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Dermatology 1999

Autoantibodies against oxidatively modified low-density lipoprotein in patients with Behçet's disease.

Straipsnius versti gali tik registruoti vartotojai
Prisijungti Registracija
Nuoroda įrašoma į mainų sritį
A Orem
G Cimşit
O Değer
B Vanizor
S C Karahan

Raktažodžiai

Santrauka

BACKGROUND

Change of lipids and lipoprotein metabolism and an imbalance of the oxidant-antioxidant system related to the disease activity have been reported in Behçet's disease. Therefore, there is a tendency of oxidative modification of lipids and lipoproteins in patients with the disease.

OBJECTIVE

To investigate serum autoantibodies against oxidatively modified low-density lipoprotein (oxLDL) as a marker for the degree of in vivo oxidation of lipoproteins in Behçet's disease.

METHODS

Serum autoantibodies against oxLDL, total cholesterol, triacylglycerol, HDL cholesterol, LDL cholesterol, apolipoprotein (Apo) AI, Apo B, alpha1-antitrypsin, alpha2-macroglobulin and erythrocyte sedimentation rate were determined in 37 patients and 30 sex- and age-matched healthy volunteers. Autoantibodies against oxLDL were measured by a commercial enzyme-linked immunosorbent assay.

RESULTS

Serum autoantibody levels against oxLDL were significantly higher in patients than in controls (425 +/- 365 and 187 +/- 132 mU/ml, respectively; p < 0.05). The levels of autoantibodies against oxLDL in the patients were found to correlate with total cholesterol, LDL cholesterol, HDL cholesterol and alpha1-antitrypsin levels (r = 0.38, p < 0.05; r = 0.42, p < 0.05; r = -0.38, p < 0.05; r = 0.42, p < 0. 05, respectively).

CONCLUSIONS

It has been shown in previous studies that high autoantibody titers against oxLDL may be important in diseases with atherosclerosis as seen in systemic lupus erythematosus and rheumatoid arthritis. High autoantibody titers against oxLDL are not specific for Behçet's disease but probably important for pathologic processes in the disease. We suggest that increased levels of autoantibodies against oxLDL may be a factor responsible for endothelial dysfunction and development of vascular pathology in Behçet's disease.

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