Abstract
Patients with systemic lupus erythematosus are at increased risk for premature atherosclerosis. We examined one possible etiologic factor, dyslipoproteinemia, both before and after corticosteroid therapy. We identified 2 distinct patterns of dyslipoproteinemia. One is attributable to active disease; the other is attributable, in part, to corticosteroid therapy. The dyslipoprotinemia of active disease consists of depressed high density lipoprotein cholesterol and apoprotein A-I with elevated very low density lipoprotein cholesterol and triglyceride, while the dyslipoproteinemia after corticosteroid therapy consists of increased total cholesterol, very low density lipoprotein cholesterol, and triglyceride. The possible pathophysiologic mechanisms responsible for these patterns, as well as the possible roles in premature atherosclerosis seen in systemic lupus erythematosus patients, are discussed.
Original language | English (US) |
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Pages (from-to) | 859-863 |
Number of pages | 5 |
Journal | Arthritis and Rheumatism |
Volume | 31 |
Issue number | 7 |
State | Published - 1988 |
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ASJC Scopus subject areas
- Immunology
- Rheumatology
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Dyslipoproteinemia in pediatric systemic lupus erythematosus. / Ilowite, Norman Todd; Samuel, P.; Ginzler, E.; Jacobson, M. S.
In: Arthritis and Rheumatism, Vol. 31, No. 7, 1988, p. 859-863.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Dyslipoproteinemia in pediatric systemic lupus erythematosus
AU - Ilowite, Norman Todd
AU - Samuel, P.
AU - Ginzler, E.
AU - Jacobson, M. S.
PY - 1988
Y1 - 1988
N2 - Patients with systemic lupus erythematosus are at increased risk for premature atherosclerosis. We examined one possible etiologic factor, dyslipoproteinemia, both before and after corticosteroid therapy. We identified 2 distinct patterns of dyslipoproteinemia. One is attributable to active disease; the other is attributable, in part, to corticosteroid therapy. The dyslipoprotinemia of active disease consists of depressed high density lipoprotein cholesterol and apoprotein A-I with elevated very low density lipoprotein cholesterol and triglyceride, while the dyslipoproteinemia after corticosteroid therapy consists of increased total cholesterol, very low density lipoprotein cholesterol, and triglyceride. The possible pathophysiologic mechanisms responsible for these patterns, as well as the possible roles in premature atherosclerosis seen in systemic lupus erythematosus patients, are discussed.
AB - Patients with systemic lupus erythematosus are at increased risk for premature atherosclerosis. We examined one possible etiologic factor, dyslipoproteinemia, both before and after corticosteroid therapy. We identified 2 distinct patterns of dyslipoproteinemia. One is attributable to active disease; the other is attributable, in part, to corticosteroid therapy. The dyslipoprotinemia of active disease consists of depressed high density lipoprotein cholesterol and apoprotein A-I with elevated very low density lipoprotein cholesterol and triglyceride, while the dyslipoproteinemia after corticosteroid therapy consists of increased total cholesterol, very low density lipoprotein cholesterol, and triglyceride. The possible pathophysiologic mechanisms responsible for these patterns, as well as the possible roles in premature atherosclerosis seen in systemic lupus erythematosus patients, are discussed.
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M3 - Article
C2 - 3134897
AN - SCOPUS:0023792957
VL - 31
SP - 859
EP - 863
JO - Arthritis and Rheumatology
JF - Arthritis and Rheumatology
SN - 2326-5191
IS - 7
ER -