ЛИПИД-БЕЛКОВЫЕ СИСТЕМЫ ТРАНСПОРТА ХОЛЕСТЕРИНА КРОВИ У БОЛЬНЫХ СИСТЕМНОЙ КРАСНОЙ ВОЛЧАНКОЙ В ЗАВИСИМОСТИ ОТ АНТИФОСФОЛИПИДНОГО СИНДРОМА

2001 
Objective. To stude the indices of lipid-protein blood spectrum in SLE pts with A PS as one of the risk factors of atherosclerosis development. Material and methods. 60 pts (45 females and 15 males) with definite SLE (ARA criteria, 1982) were examined; age 15-44 (median age 28.9+8.1; M+G), disease duration from 2 months to 28 years (median 8.6+6.6 years) APS was diagnosed in 39 out of them( G.R.V.Huges and E.N.Harris criteria, 1986) with subsequent isolation of Wr' -wKable, possible and unreliable A PS; thrombotic complications were observed in 23 out of 39 SLE pts with APS. Control group was composed of 35 practically healthy persons without risk factors of atherosclerosis and related diseases development. Results. There were no difference in the levels of cholesterol, triglycerides low density lipoproteid cholesterol and apolipoprotein В in SLE pts with APS as compared with SLE pts without APS. Concentration of high density lipoproteid cholesterol (HD LP C) and apolipoprotein AI (apo A!) was higher in SLE pts with APS as compared with SLE pis without APS and reached for HD LPC- 46. I±11.0mg/dl against 40.5±8.1 mg/dl, for apoAl - 133.7±28.1 tng/cll against 118.5±28.2 mg/dl correspondingly (p=0.04 and p-0.05). There was no difference in the content oJHD LP phospholipids in the group of SLE pts with and without APS. The level ofHD LP phospholipids in the group of SLE pts with APS was lower (91, 8±21.2 mg/dl) as compared to the control group (131.8+3 5.1 mg/dl)(p=0.001), The relation ofHD LP С/apoAl in SLE pts with APS: 0.35+0.06 against 0.38±0.08 in persons from the control group (p-0.04). With the decreased level ofHD LP in basic groups of pts as,compared with control statistically reliable difference of all HD LP phospholipids was found (p<0.001). Иге level of apoAl was lower in pts with unreliable APS as compared with such in pts with definite APS (137.4+26,6 mg/dl and 103.8±23.5 mg/dl (p-0.002). Conclusion. In SLE pts with APS there are interrelated pathogenic mechanisms, which could lead to thrombotic complications as well as to atherosclerotic vascular damage.
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