الفهرس 
Pathogenesis of Systemic Lupus ErythematosusOnly 14 pages are availabe for public view
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Abstract
Objective: To study the lipid profile in systemic lupus erythematosus
(SLE) patients and to correlate it with various disease activity parameters.
Patients and methods: 48 female SLE patients fulfilling the updated
ACR 1997 revised criteria for classification of SLE were subjected to:
Full history taking, clinical examination and routine laboratory tests to
assess SLE including: Complete blood count, erythrocyte sedimentation
rate, liver function tests, kidney function tests, complement components,
complete urine analysis and fasting lipid profile. Total cholesterol (TC)
and triglycerides (TG) were measured in plasma by the calometric
method. High density lipid cholesterol (HDL-C) was measured using
direct HDL method (Hitachi 917). Low density lipid cholesterol (LDL-C)
and very low density lipid cholesterol (VLDL) were calculated using
formulas LDL-C= TC – (TG/2.2+ HDL-C) and VLDL= TG × 0.45.
Systolic and diastolic blood pressures were measured.
Results: Hypercholesterolemia (>200mg/dl) was present in 23 patients
(47.9%). Lupus nephritis was detected in 38 patients (79.1%),
hematological disorders were found in 33 patients (68.75%), joint
affection in 27 patients (56.3%), muco-cutaneous lesions in 25 patients
(52%), hypertension in 24 patients (50%), respiratory affection and
Raynauds’ in 15 patients each (31.3%) and cardiovascular affection in 6
patients (12.5%). Systemic lupus activity measure (SLAM) index
correlated significantly with TG (r=0.295, p=0.041) and with VLDL
(r=0.296, p=0.041) respectively. A significant negative correlation was
found between SLAM and C3 level (r=-0.403, p=0.004) and between
SLAM and administration of antimalarial drugs (r=-0.0297, p=0.041). HDL-C was negatively correlated with the SLAM score, however, the
correlation did not reach statistical significance (r=-0.079, p=0.598).
Correlation of the lipid profile with C3, C4, ESR and platelet levels did
not reach statistical significance.
Conclusion: Disease activity correlated with elevated TG and VLDL
levels. An oral steroid dose of ≤ 10 mg/d was associated with a lower
lipid profile than that of patients not receiving any steroids. On increasing
the dose to > 10 mg/d all the lipid components showed an increase which
was statistically insignificant. Patients not receiving antimalarial drugs
showed higher plasma lipid levels than those receiving the drug. There
was a further decrease in TG, VLDL and HDL-C levels on increasing the
antimalarial dose from 200mg/d to 400 mg/d. However, the difference in
plasma lipid levels between the two doses did not reach statistical
significance.