,
Mukai S, et al. Establishment of a high sensitivity plasma
assay for human pentraxin3 as a marker for unstable angina
pectoris. Arterioscler. Thromb. Vasc. Biol 2007;27(1):161-
7.
23.Mackness M, Mackness B. Paraoxonase 1 and
atherosclerosis: is the gene or the protein more important?
Free Radic Biol Med 2004;37(9):1317-23.