Background There is evidence that opium addiction has immunosuppressant effects. Coronary artery disease (CAD) is a condition resulted from atherosclerosis which is dependent on the immune response. Purpose To evaluate plasma levels of interleukin-6 and interleukin-1Ra in 30 patients with three-vessel coronary artery disease, ejection fraction of more than 35% and to evaluate their changes after prognostic treadmill test in 15 opium addicted and 15 non-addicted patients. Methods The participants underwent prognostic treadmill test and plasma levels of interleukin-6 (IL-6) and interleukin-1Ra (IL-1Ra) were evaluated with ELISA method before, just after and 4 hours after the test. Results IL-1Ra (2183 pg/ml) tended to decrease over time in the opium addicted group (1372 pg/ml after prognostic treadmill test and 1034 pg/ml 4 hours after that), although such decrease did not reach the statistical significance. IL-1Ra levels were significantly higher in opium addicted than in non addicted patients. Opium addiction had no significant effect on IL-6 changes. Conclusion Consumption of opium in CAD patients is associated with higher IL-1Ra levels.
References
[1]
Kleemann R, Zadelaar S, Kooistra T (2008) Cytokines and atherosclerosis: a comprehensive review of studies in mice. Cardiovasc Res.
[2]
Apostolakis S, Vogiatzi K, Krambovitis E, Spandidos DA (2008) IL-1 cytokines in cardiovascular disease: diagnostic, prognostic and therapeutic implications. Cardiovasc Hematol Agents Med Chem 6: 150–158.
[3]
Fiotti N, Giansante C, Ponte E, Delbello C, Calabrese S, et al. (1999) Atherosclerosis and inflammation. Patterns of cytokine regulation in patients with peripheral arterial disease. Atherosclerosis 145: 51–60.
[4]
Biasucci LM, Liuzzo G, Fantuzzi G, Caligiuri G, Rebuzzi AG, et al. (1999) Increasing levels of interleukin (IL)-1Ra and IL-6 during the first 2 days of hospitalization in unstable angina are associated with increased risk of in-hospital coronary events. Circulation 99: 2079–2084.
[5]
Biasucci LM, Vitelli A, Liuzzo G, Altamura S, Caligiuri G, et al. (1996) Elevated levels of interleukin-6 in unstable angina. Circulation 94: 874–877.
[6]
Azimzade-Sarwar B, Yousefzade G, Narooey S (2005) A case-control study of effect of opium addiction on myocardial infarction. American Journal of Applied Sciences 2: 1134–1135.
[7]
Davoodi G, Sadeghian S, Akhondzadeh S, Darvish S, Alidoosti M, et al. (2006) Comparison of Specifications, Short Term Outcome and Prognosis of Acute Myocardial Infarction in Opium Dependent Patients and Nondependents. Journal Of Tehran Heart Center 1: 43–47.
[8]
Sadr Bafghi SM, Rafiei M, Bahadrzadeh L, Namayandeh SM, Soltani MH, et al. (2005) Is opium addiction a risk factor for acute myocardial infarction? Acta Medica Iranica 43: 218–222.
[9]
Peng X, Mosser DM, Adler MW, Rogers TJ, Meissler JJ Jr, et al. (2000) Morphine enhances interleukin-12 and the production of other pro-inflammatory cytokines in mouse peritoneal macrophages. J Leukoc Biol 68: 723–728.
[10]
Wang J, Charboneau R, Balasubramanian S, Barke RA, Loh HH, et al. (2002) The immunosuppressive effects of chronic morphine treatment are partially dependent on corticosterone and mediated by the mu-opioid receptor. J Leukoc Biol 71: 782–790.
[11]
Holan V, Zajicova A, Krulova M, Blahoutova V, Wilczek H (2003) Augmented production of proinflammatory cytokines and accelerated allotransplantation reactions in heroin-treated mice. Clin Exp Immunol 132: 40–45.
[12]
Roy S, Wang J, Gupta S, Charboneau R, Loh HH, et al. (2004) Chronic morphine treatment differentiates T helper cells to Th2 effector cells by modulating transcription factors GATA 3 and T-bet. Journal of Neuroimmunology 147: 78–81.
[13]
Ross R (1993) The pathogenesis of atherosclerosis: a perspective for the 1990s. Nature 362: 801–809.
[14]
Dinarello CA (1996) Biologic basis for interleukin-1 in disease. Blood 87: 2095–2147.
[15]
Arend WP, Smith MF Jr, Janson RW, Joslin FG (1991) IL-1 receptor antagonist and IL-1 beta production in human monocytes are regulated differently. J Immunol 147: 1530–1536.
[16]
Fenton MJ, Buras JA, Donnelly RP (1992) IL-4 reciprocally regulates IL-1 and IL-1 receptor antagonist expression in human monocytes. J Immunol 149: 1283–1288.
[17]
Chomarat P, Vannier E, Dechanet J, Rissoan MC, Banchereau J, et al. (1995) Balance of IL-1 receptor antagonist/IL-1 beta in rheumatoid synovium and its regulation by IL-4 and IL-10. J Immunol 154: 1432–1439.
[18]
Fisher CJ Jr, Slotman GJ, Opal SM, Pribble JP, Bone RC, et al. (1994) Initial evaluation of human recombinant interleukin-1 receptor antagonist in the treatment of sepsis syndrome: a randomized, open-label, placebo-controlled multicenter trial. Crit Care Med 22: 12–21.
[19]
Ikonomidis I, Athanassopoulos G, Lekakis J, Venetsanou K, Marinou M, et al. (2005) Myocardial ischemia induces interleukin-6 and tissue factor production in patients with coronary artery disease: a dobutamine stress echocardiography study. Circulation 112: 3272–3279.
[20]
Ikonomidis I, Stamatelopoulos K, Lekakis J, Vamvakou GD, Kremastinos DT (2008) Inflammatory and non-invasive vascular markers: the multimarker approach for risk stratification in coronary artery disease. Atherosclerosis 199: 3–11.
[21]
Wassmann S, Stumpf M, Strehlow K, Schmid A (2004) Schieffer B, et al (2004) Interleukin-6 induces oxidative stress and endothelial dysfunction by overexpression of the angiotensin II type 1 receptor. Circ Res 94: 534–541.
[22]
Szotowski B, Antoniak S, Poller W, Schultheiss HP, Rauch U (2005) Procoagulant soluble tissue factor is released from endothelial cells in response to inflammatory cytokines. Circ Res 96: 1233–1239.
[23]
Kukielka GL, Smith CW, Manning AM, Youker KA, Michael LH, et al. (1995) Induction of interleukin-6 synthesis in the myocardium. Potential role in postreperfusion inflammatory injury. Circulation 92: 1866–1875.
[24]
Finkel MS, Hoffman RA, Shen L, Oddis CV, Simmons RL, et al. (1993) Interleukin-6 (IL-6) as a mediator of stunned myocardium. Am J Cardiol 71: 1231–1232.
[25]
Deng MC, Erren M, Lutgen A, Zimmermann P, Brisse B, et al. (1996) Interleukin-6 correlates with hemodynamic impairment during dobutamine administration in chronic heart failure. Int J Cardiol 57: 129–134.
[26]
James SK, Oldgren J, Lindback J, Johnston N, Siegbahn A, et al. (2005) An acute inflammatory reaction induced by myocardial damage is superimposed on a chronic inflammation in unstable coronary artery disease. Am Heart J 149: 619–626.
[27]
Fisman EZ, Benderly M, Esper RJ, Behar S, Boyko V, et al. (2006) Interleukin-6 and the risk of future cardiovascular events in patients with angina pectoris and/or healed myocardial infarction. Am J Cardiol 98: 14–18.
[28]
Hoffmeister A, Rothenbacher D, Kunze M, Brenner H, Koenig W (2005) Prognostic value of inflammatory markers alone and in combination with blood lipids in patients with stable coronary artery disease. Eur J Intern Med 16: 47–52.
[29]
Koukkunen H, Penttila K, Kemppainen A, Halinen M, Penttila I, et al. (2001) C-reactive protein, fibrinogen, interleukin-6 and tumour necrosis factor-alpha in the prognostic classification of unstable angina pectoris. Ann Med 33: 37–47.
[30]
Helle M, Brakenhoff JP, De Groot ER, Aarden LA (1988) Interleukin 6 is involved in interleukin 1-induced activities. Eur J Immunol 18: 957–959.
[31]
Kusuhara H, Matsuyuki H, Okumoto T (1997) Effects of nonsteroidal anti-inflammatory drugs on interleukin-1 receptor antagonist production in cultured human peripheral blood mononuclear cells. Prostaglandins 54: 795–804.