The effect of Etofibrate (Lipo-Merz) on "in vitro" cellular immune response and on lipid parameters of men with myocardial infarction and with arteriosclerosis obliterans.
Earlier specific cell-mediated immune reactions and their modulation by different drugs were reported against human vascular antigens in patients with vascular diseases. Presently the effect of Etofibrate (Lipo-Merz) was studied on cellular immune reactions induced by human aorta with lipid plaques and on serum lipid parameters in 46 men with acute myocardial infarction and in 48 men with arteriosclerosis obliterans compared to 40 healthy controls. Leucocyte migration test and lymphocyte-mediated cytotoxicity were repeatedly investigated in the presence of human aortic extract with or without Etofibrate (2 micrograms/50 microliters). The degree of leucocyte migration inhibition and of lymphocyte-mediated cytotoxicity proved to be similar in hypherlipaemic and in normolipaemic groups. Etofibrate could decrease cellular immune reactions both in hyperlipaemic and normolipaemic patients, but its effect was more expressive in the hyperlipaemic than normolipaemic group. Three months later a reduction of cellular immune reactions was found mainly in normolipaemic patients. Ten patients with myocardial infarction and 10 arteriosclerosis obliterans patients were treated with Etofibrate (900 mg/day) for 12 weeks. After therapy, cholesterol, triglycerides, LDL concentrations were reduced, HDL level was increased and the rate of LDL:HDL decreased. Leucocyte migration inhibition and lymphocyte-mediated cytotoxicity were also diminished. This time the cellular immune reactions of treated patients were only slightly reduced "in vitro" by Etofibrate in contrast with non treated hyper- and normolipaemic patients in whom cellular immune reactions were decreased by Etofibrate similarly to the first determinations. On the basis of our observations Etofibrate may be useful in the therapy of arteriosclerotic vascular diseases with or without hyperlipaemia, because it could decrease the cellular sensitization against aortic tissue.
Horváth
M
M
3rd Department of Medicine, Semmelweis Medical University, Budapest, Hungary.
Varsányl
M
M
Jovanovich
N
N
Romics
L
L
Gerö
S
S
D000328:Adult; D000368:Aged; D001011:Aorta / Q000276:immunology; D001162:Arteriosclerosis Obliterans / Q000097:blood / Q000276:immunology*; D002464:Cell Migration Inhibition; D002994:Clofibrate / Q000031:analogs & derivatives*; D002995:Clofibric Acid / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use; D003601:Cytotoxicity Tests, Immunologic; D006801:Humans; D006949:Hyperlipidemias / Q000097:blood / Q000188:drug therapy / Q000276:immunology*; D000960:Hypolipidemic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D007111:Immunity, Cellular / Q000187:drug effects*; D008055:Lipids / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000276:immunology*; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology
D000960:Hypolipidemic Agents; D008055:Lipids; C009746:etofibrate; D002995:Clofibric Acid; D002994:Clofibrate