[Tumor necrosis factor alpha and its soluble receptors in serum of patients with coronary artery disease].
TNF-alpha as a pleiotropic, proinflammatory cytokine seems to play a role in the pathogenesis of atherosclerosis and coronary artery disease (CAD). TNF-alpha is binding to two cell surface receptors and its serum activity is modified by soluble forms of these receptors: sTNF-R I and sTNF-R II. The aim of this study was to assess serum concentrations of TNF-alpha, sTNF-R I and sTNF-R II in patients (pts) with CAD. We examined serum concentrations of TNF-alpha, sTNF-R I and sTNF-R II by ELISA in: 45 pts with stable exertional angina (group I); 32 pts with unstable angina (group II) within 6, 24, and 48 h after the chest pain; and 23 pts before and 6, 24, and 48 h after PTCA (group III). The control group (group C) consisted of 20 healthy subjects. We evaluated: clinical state of patients and results of some diagnostic examinations (lipids, ECG, echocardiography, coronary angiography). Mean serum concentrations of TNF-alpha were significantly higher in pts ith CAD (group I: 18.25 +/- 5.5 pg/ml; group II: 17.24 +/- 4.0 pg/ml; group III: 18.70 +/- 0.6 pg/ml; p < 0.001) than in healthy pts (8.31 +/- 1.4 pg/ml). In turn mean serum concentrations of sTNF-R I were significantly higher both in group I (1399.6 +/- 536.3 pg/ml; p < 0.05) and III (1544.0 +/- 391.4 pg/ml; p < 0.01) than in control group (1093.9 +/- 456.9 pg/ml). There were not differences in mean serum concentrations of sTNF-R II. We found no differences between mean serum concentrations of TNF-alpha, sTNF-R I and sTNF-R II either after the chest pain (group II); or before and after PTCA (group III). In group I mean TNF-alpha correlated with serum triglycerides and HDL-cholesterol (r = 0.412 and r = -0.424; p < 0.01); sTNF-R I correlated with LDL-cholesterol (r = -0.309; p < 0.05); and sTNF-R II correlated with total cholesterol and LDL-cholesterol (r = 0.311 and r = 0.316; p < 0.05). The serum concentrations of TNF-alpha are increased in patients with CAD, but this does not reflect the clinical state of patients. In pts with stable angina these increased levels of TNF-alpha may be accompanied with higher concentrations of sTNF-R I--it seems to be the compensatory mechanism in long-term atherosclerosis. Lipid disturbances may influence the cytokines metabolism in pts with CAD.
Mizia-Stec
K
K
II Katedra i Zakład Patofizjologii Sl. AM w Katowicach.
Mandecki
T
T
Zahorska-Markiewicz
B
B
Janowska
J
J
Szulc
A
A
Jastrzebska-Maj
E
E
Szymański
L
L
D015906:Angioplasty, Balloon, Coronary; D003327:Coronary Disease / Q000097:blood* / Q000601:surgery; D004562:Electrocardiography; D004797:Enzyme-Linked Immunosorbent Assay; D000068800:Etanercept; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood*; D008297:Male; D008875:Middle Aged; D018124:Receptors, Tumor Necrosis Factor / Q000097:blood*; D014280:Triglycerides / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
D007074:Immunoglobulin G; D018124:Receptors, Tumor Necrosis Factor; D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha; D000068800:Etanercept