الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
SLE patients have an increased frequency of traditional risk factors for CVD, such as hypertension, dyslipidemia, obesity, and diabetes mellitus and nontraditional risk factors as homocysteine. This would most likely be further increased in LN, as these patients may be hypertensive, and have hyperlipidemia related to steroids, nephrotic syndrome and chronic renal impairment. Abnormal lipid profile has been reported in SLE and Lp (a) has been reported to elevate in lupus nephritis.
The aim of this work is to assess lipid status and oxidative stress in different groups of SLE and the effect of different drug regimen and disease activity on the studied parameters. Also, this work aims to study the effect of disease pathogenesis on internal lipid distribution in the major lipoprotein classes.
The present study included 120 SLE adult patients (104 females and 16 males) selected from Internal Medicine Department and Rheumatology and Rehabilitation outpatient Clinic of Mansoura University Hospital between August 2009 and May 2011. Thirty healthy subjects with matched age, sex and BMI were included as healthy controls.
It was found that:
Dyslipidemia in SLE include elevated TC, TG, LDL-C, ox- LDL, MDA, and reduced HDL-C and its associated anti-oxidant component Apo A-1.
SLE causes qualitative disturbance in different lipoprotein classes in the form of increased TG content in relation to their cholesterol content.
Increased levels of oxidant status in the form of MDA and ox-LDL promote LDL and other lipoprotein oxidation that pave the way to premature atherosclerosis in SLE
SLE complication, disease activity, as well as drug therapy all together contributes to dyslipidemia and hence cardiovascular risk associated with SLE.
Elevation of Lp (a) which is considered an independent risk factor for CVD could share in premature atheroscelerosis in these patients.